You searched for subject:(MyoD).
Showing records 1 – 30 of
37 total matches.
◁ [1] [2] ▶
Duke University
1.
Kabadi, Ami Meda.
Engineering Transcription Factors to Program Cell Fate Decisions
.
Degree: 2015, Duke University
URL: http://hdl.handle.net/10161/9831 
► Technologies for engineering new functions into proteins are advancing biological research, biotechnology, and medicine at an astounding rate. Building on fundamental research of natural…
(more)
▼ Technologies for engineering new functions into proteins are advancing biological research, biotechnology, and medicine at an astounding rate. Building on fundamental research of natural protein structure and function, scientists are identifying new protein domains with previously undescribed properties and engineering new proteins with expanded functionalities. Such tools are enabling the precise study of fundamental aspects of cellular behavior and the development of a new class of gene therapies that manipulate the expression of endogenous genes. The applications of these gene regulation technologies include but are not limited to controlling cell fate decisions, reprogramming cell lineage commitment, monitoring cellular states, and stimulating expression of therapeutic factors. While the field has come a long way in the past 20 years, there are still many limitations. Historically, gene therapy and gene replacement therapies have relied on over-expression of natural transcription factors that activate specific endogenous gene networks. However, natural transcription factors are often inadequate for generating efficient, fast, and homogenous cellular responses. Furthermore, most natural transcription factors have complex structures and functions that are difficult to improve or alter by rational design. This thesis presents three novel and widely applicable methods for engineering transcription factors for programming cell fate decisions in primary human cells.
MyoD is the master transcription factor defining the myogenic lineage. Expression of
MyoD in certain non-myogenic lineages induces a coordinated change in differentiation state. We use
MyoD as a model for developing our protein engineering techniques because myogenesis is a well-studied pathway that is characterized by an easily detected change in phenotype from mono-nucleated to multinucleated cells. Furthermore, efficient generation of myocytes in vitro presents an attractive patient-specific method by which to treat muscle-wasting diseases such as muscular dystrophy. We first demonstrate that we can improve the ability of
MyoD to convert human dermal fibroblasts and human adipose-derived stem cells into myocyte-like cells. By fusing potent modular activation domains to the
MyoD protein, we increased myogenic gene expression, myofiber formation, cell fusion, and global reprogramming of the myogenic gene network. The engineered
MyoD transcription factor induced myogenisis in a little as ten days, a process that takes three or more weeks with the natural
MyoD protein. While increasing the potency of transcriptional activation is one mechanism by which to improve transcription factor function, there are many other possible routes such as increasing DNA-binding affinity, increasing protein stability, altering interactions with co-factors, or inducing post-translational modifications. Endogenous regulatory pathways are complex, and it is difficult to predict specific amino acid changes that will produce the desired outcome. Therefore, we…
Advisors/Committee Members: Gersbach, Charles A (advisor).
Subjects/Keywords: Biomedical engineering;
MyoD;
Myogenesis;
Transcription Factor
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Kabadi, A. M. (2015). Engineering Transcription Factors to Program Cell Fate Decisions
. (Thesis). Duke University. Retrieved from http://hdl.handle.net/10161/9831
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Kabadi, Ami Meda. “Engineering Transcription Factors to Program Cell Fate Decisions
.” 2015. Thesis, Duke University. Accessed February 28, 2021.
http://hdl.handle.net/10161/9831.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Kabadi, Ami Meda. “Engineering Transcription Factors to Program Cell Fate Decisions
.” 2015. Web. 28 Feb 2021.
Vancouver:
Kabadi AM. Engineering Transcription Factors to Program Cell Fate Decisions
. [Internet] [Thesis]. Duke University; 2015. [cited 2021 Feb 28].
Available from: http://hdl.handle.net/10161/9831.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Kabadi AM. Engineering Transcription Factors to Program Cell Fate Decisions
. [Thesis]. Duke University; 2015. Available from: http://hdl.handle.net/10161/9831
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
2.
Scionti, Isabella.
Epigenetic Regulation of Skeletal Muscle Differentiation : Régulation épigénétique de la différenciation du muscle squelettique.
Degree: Docteur es, Biologie, 2017, Lyon
URL: http://www.theses.fr/2017LYSEN084
► LSD1 et PHF2 sont des déméthylases de lysines capables de déméthyler à la fois les protéines histones qui influencent l’expression génique et les protéines non…
(more)
▼ LSD1 et PHF2 sont des déméthylases de lysines capables de déméthyler à la fois les protéines histones qui influencent l’expression génique et les protéines non histones en affectant leurs activités ou stabilités. Des approches fonctionnelles d’inactivation de Lsd1 ou Phf2 chez la souris ont démontré l’implication de ces enzymes dans l'engagement des cellules progénitrices au cours de la différenciation. La myogenèse est l'un des exemples les mieux caractérisés sur la façon dont les cellules progénitrices se multiplient et se différencient pour former un organe fonctionnel. Elle est initiée par une expression temporelle spécifique des gènes régulateurs cibles. Parmi ces facteurs, MYOD est un régulateur clé de l'engagement dans la différenciation des cellules progénitrices musculaires. Bien que l’action de MYOD au cours de la différenciation cellulaire ait été largement étudiée, peu de chose sont connus sur les événements de remodelage de la chromatine associés à l'activation de l'expression de MyoD. Parmi les régions régulatrices de l'expression de MyoD, la région Core Enhancer (CE) qui est transcrite en ARN activateur non codant (CEeRNA) a été démontrée pour contrôler l'initiation de l'expression de MyoD au cours de l'engagement de myoblastes dans la différenciation.Nous avons identifié LSD1 et PHF2 comme des activateurs clés du CE de MyoD. L'invalidation in vitro et in vivo de LSD1 ou l'inhibition de l'activité enzymatique de LSD1 empêche le recrutement de l'ARN PolII sur le CE, empêchant l’expression du CEeRNA. D’après nos résultats, l'expression forcée du CEeRNA restaure efficacement l'expression de MyoD et la fusion myoblastique en l'absence de LSD1. De plus, PHF2 interagit avec LSD1 en régulant sa stabilité protéique.En effet, l'ablation in vitro de PHF2 entraîne une dégradation massive de LSD1 et donc une absence d'expression du CEeRNA. Cependant, toutes les modifications d'histones qui ont lieu dans la région du CE lors de l'activation de la différenciation ne peuvent pas être directement attribuées à l'activité enzymatique de LSD1 ou PHF2. Ces résultats soulèvent la question de l'identité des partenaires de LSD1 et PHF2, qui co-participeraient à l'expression du CEeRNA et donc à l'engagement des myoblastes dans la différenciation cellulaire.
LSD1 and PHF2 are lysine de-methylases that can de-methylate both histone proteins, influencing gene expression and non-histone proteins, affecting their activity or stability. Functional approaches using Lsd1 or Phf2 inactivation in mouse have demonstrated the involvement of these enzymes in the engagement of progenitor cells into differentiation. One of the best-characterized examples of how progenitor cells multiply and differentiate to form functional organ is myogenesis. It is initiated by the specific timing expression of the specific regulatory genes; among these factors, MYOD is a key regulator of the engagement into differentiation of muscle progenitor cells. Although the action of MYOD during muscle differentiation has been extensively studied, still little is…
Advisors/Committee Members: Schaeffer, Laurent (thesis director).
Subjects/Keywords: LSD1; PHF2; MyoD; ARN enhancer; Muscle; Différenciation; LSD1; PHF2; MyoD; RNA enhancer; Muscle; Differenciation
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Scionti, I. (2017). Epigenetic Regulation of Skeletal Muscle Differentiation : Régulation épigénétique de la différenciation du muscle squelettique. (Doctoral Dissertation). Lyon. Retrieved from http://www.theses.fr/2017LYSEN084
Chicago Manual of Style (16th Edition):
Scionti, Isabella. “Epigenetic Regulation of Skeletal Muscle Differentiation : Régulation épigénétique de la différenciation du muscle squelettique.” 2017. Doctoral Dissertation, Lyon. Accessed February 28, 2021.
http://www.theses.fr/2017LYSEN084.
MLA Handbook (7th Edition):
Scionti, Isabella. “Epigenetic Regulation of Skeletal Muscle Differentiation : Régulation épigénétique de la différenciation du muscle squelettique.” 2017. Web. 28 Feb 2021.
Vancouver:
Scionti I. Epigenetic Regulation of Skeletal Muscle Differentiation : Régulation épigénétique de la différenciation du muscle squelettique. [Internet] [Doctoral dissertation]. Lyon; 2017. [cited 2021 Feb 28].
Available from: http://www.theses.fr/2017LYSEN084.
Council of Science Editors:
Scionti I. Epigenetic Regulation of Skeletal Muscle Differentiation : Régulation épigénétique de la différenciation du muscle squelettique. [Doctoral Dissertation]. Lyon; 2017. Available from: http://www.theses.fr/2017LYSEN084
3.
Roberto Farina Piovesan.
Efeito do anabolizante decanoato de nandrolona na expressão de marcadores miogênicos e no processo de reparo muscular após criolesão.
Degree: 2010, Universidade Nove de Julho
URL: http://www4.uninove.br/tedeSimplificado/tde_busca/arquivo.php?codArquivo=395
► O objetivo desse estudo foi analisar o efeito do anabolizante esteróide decanoato de nandrolona sobre o reparo muscular e a expressão de marcadores miogenicos após…
(more)
▼ O objetivo desse estudo foi analisar o efeito do anabolizante esteróide decanoato de nandrolona sobre o reparo muscular e a expressão de marcadores miogenicos após criolesão em músculo esquelético de ratos. Foram utilizados 100 ratos Wistar machos divididos em 4 grupos sendo: (1) Controle (n=10); (2) controle sham (n=10) apenas submetido a incisão e exposição do músculo tibial anterior, (3) Criolesionados e tratados com anabolizante e sacrificados após 1, 7, 14 e 21 dias (n=40); (4) Criolesionados e tratados com veículo e sacrificados após 1, 7, 14 e 21 dias (n=40). O tratamento com o anabolizante consistiu de injeções de Decanoato de nandrolona intramuscular duas vezes por semana 5mg/kg. Os animais foram sacrificados e o TA foi removido para a extração do RNA total para análise da expressão de MyoD e miogenina por PCR em tempo real e para a análise morfológica do processo de reparo utilizando a coloração com hematoxilina-eosina. Os resultados evidenciaram um aumento significativo de RNAm de Myod no grupo 7 dias criolesionado e tratado com anabolizante quando comparado ao seu respectivo grupo sem criolesão e tratado com anabolizante e aos grupos veículo com ou sem lesão, neste mesmo período. Com relação a miogenina, após 21 dias foi possível verificar um aumento significativo em sua expressão no grupo lesão tratado com anabolizante em comparação aos demais grupos deste mesmo período. A análise morfológica permitiu verificar que após 7 dias houve ausência de edema e mionecrose e em 14 dias ausência de edema e infiltrado inflamatório somente no grupo com lesão e tratado com anabolizante em comparação aos demais grupos do mesmo período. Em conclusão, o anabolizante Decanoato de Nandrolona acelera o processo de reparo tecidual em ratos machos após criolesão e induz um aumento significativo na expressão de MyoD após 7 dias e de miogenina após 21 dias de lesão.
The objective of this study was to analyze the effect of the anabolic steroid nandrolone decanoate on muscle repair and expression of myogenic markers after cryolesion in rat skeletal muscle. We studied 100 male Wistar rats were divided into four groups: (1) Control (n = 10), (2) sham control (n = 10) only underwent incision and exposure of the anterior tibial muscle (3) and cryolesioned treated with anabolic and sacrificed after 1, 7, 14 and 21 days (n = 40), (4) cryolesioned and treated with vehicle and sacrificed after 1, 7, 14 and 21 days (n = 40). Treatment with steroid injections consisted of Nandrolone decanoate intramuscular 5mg/kg twice a week. The animals were sacrificed and the TA was removed for total RNA extraction for analysis of MyoD and myogenin by real time PCR and morphological analysis of the repair process using hematoxylin-eosin. The results showed a significant increase in MyoD mRNA in group cryolesioned 7 days and treated with steroid compared to its respective group without cryolesion and treated with steroid and vehicle groups with or without injury, this same period. With respect to myogenin, 21 days after it was verified a significant…
Advisors/Committee Members: Kristiane Santos Porta Fernandes, Manoela Domingues Martins, Flávio Aimbire Soares de Carvalho, Raquel Agnelli Mesquita Ferrari, José António Silva Júnior.
Subjects/Keywords: Miogenina.; OUTROS; Muscle Injury; Cryolesion; Decanoate Nandrolone; Myod; Lesão muscular; Criolesão; Decanoato de Nandrolona; Myogenin.; Myod
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Piovesan, R. F. (2010). Efeito do anabolizante decanoato de nandrolona na expressão de marcadores miogênicos e no processo de reparo muscular após criolesão. (Thesis). Universidade Nove de Julho. Retrieved from http://www4.uninove.br/tedeSimplificado/tde_busca/arquivo.php?codArquivo=395
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Piovesan, Roberto Farina. “Efeito do anabolizante decanoato de nandrolona na expressão de marcadores miogênicos e no processo de reparo muscular após criolesão.” 2010. Thesis, Universidade Nove de Julho. Accessed February 28, 2021.
http://www4.uninove.br/tedeSimplificado/tde_busca/arquivo.php?codArquivo=395.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Piovesan, Roberto Farina. “Efeito do anabolizante decanoato de nandrolona na expressão de marcadores miogênicos e no processo de reparo muscular após criolesão.” 2010. Web. 28 Feb 2021.
Vancouver:
Piovesan RF. Efeito do anabolizante decanoato de nandrolona na expressão de marcadores miogênicos e no processo de reparo muscular após criolesão. [Internet] [Thesis]. Universidade Nove de Julho; 2010. [cited 2021 Feb 28].
Available from: http://www4.uninove.br/tedeSimplificado/tde_busca/arquivo.php?codArquivo=395.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Piovesan RF. Efeito do anabolizante decanoato de nandrolona na expressão de marcadores miogênicos e no processo de reparo muscular após criolesão. [Thesis]. Universidade Nove de Julho; 2010. Available from: http://www4.uninove.br/tedeSimplificado/tde_busca/arquivo.php?codArquivo=395
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Universiteit Utrecht
4.
Bourajjaj, M.
Nuclear Factor of Activated T cells (NFAT): key regulator of cardiac hypertrophy and skeletal muscle adaptation.
Degree: 2008, Universiteit Utrecht
URL: http://dspace.library.uu.nl:8080/handle/1874/29300
► Despite significant progress in the prevention and treatment of cardiovascular diseases, heart failure is still a leading cause of morbidity and mortality in industrial countries.…
(more)
▼ Despite significant progress in the prevention and treatment of cardiovascular diseases, heart failure is still a leading cause of morbidity and mortality in industrial countries. Sustained cardiac hypertrophy, which is defined as an increase in heart size resulting from an increase in cardiomyocyte cell volume, has been recognized as the single most important risk factor for heart failure development. Cardiac hypertrophy can be initiated by a wide array of (neuro/humoral) growth factors in response to increased workload, injury, or intrinsic defects in contractile performance. To understand the molecular determinants of the hypertrophic response and to achieve future rational drug design to treat heart failure, investigation currently focuses on identifying and characterizing intracellular signal transduction pathways in the heart. The experiments presented in this thesis focus on a signaling pathway which plays a role in the hypertrophic transcriptional response of the myocyte. This signaling route employs the Ca2+-calmodulin-dependent phosphatase calcineurin and its immediate downstream transcriptional effector Nuclear Factor of Activated T-cells (NFAT), and further focuses on the immediate downstream NFAT target genes in cardiac muscle.
Subjects/Keywords: Geneeskunde; cardiac hypertrophy; heart failure; calcineurin; NFAT; myogenesis; MyoD
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Bourajjaj, M. (2008). Nuclear Factor of Activated T cells (NFAT): key regulator of cardiac hypertrophy and skeletal muscle adaptation. (Doctoral Dissertation). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/29300
Chicago Manual of Style (16th Edition):
Bourajjaj, M. “Nuclear Factor of Activated T cells (NFAT): key regulator of cardiac hypertrophy and skeletal muscle adaptation.” 2008. Doctoral Dissertation, Universiteit Utrecht. Accessed February 28, 2021.
http://dspace.library.uu.nl:8080/handle/1874/29300.
MLA Handbook (7th Edition):
Bourajjaj, M. “Nuclear Factor of Activated T cells (NFAT): key regulator of cardiac hypertrophy and skeletal muscle adaptation.” 2008. Web. 28 Feb 2021.
Vancouver:
Bourajjaj M. Nuclear Factor of Activated T cells (NFAT): key regulator of cardiac hypertrophy and skeletal muscle adaptation. [Internet] [Doctoral dissertation]. Universiteit Utrecht; 2008. [cited 2021 Feb 28].
Available from: http://dspace.library.uu.nl:8080/handle/1874/29300.
Council of Science Editors:
Bourajjaj M. Nuclear Factor of Activated T cells (NFAT): key regulator of cardiac hypertrophy and skeletal muscle adaptation. [Doctoral Dissertation]. Universiteit Utrecht; 2008. Available from: http://dspace.library.uu.nl:8080/handle/1874/29300
University of Minnesota
5.
Lee, Catherine Ann Alsager.
Isolation and identification of De Novo long noncoding
RNAs from mouse myoblasts and embryonic stem cells.
Degree: MS, Stem Cell Biology, 2013, University of Minnesota
URL: http://purl.umn.edu/146424
► University of Minnesota M.S. thesis. January 2013. Major: Stem Cell Biology. Advisor: Nobuaki Kikyo. 1 computer file (PDF); vii, 46 pages.
Long noncoding RNAs (lncRNAs)…
(more)
▼ University of Minnesota M.S. thesis. January 2013.
Major: Stem Cell Biology. Advisor: Nobuaki Kikyo. 1 computer file
(PDF); vii, 46 pages.
Long noncoding RNAs (lncRNAs) are a pervasive class
of transcripts whose importance and biological relevance are only
beginning to be elucidated. LncRNAs have been detected in nearly
every cell type and found to be fundamentally involved in many
biological processes; however, studies that characterize lncRNA
expression during certain periods of development are largely
missing. Here, we demonstrate how a pool of potentially relevant
lncRNAs can be identified using a RNA-chromatin immunoprecipitation
(RNA-ChIP) technique that pulls down sufficient amount of RNA to
send for sequencing. In our initial experiment, we attempted to
identify lncRNAs bound to the MyoD protein in myoblast cells;
however, the lack of immunoprecipitation-compatible highly specific
antibodies against MyoD prevented us from pursuing this project. As
an alternative, we successfully identified lncRNAs bound to the
histone-modifying complex COMPASS, as well as those bound to the
master pluripotency factors Oct4 and Sox2 in mouse embryonic stem
cells. This study provides a proof-of-principle to identify lncRNAs
potentially involved in chromatin regulation of
pluripotency.
Advisors/Committee Members: Nobuaki Kikyo.
Subjects/Keywords: ChIP; MyoD; Pluripotency; RNA-ChIP; RNA-seq; Trithorax-group
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Lee, C. A. A. (2013). Isolation and identification of De Novo long noncoding
RNAs from mouse myoblasts and embryonic stem cells. (Masters Thesis). University of Minnesota. Retrieved from http://purl.umn.edu/146424
Chicago Manual of Style (16th Edition):
Lee, Catherine Ann Alsager. “Isolation and identification of De Novo long noncoding
RNAs from mouse myoblasts and embryonic stem cells.” 2013. Masters Thesis, University of Minnesota. Accessed February 28, 2021.
http://purl.umn.edu/146424.
MLA Handbook (7th Edition):
Lee, Catherine Ann Alsager. “Isolation and identification of De Novo long noncoding
RNAs from mouse myoblasts and embryonic stem cells.” 2013. Web. 28 Feb 2021.
Vancouver:
Lee CAA. Isolation and identification of De Novo long noncoding
RNAs from mouse myoblasts and embryonic stem cells. [Internet] [Masters thesis]. University of Minnesota; 2013. [cited 2021 Feb 28].
Available from: http://purl.umn.edu/146424.
Council of Science Editors:
Lee CAA. Isolation and identification of De Novo long noncoding
RNAs from mouse myoblasts and embryonic stem cells. [Masters Thesis]. University of Minnesota; 2013. Available from: http://purl.umn.edu/146424
University of Ottawa
6.
Liu, Yubing.
The Role of Six1 in Transcriptional Regulation during Myogenesis
.
Degree: 2017, University of Ottawa
URL: http://hdl.handle.net/10393/35952
► Skeletal myogenesis is under the control of a combinatorial network of transcription factors. It has been shown that the homeobox protein Six1 is required for…
(more)
▼ Skeletal myogenesis is under the control of a combinatorial network of transcription factors. It has been shown that the homeobox protein Six1 is required for embryonic myogenesis. Using functional genomics approaches, I determined that Six1 is required for myoblasts differentiation through direct binding to a cluster of genes that are related to muscle function and muscle structure during my Master’s studies. However, it was still not fully understood how Six1 selects its genomic targets and whether Six1 regulates the expression of Myod directly. I devoted my PhD work to study three central aspects of Six1 function: through what DNA motif it binds to DNA, how it regulates the expression of the myogenic regulatory factor MyoD, and how it might regulate chromatin structure at the enhancer regions of muscle genes. A more degenerate MEF3-like DNA sequence consensus has been identified from Six1 ChIP-on-chip experiments. This MEF3 motif was further optimized using bioinformatic methods and was proved to discover Six1 binding sites with improved specificity and sensitivity. Myod, a member of myogenic regulatory factors (MRFs), is a master regulator in the myogenic lineage. Multiple MEF3 sites were identified on the regulatory regions of Myod, including two MEF3 sites within its core enhancer region (CER). Six1 was able to bind to the CER directly through these two MEF3 sites and regulated the Myod expression in cultured primary myoblasts. Previous work has suggested that the CER is also bound by Myod in myoblasts. I demonstrated that the binding of Myod to the CER depended on the presence of Six1. Six1 was also involved in maintaining a relatively ‘open’ chromatin structure at the CER, suggesting that Six1 may play a direct or indirect role in chromatin remodeling. During my Master’s studies, I demonstrated a synergistic regulation by the Six and MRF families. This synergistic function gains potential importance by the fact that ~25% of Six1 genomic targets are also bound by Myod. I decided to study whether the co-occupancy of Six1 and Myod was essential to maintain the proper global chromatin structure at these loci. Six1 and Myod co-bound genomic regions correlated with more accessible chromatin, which was detected by the formaldehyde-assisted isolation of regulatory elements (FAIRE) assay followed by DNA deep sequencing (FAIRE-seq). When combined with small interfering RNA-mediated gene knockdown of Six1 or Myod, FAIRE-seq data suggested that Six1, but not Myod, was involved in regulating the chromatin accessibility at these co-bound DNA loci. To shed light on the mechanism by which Six1 functions, proteomics approaches were used and revealed that proteins involved in “regulation of transcription” and “chromatin organization” were enriched among Six1-bound proteins. Cdk9 and its partner cyclin T have been shown to stimulate gene expression by releasing RNA polymerase II from transcriptional pause, but they can also function at gene enhancers. I determined that Six1 and Cdk9 participated in the same protein complex, and…
Subjects/Keywords: Six1;
Myod;
Myogenesis;
transcription;
MEF3 DNA motif;
Cdk9
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Liu, Y. (2017). The Role of Six1 in Transcriptional Regulation during Myogenesis
. (Thesis). University of Ottawa. Retrieved from http://hdl.handle.net/10393/35952
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Liu, Yubing. “The Role of Six1 in Transcriptional Regulation during Myogenesis
.” 2017. Thesis, University of Ottawa. Accessed February 28, 2021.
http://hdl.handle.net/10393/35952.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Liu, Yubing. “The Role of Six1 in Transcriptional Regulation during Myogenesis
.” 2017. Web. 28 Feb 2021.
Vancouver:
Liu Y. The Role of Six1 in Transcriptional Regulation during Myogenesis
. [Internet] [Thesis]. University of Ottawa; 2017. [cited 2021 Feb 28].
Available from: http://hdl.handle.net/10393/35952.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Liu Y. The Role of Six1 in Transcriptional Regulation during Myogenesis
. [Thesis]. University of Ottawa; 2017. Available from: http://hdl.handle.net/10393/35952
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Texas Southwestern Medical Center
7.
Casey, Bradford Harris.
Intrinsic Specificity of Binding and Regulatory Function of Class II bHLH Transcription Factors.
Degree: 2016, University of Texas Southwestern Medical Center
URL: http://hdl.handle.net/2152.5/6137
► Embryonic development begins with a single cell, and gives rise to the many diverse cells which comprise the complex structures of the adult animal. Distinct…
(more)
▼ Embryonic development begins with a single cell, and gives rise to the many diverse cells which comprise the complex structures of the adult animal. Distinct cell fates require precise regulation to develop and maintain their functional characteristics. Transcription factors provide a mechanism to select tissue-specific programs of gene expression from the shared genome. ASCL1, ASCL2, and
MYOD are class II basic Helix-Loop-Helix (bHLH) transcription factors which play crucial roles in lineage specification in the developing embryo. In vivo, these factors bind to distinct genomic sites, and regulate distinct transcriptional programs. The mechanisms by which they select their cognate binding sites remain poorly defined. Here, we utilize an inducible system to express these master regulatory factors in embryonic stem cells to characterize early events in bHLH factor binding and function in a common cellular context, removed from their role as endogenous master regulators of lineage specification. Using genome-wide sequencing approaches, we demonstrate that these factors maintain distinct binding when ectopically expressed in a common context. We observe that they initiate distinct transcriptional programs, which include key regulators in lineage specification. By comparing chromatin accessibility of bHLH binding sites, we reveal a shared ability for these factors to bind nucleosome-occupied sites, and meet the criteria which define pioneer transcription factors. We further characterize epigenetic features of the empirically observed genome-wide binding sites of these factors, and compare these findings to the conventional understanding of bHLH factor function. This work represents the first comprehensive approach to direct comparison of early events in the binding and transcriptional profiles of ASCL1, ASCL2, and
MYOD.
Advisors/Committee Members: Krämer, Helmut, Johnson, Jane E., Konopka, Genevieve, MacDonald, Raymond J..
Subjects/Keywords: Basic Helix-Loop-Helix Transcription Factors; DNA-Binding Proteins; MyoD Protein
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Casey, B. H. (2016). Intrinsic Specificity of Binding and Regulatory Function of Class II bHLH Transcription Factors. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/6137
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Casey, Bradford Harris. “Intrinsic Specificity of Binding and Regulatory Function of Class II bHLH Transcription Factors.” 2016. Thesis, University of Texas Southwestern Medical Center. Accessed February 28, 2021.
http://hdl.handle.net/2152.5/6137.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Casey, Bradford Harris. “Intrinsic Specificity of Binding and Regulatory Function of Class II bHLH Transcription Factors.” 2016. Web. 28 Feb 2021.
Vancouver:
Casey BH. Intrinsic Specificity of Binding and Regulatory Function of Class II bHLH Transcription Factors. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2016. [cited 2021 Feb 28].
Available from: http://hdl.handle.net/2152.5/6137.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Casey BH. Intrinsic Specificity of Binding and Regulatory Function of Class II bHLH Transcription Factors. [Thesis]. University of Texas Southwestern Medical Center; 2016. Available from: http://hdl.handle.net/2152.5/6137
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
8.
Hamed, Munerah.
Effect of p300 HAT Activity on Myogenic Differentiation
.
Degree: 2013, University of Ottawa
URL: http://hdl.handle.net/10393/23707
► Skeletal muscle specification and differentiation programs are regulated by the myogenic regulatory factors which include Myf5, MyoD, myogenin and Mrf4. Upstream of the MRFs, the…
(more)
▼ Skeletal muscle specification and differentiation programs are regulated by the myogenic regulatory factors which include Myf5, MyoD, myogenin and Mrf4. Upstream of the MRFs, the transcription co-activators and other intracellular and extracellular signals play crucial roles in regulating skeletal myogenesis. Histone acetyltransferase activity of p300 is required for Myf5 and MyoD expression. Furthermore, the MyoD core enhancer region is indispensable for MyoD expression. However, the mechanism by which p300 activates MyoD gene expression is to be determined. The histone acetyltransferase activity of p300 can be inhibited by small molecule inhibitors such as curcumin. Thus, using the inhibitor approach on stem cells is useful to investigate the role of p300 in activating MyoD expression during myogenesis. We here show that curcumin was able to inhibit stem cell determination and differentiation into skeletal myocytes. We also show that p300 is present, and histone acetylation is high at the core enhancer region. Therefore, we provide evidence that p300 is directly involved in MyoD gene expression during skeletal myogenesis.
Subjects/Keywords: p300;
myod;
histone acetylation
…MyoD: Myogenic Differentiation Antigen
Mrf4: Muscle Regulatory Factor 4
MEF2: Myocyte… …myogenesis, in MyoD regulation.
Skeletal myogenesis
Skeletal myogenesis is a complex process that… …including Myf5, MyoD,
myogenin and Mrf4 in which they initiate myoblast identity and terminal… …regulators: Myf5, MyoD, myogenin and Mrf4 (Gianakopoulos et al., 2010;
Puri et al., 1997… …of MRFs in skeletal myogenesis. Myf5 and
MyoD expression is the key step that results in…
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Hamed, M. (2013). Effect of p300 HAT Activity on Myogenic Differentiation
. (Thesis). University of Ottawa. Retrieved from http://hdl.handle.net/10393/23707
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Hamed, Munerah. “Effect of p300 HAT Activity on Myogenic Differentiation
.” 2013. Thesis, University of Ottawa. Accessed February 28, 2021.
http://hdl.handle.net/10393/23707.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Hamed, Munerah. “Effect of p300 HAT Activity on Myogenic Differentiation
.” 2013. Web. 28 Feb 2021.
Vancouver:
Hamed M. Effect of p300 HAT Activity on Myogenic Differentiation
. [Internet] [Thesis]. University of Ottawa; 2013. [cited 2021 Feb 28].
Available from: http://hdl.handle.net/10393/23707.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Hamed M. Effect of p300 HAT Activity on Myogenic Differentiation
. [Thesis]. University of Ottawa; 2013. Available from: http://hdl.handle.net/10393/23707
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Ottawa
9.
Li, Grace T.Y.
C/EBPbeta is a Negative Regulator of Skeletal Muscle Differentiation
.
Degree: 2011, University of Ottawa
URL: http://hdl.handle.net/10393/20110
► C/EBPβ is a bZIP transcription factor known to be involved in various physiological processes, including adipogenesis, osteogenesis and liver development. Previous studies in this laboratory…
(more)
▼ C/EBPβ is a bZIP transcription factor known to be involved in various physiological processes, including adipogenesis, osteogenesis and liver development. Previous studies in this laboratory revealed an inhibition of myogenesis and reduced myogenic protein expression in 5-azacytidine treated mesenchymal stem cells retrovirally transduced to overexpress C/EBPβ. The goal of this thesis was to evaluate the role of C/EBPβ in myogenic differentiation by overexpression in C2C12 myoblasts and primary myoblasts. We demonstrate reduced MyoD protein expression and subsequent downregulation of myogenic proteins during differentiation following C/EBPβ overexpression. We localized C/EBPβ to the quiescent Pax7+ satellite cells associated with the muscle fiber. Upon satellite cell activation, we observed the downregulation of C/EBPβ protein expression prior to MyoD protein expression. Furthermore, the re-expression of C/EBPβ correlated with the loss of MyoD expression later in differentiation. Histological analysis of C/EBPβ-/- mice revealed smaller fibers and a reduced Pax7+ satellite cell population as compared to control animals. In this thesis, we propose that C/EBPβ is a negative regulator of skeletal muscle differentiation by inhibiting the expression of MyoD, thus impairing proper progression through the myogenic program. In addition, we propose a role for C/EBPβ in the maintenance of undifferentiatied satellite cells.
Subjects/Keywords: C/EBPbeta;
satellite cells;
skeletal muscle differentiation;
MyoD
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Li, G. T. Y. (2011). C/EBPbeta is a Negative Regulator of Skeletal Muscle Differentiation
. (Thesis). University of Ottawa. Retrieved from http://hdl.handle.net/10393/20110
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Li, Grace T Y. “C/EBPbeta is a Negative Regulator of Skeletal Muscle Differentiation
.” 2011. Thesis, University of Ottawa. Accessed February 28, 2021.
http://hdl.handle.net/10393/20110.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Li, Grace T Y. “C/EBPbeta is a Negative Regulator of Skeletal Muscle Differentiation
.” 2011. Web. 28 Feb 2021.
Vancouver:
Li GTY. C/EBPbeta is a Negative Regulator of Skeletal Muscle Differentiation
. [Internet] [Thesis]. University of Ottawa; 2011. [cited 2021 Feb 28].
Available from: http://hdl.handle.net/10393/20110.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Li GTY. C/EBPbeta is a Negative Regulator of Skeletal Muscle Differentiation
. [Thesis]. University of Ottawa; 2011. Available from: http://hdl.handle.net/10393/20110
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of California – San Francisco
10.
Ehlers Stewart, Melissa Laura.
NFATc1 controls skeletal muscle fiber type and is a negative regulator of MyoD transcriptional activity.
Degree: Biomedical Sciences, 2012, University of California – San Francisco
URL: http://www.escholarship.org/uc/item/1sc5t4kg
► The NFAT family of transcription factors regulates cell differentiation programs in a variety of cellular contexts, including immune cell activation, cardiac valve development, osteoclast differentiation,…
(more)
▼ The NFAT family of transcription factors regulates cell differentiation programs in a variety of cellular contexts, including immune cell activation, cardiac valve development, osteoclast differentiation, and fiber type in skeletal muscle. NFAT proteins are activated by the phosphatase calcineurin in response to increases in intracellular calcium levels, and can function as either activators or repressors, depending on co-factor interactions. Four of the five known NFAT transcription factors are expressed in skeletal muscle, of which NFATc2 and NFATc3 have a known function in skeletal muscle in vivo. However, studies interrogating the role of NFATc1 in skeletal muscle in vivo have been limited because Nfatc1-null mice die around E12.5 due to cardiac valve defects. We identified a novel function for NFATc1 in skeletal muscle as a repressor of the skeletal muscle specific bHLH transcription factor MyoD. We found that NFATc1, but not other NFAT isoforms, inhibits MyoD transactivation function. We found that NFATc1 physically interacts with MyoD via the N-terminal transactivation domain of MyoD and inhibits MyoD-mediated conversion of C3H10T1/2 fibroblasts into myosin expressing myotubes. We show that, and that NFATc1 is able to inhibit the transactivation ability of MyoD. To further verify NFATc1 repression of MyoD and to study the role of NFATc1 in vivo, we used Cre-Lox technology to generate a skeletal-muscle specific nfatc1 knockout mouse (nfatc1SkM-KO). We show that NFATc1 controls skeletal muscle fiber type composition in adult mice. The balance between Type I (slow) and Type II (fast) myofibers is altered in mice lacking nfatc1, with these mice exhibiting an increase in the number of Type II (fast) myofibers compared to wild type mice. In addition, we found that NFATc1 is required for proper fiber type switching of myofibers from the fast-to-slow fiber type phenotype in response to endurance exercise training. Finally, we examined the expression levels of several known MyoD target genes in muscle of nfatc1 SkM-KO mice, and found that the majority of genes analyzed are upregulated, providing in vivo support of our findings that NFATc1 negatively regulates MyoD. We propose a model whereby NFATc1 represses MyoD transactivation ability, at least in part, to promote the slow fiber phenotype through repression of fast fiber genes regulated by MyoD.
Subjects/Keywords: Molecular biology; Biochemistry; Developmental biology; MyoD; NFATc1; skeletal muscle
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Ehlers Stewart, M. L. (2012). NFATc1 controls skeletal muscle fiber type and is a negative regulator of MyoD transcriptional activity. (Thesis). University of California – San Francisco. Retrieved from http://www.escholarship.org/uc/item/1sc5t4kg
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Ehlers Stewart, Melissa Laura. “NFATc1 controls skeletal muscle fiber type and is a negative regulator of MyoD transcriptional activity.” 2012. Thesis, University of California – San Francisco. Accessed February 28, 2021.
http://www.escholarship.org/uc/item/1sc5t4kg.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Ehlers Stewart, Melissa Laura. “NFATc1 controls skeletal muscle fiber type and is a negative regulator of MyoD transcriptional activity.” 2012. Web. 28 Feb 2021.
Vancouver:
Ehlers Stewart ML. NFATc1 controls skeletal muscle fiber type and is a negative regulator of MyoD transcriptional activity. [Internet] [Thesis]. University of California – San Francisco; 2012. [cited 2021 Feb 28].
Available from: http://www.escholarship.org/uc/item/1sc5t4kg.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Ehlers Stewart ML. NFATc1 controls skeletal muscle fiber type and is a negative regulator of MyoD transcriptional activity. [Thesis]. University of California – San Francisco; 2012. Available from: http://www.escholarship.org/uc/item/1sc5t4kg
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Toronto
11.
Law, Cindy Tsz Ling.
Characterizing the Role of Post-Translational Modifications of Histone Variant H2A.Z in Mammalian Cells.
Degree: PhD, 2014, University of Toronto
URL: http://hdl.handle.net/1807/94561
H2A.Z is a histone H2A variant that has an essential role in the development of mice,
2016-06-17 00:00:00
Advisors/Committee Members: Cheung, Peter, Medical Biophysics.Subjects/Keywords: Enhancers; Epigenetics; H2A.Z; Histone acetylation; Histone Variants; MyoD; 0307
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Law, C. T. L. (2014). Characterizing the Role of Post-Translational Modifications of Histone Variant H2A.Z in Mammalian Cells. (Doctoral Dissertation). University of Toronto. Retrieved from http://hdl.handle.net/1807/94561
Chicago Manual of Style (16th Edition):
Law, Cindy Tsz Ling. “Characterizing the Role of Post-Translational Modifications of Histone Variant H2A.Z in Mammalian Cells.” 2014. Doctoral Dissertation, University of Toronto. Accessed February 28, 2021.
http://hdl.handle.net/1807/94561.
MLA Handbook (7th Edition):
Law, Cindy Tsz Ling. “Characterizing the Role of Post-Translational Modifications of Histone Variant H2A.Z in Mammalian Cells.” 2014. Web. 28 Feb 2021.
Vancouver:
Law CTL. Characterizing the Role of Post-Translational Modifications of Histone Variant H2A.Z in Mammalian Cells. [Internet] [Doctoral dissertation]. University of Toronto; 2014. [cited 2021 Feb 28].
Available from: http://hdl.handle.net/1807/94561.
Council of Science Editors:
Law CTL. Characterizing the Role of Post-Translational Modifications of Histone Variant H2A.Z in Mammalian Cells. [Doctoral Dissertation]. University of Toronto; 2014. Available from: http://hdl.handle.net/1807/94561
University of Minnesota
12.
Lee, Catherine Ann Alsager.
Isolation and identification of De Novo long noncoding RNAs from mouse myoblasts and embryonic stem cells.
Degree: MS, Stem Cell Biology, 2013, University of Minnesota
URL: http://purl.umn.edu/146424
► Long noncoding RNAs (lncRNAs) are a pervasive class of transcripts whose importance and biological relevance are only beginning to be elucidated. LncRNAs have been detected…
(more)
▼ Long noncoding RNAs (lncRNAs) are a pervasive class of transcripts whose importance and biological relevance are only beginning to be elucidated. LncRNAs have been detected in nearly every cell type and found to be fundamentally involved in many biological processes; however, studies that characterize lncRNA expression during certain periods of development are largely missing. Here, we demonstrate how a pool of potentially relevant lncRNAs can be identified using a RNA-chromatin immunoprecipitation (RNA-ChIP) technique that pulls down sufficient amount of RNA to send for sequencing. In our initial experiment, we attempted to identify lncRNAs bound to the MyoD protein in myoblast cells; however, the lack of immunoprecipitation-compatible highly specific antibodies against MyoD prevented us from pursuing this project. As an alternative, we successfully identified lncRNAs bound to the histone-modifying complex COMPASS, as well as those bound to the master pluripotency factors Oct4 and Sox2 in mouse embryonic stem cells. This study provides a proof-of-principle to identify lncRNAs potentially involved in chromatin regulation of pluripotency.
Subjects/Keywords: ChIP; MyoD; Pluripotency; RNA-ChIP; RNA-seq; Trithorax-group
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Lee, C. A. A. (2013). Isolation and identification of De Novo long noncoding RNAs from mouse myoblasts and embryonic stem cells. (Masters Thesis). University of Minnesota. Retrieved from http://purl.umn.edu/146424
Chicago Manual of Style (16th Edition):
Lee, Catherine Ann Alsager. “Isolation and identification of De Novo long noncoding RNAs from mouse myoblasts and embryonic stem cells.” 2013. Masters Thesis, University of Minnesota. Accessed February 28, 2021.
http://purl.umn.edu/146424.
MLA Handbook (7th Edition):
Lee, Catherine Ann Alsager. “Isolation and identification of De Novo long noncoding RNAs from mouse myoblasts and embryonic stem cells.” 2013. Web. 28 Feb 2021.
Vancouver:
Lee CAA. Isolation and identification of De Novo long noncoding RNAs from mouse myoblasts and embryonic stem cells. [Internet] [Masters thesis]. University of Minnesota; 2013. [cited 2021 Feb 28].
Available from: http://purl.umn.edu/146424.
Council of Science Editors:
Lee CAA. Isolation and identification of De Novo long noncoding RNAs from mouse myoblasts and embryonic stem cells. [Masters Thesis]. University of Minnesota; 2013. Available from: http://purl.umn.edu/146424
University of Southern California
13.
Jensky, Nicole Elizabeth.
The influence of eccentric and concentric exercise on mRNA
expression of skeletal muscle regulators in young women.
Degree: PhD, Biokinesiology, 2008, University of Southern California
URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/62481/rec/6881
► We hypothesized that high intensity eccentric exercise (EE) and concentric exercise (CE) would differentially affect important regulators of skeletal muscle hypertrophy. We therefore sought to…
(more)
▼ We hypothesized that high intensity eccentric exercise
(EE) and concentric exercise (CE) would differentially affect
important regulators of skeletal muscle hypertrophy. We therefore
sought to evaluate changes in myostatin, follistatin and
MyoD mRNA
gene expression using EE and CE as probes to better understand the
mechanisms of muscle hypertrophy in young women. Twelve
recreationally active women performed single-leg maximal eccentric
[n=6, 25±1yr (mean±SD), 59±7kg] or concentric [n=6, 24±1 yr,
65±7kg] isokinetic exercise at 60°/s. Participants performed 10
sets of 10 maximal repetitions with 20 second rest between sets.
Three muscle biopsies of the vastus lateralis were obtained from
the exercised leg at baseline (biopsy1), 8 hours after the first
exercise bout (biopsy #2), and 8 hours after the seventh and final
exercise bout performed 2 weeks after the first exercise session
(biopsy #3). mRNA gene expression was determined using RT-PCR. For
the CE group, there were no changes in myostatin, follistatin, and
MyoD mRNA gene expression between biopsies #1 and #2, biopsy #1 and
#3 (P equal to or greater than 0.07). For the EE group, there were
no changes for the same variables (P equal to or greater than 0.17)
except for
MyoD expression which increased after one exercise bout
(P=0.02). Differences between the EE and CE groups were not
significant (P equal to or greater than 0.05). These data suggest
that a single bout or multiple bouts of maximal EE or CE do not
significantly alter myostatin or follistatin mRNA gene expression
in young women. However
MyoD mRNA expression appears to increase
after EE. Therefore, the type of exercise stimulus may not
differentially alter specific myogenic regulators.
Advisors/Committee Members: Schroeder, E. ToddGordon, James (Committee Chair), Sattler, Fred R. (Committee Member), Hawkins, Steven (Committee Member), Rice, Judd (Committee Member).
Subjects/Keywords: myostatin; follistatin; MyoD; resistance exercise
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Jensky, N. E. (2008). The influence of eccentric and concentric exercise on mRNA
expression of skeletal muscle regulators in young women. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/62481/rec/6881
Chicago Manual of Style (16th Edition):
Jensky, Nicole Elizabeth. “The influence of eccentric and concentric exercise on mRNA
expression of skeletal muscle regulators in young women.” 2008. Doctoral Dissertation, University of Southern California. Accessed February 28, 2021.
http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/62481/rec/6881.
MLA Handbook (7th Edition):
Jensky, Nicole Elizabeth. “The influence of eccentric and concentric exercise on mRNA
expression of skeletal muscle regulators in young women.” 2008. Web. 28 Feb 2021.
Vancouver:
Jensky NE. The influence of eccentric and concentric exercise on mRNA
expression of skeletal muscle regulators in young women. [Internet] [Doctoral dissertation]. University of Southern California; 2008. [cited 2021 Feb 28].
Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/62481/rec/6881.
Council of Science Editors:
Jensky NE. The influence of eccentric and concentric exercise on mRNA
expression of skeletal muscle regulators in young women. [Doctoral Dissertation]. University of Southern California; 2008. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/62481/rec/6881
Cleveland State University
14.
Ross, Jason Allen.
Basal Signaling Through Death Receptor 5 and Caspase 3
Activates p38 Kinase to Regulate Serum Response Factor – Mediated
MyoD Transcription.
Degree: PhD, College of Sciences and Health Professions, 2020, Cleveland State University
URL: http://rave.ohiolink.edu/etdc/view?acc_num=csu160915772455676
► The formation of functional skeletal muscle is the consequence of both the differentiation and apoptosis of skeletal myoblasts. Ex vivo culture of skeletal myoblasts provides…
(more)
▼ The formation of functional skeletal muscle is the
consequence of both the differentiation and apoptosis of skeletal
myoblasts. Ex vivo culture of skeletal myoblasts provides a
tractable model for the study of these two coordinately regulated
processes. We have previously reported that 23A2 myoblasts stably
expressing a dominant negative Death Receptor 5 (A2:dnDR5
myoblasts) exhibit decreased basal mRNA and protein expression of
the master muscle regulatory transcription factor
MyoD. This
decrease at the mRNA level is not a consequence of altered
stability. Binding of the transcription factor SRF to a
non-canonical CArG box within a serum response element (SRE) in the
distal regulatory region (DRR) of the
MyoD gene is required for
basal
MyoD expression. Herein, we report that A2:dnDR5 myoblasts
exhibit a decrease in the amount of SRF bound at this CArG box.
Additionally, in A2:dnDR5 myoblasts, we observe a decrease in the
phosphorylation indicative of activation of SRF as well as a
decrease in the phosphorylation indicative of activation of the
mitogen-activated protein kinase p38, which is known to activate
SRF. Pharmacological inhibition of p38, or of caspase-3, in
parental 23A2 myoblasts mimics the decreased activation of SRF and
p38, the decreased binding of SRF to the
MyoD CArG box, and the
decreased levels of
MyoD mRNA and protein detected in the A2:dnDR5
myoblasts. Taken together, these results suggest that basal
signaling through DR5 to caspase 3 leads to the activation of p38
and subsequently SRF to maintain basal expression of
MyoD.
Advisors/Committee Members: Weyman, Crystal (Advisor).
Subjects/Keywords: Biology; Cellular Biology; Molecular Biology; MyoD; DR5; basal signaling; SRF; p38
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Ross, J. A. (2020). Basal Signaling Through Death Receptor 5 and Caspase 3
Activates p38 Kinase to Regulate Serum Response Factor – Mediated
MyoD Transcription. (Doctoral Dissertation). Cleveland State University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=csu160915772455676
Chicago Manual of Style (16th Edition):
Ross, Jason Allen. “Basal Signaling Through Death Receptor 5 and Caspase 3
Activates p38 Kinase to Regulate Serum Response Factor – Mediated
MyoD Transcription.” 2020. Doctoral Dissertation, Cleveland State University. Accessed February 28, 2021.
http://rave.ohiolink.edu/etdc/view?acc_num=csu160915772455676.
MLA Handbook (7th Edition):
Ross, Jason Allen. “Basal Signaling Through Death Receptor 5 and Caspase 3
Activates p38 Kinase to Regulate Serum Response Factor – Mediated
MyoD Transcription.” 2020. Web. 28 Feb 2021.
Vancouver:
Ross JA. Basal Signaling Through Death Receptor 5 and Caspase 3
Activates p38 Kinase to Regulate Serum Response Factor – Mediated
MyoD Transcription. [Internet] [Doctoral dissertation]. Cleveland State University; 2020. [cited 2021 Feb 28].
Available from: http://rave.ohiolink.edu/etdc/view?acc_num=csu160915772455676.
Council of Science Editors:
Ross JA. Basal Signaling Through Death Receptor 5 and Caspase 3
Activates p38 Kinase to Regulate Serum Response Factor – Mediated
MyoD Transcription. [Doctoral Dissertation]. Cleveland State University; 2020. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=csu160915772455676
Université de Bordeaux I
15.
Stuelsatz, Pascal.
Implication de la protéase calpaïne 3 dans la régulation de l’activité transcriptionnelle du facteur MyoD au cours du processus de myogénèse : Investigation of zinc oxides and fluorides : opto-electronic and magnetic properties.
Degree: Docteur es, Nutrition, 2008, Université de Bordeaux I
URL: http://www.theses.fr/2008BOR13748
► Calpaïne 3 est une cystéine protéase retrouvée principalement au niveau du tissu musculaire. Cette enzyme joue un rôle clef dans le maintient de l’intégrité des…
(more)
▼ Calpaïne 3 est une cystéine protéase retrouvée principalement au niveau du tissu musculaire. Cette enzyme joue un rôle clef dans le maintient de l’intégrité des fibres musculaires. En effet, des mutations au niveau du gène de calpaïne 3 ont été identifiées comme étant responsables d’une dystrophie musculaire autosomale récessive, la LGMD2A (Limb-girdle muscular dystrophy type 2A), caractérisée par une atrophie progressive des muscles des ceintures scapulaires et pelviennes. Nos travaux montrent que calpaïne 3 inhibe l’activité transcriptionnelle de MyoD. Ce facteur de transcription myogénique (MRF) joue un rôle central dans le contrôle de la myogenèse aussi bien au cours du développement embryonnaire que chez un individu adulte au cours du processus de régénération musculaire. Cette diminution d’activité transcriptionnelle a lieu aussi bien dans des cellules myoblastiques (C2C12) que fibroblastiques (C3H10T1/2). Par contre calpaïne 3 ne modifie pas l’activité transcriptionnelle des autres MRFs (Myf5, myogénine ou MRF4). Nous avons pu montrer que calpaïne 3 affecte spécifiquement l’activité transcriptionnelle de MyoD en entraînant une diminution de son niveau protéique (Western-blot, microscopie confocale), sans affecter son niveau d’ARNm (RT-QPCR). De plus, des expériences de détermination de la demi-vie protéique ont pu montrer que calpaïne 3 intervenait sur la dégradation protéique de MyoD. Des expériences sont en cours afin de déterminer si calpaïne 3 hydrolyse directement ou non le facteur MyoD. Nos travaux montrent que l’hydrolyse de MyoD induite par calpaïne 3 représente une voie parallèle à celle du système protéolytique protéasome ubiquitine-dépendant connu pour être impliqué dans sa dégradation. Nous avons également montré qu’une modification de l’expression de calpaïne 3, soit par surexpression soit par inhibition avec des siRNA spécifiques, entraîne une perturbation du processus de différenciation myogénique. Cet effet a été plus particulièrement étudié au sein d’une sous-population de cellules qui reste indifférenciée dans les cellules C2C12 induites en différenciation. Ces cellules, appelées cellules de réserve, s’apparentent aux cellules satellites intervenant dans la régénération musculaire. Nous avons montré que calpaïne 3 participe à la régulation du nombre des cellules de réserve au cours de la différenciation des cellules C2C12. Ce rôle de calpaïne 3 pourrait être lié à son intervention dans la dégradation du facteur MyoD. L’ensemble de ces résultats suggère ainsi que calpaïne 3 pourrait jouer un rôle in vivo dans le maintien d’un stock de cellules satellites au cours de la régénération musculaire.
Calpain 3 (CAPN3) is a calcium-dependent cysteine protease mainly expressed in skeletal muscle. This protease plays a key role in maintaining the integrity of muscular fibers. Indeed, mutations in CAPN3 encoding gene cause limb-girdle muscular dystrophy type 2A, an autosomal recessive muscular dystrophy characterized by progressive atrophy and weakness of the proximal limb muscles. Our work reveals an…
Advisors/Committee Members: Cottin, Patrick (thesis director).
Subjects/Keywords: Calpaïne 3; Régénération musculaire; Myogenèse; MyoD; Calpaïn 3; Muscular regeneration; Myogenesis; MyoD
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Stuelsatz, P. (2008). Implication de la protéase calpaïne 3 dans la régulation de l’activité transcriptionnelle du facteur MyoD au cours du processus de myogénèse : Investigation of zinc oxides and fluorides : opto-electronic and magnetic properties. (Doctoral Dissertation). Université de Bordeaux I. Retrieved from http://www.theses.fr/2008BOR13748
Chicago Manual of Style (16th Edition):
Stuelsatz, Pascal. “Implication de la protéase calpaïne 3 dans la régulation de l’activité transcriptionnelle du facteur MyoD au cours du processus de myogénèse : Investigation of zinc oxides and fluorides : opto-electronic and magnetic properties.” 2008. Doctoral Dissertation, Université de Bordeaux I. Accessed February 28, 2021.
http://www.theses.fr/2008BOR13748.
MLA Handbook (7th Edition):
Stuelsatz, Pascal. “Implication de la protéase calpaïne 3 dans la régulation de l’activité transcriptionnelle du facteur MyoD au cours du processus de myogénèse : Investigation of zinc oxides and fluorides : opto-electronic and magnetic properties.” 2008. Web. 28 Feb 2021.
Vancouver:
Stuelsatz P. Implication de la protéase calpaïne 3 dans la régulation de l’activité transcriptionnelle du facteur MyoD au cours du processus de myogénèse : Investigation of zinc oxides and fluorides : opto-electronic and magnetic properties. [Internet] [Doctoral dissertation]. Université de Bordeaux I; 2008. [cited 2021 Feb 28].
Available from: http://www.theses.fr/2008BOR13748.
Council of Science Editors:
Stuelsatz P. Implication de la protéase calpaïne 3 dans la régulation de l’activité transcriptionnelle du facteur MyoD au cours du processus de myogénèse : Investigation of zinc oxides and fluorides : opto-electronic and magnetic properties. [Doctoral Dissertation]. Université de Bordeaux I; 2008. Available from: http://www.theses.fr/2008BOR13748
16.
Manandhar, Dinesh.
Methods for Comparative Analysis of Chromatin Accessibility and Gene Expression, With Applications to Cellular Reprogramming
.
Degree: 2018, Duke University
URL: http://hdl.handle.net/10161/16843
► Cellular reprogramming processes remain poorly characterized at the level of genome- wide chromatin and gene expression changes. Specifically, the extent to which re- programmed…
(more)
▼ Cellular reprogramming processes remain poorly characterized at the level of genome- wide chromatin and gene expression changes. Specifically, the extent to which re- programmed cells differ quantitatively from both the starting cells and the target cells is unknown for most reprogramming systems. In addition, direct comparisons between the genome-wide reprogramming efficiencies in systems driven by the over- expression of endogenous versus exogenous master regulator(s) are rarely performed. This thesis presents methods for comparative analyses of genome-wide gene expres- sion and chromatin accessibility data, applied to myogenic reprogramming systems in order to assess reprogramming efficiency and generate testable hypotheses for improving the reprogramming process. First, gene expression and chromatin acces- sibility profiles of
MyoD-induced transdifferentiated primary human skin fibroblasts are compared to fibroblasts and myoblasts. Second, similar genome-wide changes are assessed for myogenic conversion of iPS cells driven by overexpression of en- dogenous
MyoD versus exogeneous
MyoD. Both studies show that (i) while many muscle marker genes are reprogrammed after
MyoD overexpression, the genome-wide accessibility and gene expression profiles are still different from those of primary my- oblast or myotube cells; (ii)
MyoD induces a continuum of changes in chromatin accessibility, with only a fraction of myogenic chromatin sites gaining a completely reprogrammed accessibility status; and (iii) chromatin-remodeling deficiencies are strongly correlated with incomplete gene expression reprogramming. Classification analyses comparing reprogrammed and non-reprogrammed genes or chromatin sites revealed discriminatory genetic and epigenetic features, suggesting ways to poten- tially improve the reprogramming efficiency. Genomic analysis of transgene
MyoD overexpression in iPS cells, compared to endogenous
MyoD activation, also showed that
MyoD is more “aggressive” in its chromatin opening behavior, showing a large number of off-target chromatin opening events. To further investigate the effects chromatin remodeling events on gene expression in reprogramming studies, a novel cross-cell type gene expression prediction framework (CPGex) is also developed. By integrating and modeling the non-linear combinatorial effects of chromatin accessi- bility as well as the expression levels of regulatory TFs, CPGex is able to weigh the importance of regulatory sites or factors for downstream targeted reprogramming of specific gene(s). The methods described in this thesis can be applied to any cellular reprogramming system in order to quantitatively assess the efficiency of reprogram- ming at the chromatin accessibility and gene expression levels, as well as to generate testable hypothesis for improved genome-wide reprogramming.
Advisors/Committee Members: Gordan, Raluca (advisor).
Subjects/Keywords: Bioinformatics;
Biostatistics;
Artificial intelligence;
comparative chromatin and gene expression analyses;
CPGex;
cross cell type gene expression prediction;
endogenous MyoD;
MyoD;
myogenic reprogramming
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Manandhar, D. (2018). Methods for Comparative Analysis of Chromatin Accessibility and Gene Expression, With Applications to Cellular Reprogramming
. (Thesis). Duke University. Retrieved from http://hdl.handle.net/10161/16843
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Manandhar, Dinesh. “Methods for Comparative Analysis of Chromatin Accessibility and Gene Expression, With Applications to Cellular Reprogramming
.” 2018. Thesis, Duke University. Accessed February 28, 2021.
http://hdl.handle.net/10161/16843.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Manandhar, Dinesh. “Methods for Comparative Analysis of Chromatin Accessibility and Gene Expression, With Applications to Cellular Reprogramming
.” 2018. Web. 28 Feb 2021.
Vancouver:
Manandhar D. Methods for Comparative Analysis of Chromatin Accessibility and Gene Expression, With Applications to Cellular Reprogramming
. [Internet] [Thesis]. Duke University; 2018. [cited 2021 Feb 28].
Available from: http://hdl.handle.net/10161/16843.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Manandhar D. Methods for Comparative Analysis of Chromatin Accessibility and Gene Expression, With Applications to Cellular Reprogramming
. [Thesis]. Duke University; 2018. Available from: http://hdl.handle.net/10161/16843
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
17.
Olga Sueli Moreira Brasileiro.
Efeito do laser de baixa intensidade sobre a regeneração do músculo esquelético em camundongos através da análise de expressão gênica com branched de DNA(bDNA)1.
Degree: 2008, Universidade Federal de São Carlos
URL: http://www.bdtd.ufscar.br/htdocs/tedeSimplificado//tde_busca/arquivo.php?codArquivo=1917
► Esta pesquisa é o resultado de quatro anos dedicados ao doutorado. Apresenta caráter pioneiro em vários aspectos. Primeiro, este trabalho utilizou a metodologia de Branched…
(more)
▼ Esta pesquisa é o resultado de quatro anos dedicados ao doutorado. Apresenta caráter pioneiro em vários aspectos. Primeiro, este trabalho utilizou a metodologia de Branched de DNA (bDNA) para análise de expressão gênica em tecidos biológicos. Inicialmente, a técnica que era destinada para cultura de células, foi adaptada para homogenatos de tecido. Primeiramente, validamos a metodologia mediante o uso do protocolo QuantiGene Reagent Systems Evaluation Program (Genospetra). Mediante este protocolo, vários ensaios experimentais foram realizados, e resultou na adequação metodológica que a empresa utilizou para padronizar os procedimentos para análise com homogenatos de tecidos animais. Atualmente, nosso protocolo faz parte do manual do Sistema de Reagentes QuantiGene Panomics que está sendo utilizado pela própria empresa para análise da expressão gênica com homogenatos de tecido muscular. Segundo, tendo em vista a existência de poucos trabalhos na literatura que investiga o efeito do laser λ=514 nm durante a regeneração do músculo esquelético, decidimos realizar esta investigação para fins de desenvolvimento do laser de argônio de baixa intensidade para fins terapêuticos. Terceiro, consiste no primeiro trabalho que investiga três comprimentos de onda de laser de baixa intensidade sobre a expressão de genes durante o processo de regeneração muscular in vivo. Ao final desse estudo obtivemos resultados relevantes que deram origem a dois manuscritos submetidos em revistas internacionais, em anexo. Para apresentação desta tese, os resultados obtidos foram organizados em capítulos que correspondem aos dois artigos apresentados a seguir.
Advisors/Committee Members: Nivaldo Antonio Parizotto.
Subjects/Keywords: Lasers; Branched DNA; Expressão gênica; MyoD; Miogenina; Camundongo; FISIOTERAPIA E TERAPIA OCUPACIONAL
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Brasileiro, O. S. M. (2008). Efeito do laser de baixa intensidade sobre a regeneração do músculo esquelético em camundongos através da análise de expressão gênica com branched de DNA(bDNA)1. (Thesis). Universidade Federal de São Carlos. Retrieved from http://www.bdtd.ufscar.br/htdocs/tedeSimplificado//tde_busca/arquivo.php?codArquivo=1917
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Brasileiro, Olga Sueli Moreira. “Efeito do laser de baixa intensidade sobre a regeneração do músculo esquelético em camundongos através da análise de expressão gênica com branched de DNA(bDNA)1.” 2008. Thesis, Universidade Federal de São Carlos. Accessed February 28, 2021.
http://www.bdtd.ufscar.br/htdocs/tedeSimplificado//tde_busca/arquivo.php?codArquivo=1917.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Brasileiro, Olga Sueli Moreira. “Efeito do laser de baixa intensidade sobre a regeneração do músculo esquelético em camundongos através da análise de expressão gênica com branched de DNA(bDNA)1.” 2008. Web. 28 Feb 2021.
Vancouver:
Brasileiro OSM. Efeito do laser de baixa intensidade sobre a regeneração do músculo esquelético em camundongos através da análise de expressão gênica com branched de DNA(bDNA)1. [Internet] [Thesis]. Universidade Federal de São Carlos; 2008. [cited 2021 Feb 28].
Available from: http://www.bdtd.ufscar.br/htdocs/tedeSimplificado//tde_busca/arquivo.php?codArquivo=1917.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Brasileiro OSM. Efeito do laser de baixa intensidade sobre a regeneração do músculo esquelético em camundongos através da análise de expressão gênica com branched de DNA(bDNA)1. [Thesis]. Universidade Federal de São Carlos; 2008. Available from: http://www.bdtd.ufscar.br/htdocs/tedeSimplificado//tde_busca/arquivo.php?codArquivo=1917
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
18.
Daou, Nissrine.
Étude de l’intéraction MyoD/NFATc2 au cours de la myogenèse chez la souris : Study the interaction MyoD/NFATc2 during the myogenesis in mice.
Degree: Docteur es, Biologie cellulaire, 2013, Université Paris Descartes – Paris V
URL: http://www.theses.fr/2013PA05T013
► La voie de signalisation calcineurine/NFAT (Nuclear Factor of Activated T-cells) est très largement impliquée dans plusieurs aspects du développement et des pathologies du muscle squelettique.…
(more)
▼ La voie de signalisation calcineurine/NFAT (Nuclear Factor of Activated T-cells) est très largement impliquée dans plusieurs aspects du développement et des pathologies du muscle squelettique. De nombreuses études ont souligné son implication dans la spécification des fibres musculaires adultes. Cependant, son rôle dans l’établissement du phénotype musculaire au cours de l’embryogenèse reste peu connu. Il faut noter que certains travaux suggèrent une implication de NFATc3 dans le nombre de fibres musculaires alors que l’isoforme NFATc2 pourrait être impliquée dans la taille des fibres musculaires. Les facteurs myogéniques (MRF) de la famille MyoD (incluant MyoD, Myf5, MRF4 et la myogénine) sont des facteurs de transcription à domaine bHLH (basic-Helix-Loop-Helix) clés pour la myogenèse squelettique. L’étude de leurs partenaires protéiques est essentielle pour bien comprendre la régulation de l’expression des gènes musculaires. Un nouveau paradigme de la transcription a été démontré (Armand et al. 2008), où une protéine NFAT pourrait coopérer spécifiquement avec un MRF : en effet, l’isoforme, NFATc3, coopère avec MyoD pour activer l’expression de la myogénine au cours de la somitogenèse. Ce rôle est spécifique du complexe NFATc3/MyoD puisque les souris mutantes myod (-/-) ; nfatc2 (-/-) ne présentent aucune modification de l’expression de la myogénine au cours de la somitogenèse. L’objectif de ce travail est d’étudier l’implication du complexe NFATc2/MyoD dans la myogenèse chez la souris. Nous montrons que l’isoforme NFATc2 coopère avec MyoD pour induire spécifiquement l’expression de la chaine lourde néonatale la myosine (MHCneo), in vitro aussi bien qu’in vivo. Cette coopération est spécifique et cruciale puisque les souris double mutantes myod (-/-) ; nfatc2 (-/-) meurent à la naissance avec une réduction spectaculaire de l’expression de la MHCneo, principale isoforme de la myosine exprimée à la naissance, alors que l’expression de cette chaine lourde de la myosine n’est pas affectée chez les simples mutants. Par des analyses d’immunoprécipitation de la chromatine et de retard sur gels, nous avons montré que les isoformes NFATc1 et NFATc3 se lient de manière préférentielle au gène codant la chaine lourde embryonnaire de la myosine (MHC emb). Ce travail, qui met en évidence pour la première fois le rôle de la voie de signalisation calcineurine/NFAT dans la construction précoce de la fibre musculaire au cours de l’embryogenèse, montre aussi l’implication spécifique du complexe NFATc2/MyoD dans le contrôle du nombre de fibres musculaires au cours de l’embryogenèse.
Cell biology
Advisors/Committee Members: Chanoine, Christophe (thesis director).
Subjects/Keywords: MyoD; NFATc2; Myogenèse; Calcineurine; Muscle squelettique; Facteurs myogéniques; Chaine lourde de myosine; Cell biology
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Daou, N. (2013). Étude de l’intéraction MyoD/NFATc2 au cours de la myogenèse chez la souris : Study the interaction MyoD/NFATc2 during the myogenesis in mice. (Doctoral Dissertation). Université Paris Descartes – Paris V. Retrieved from http://www.theses.fr/2013PA05T013
Chicago Manual of Style (16th Edition):
Daou, Nissrine. “Étude de l’intéraction MyoD/NFATc2 au cours de la myogenèse chez la souris : Study the interaction MyoD/NFATc2 during the myogenesis in mice.” 2013. Doctoral Dissertation, Université Paris Descartes – Paris V. Accessed February 28, 2021.
http://www.theses.fr/2013PA05T013.
MLA Handbook (7th Edition):
Daou, Nissrine. “Étude de l’intéraction MyoD/NFATc2 au cours de la myogenèse chez la souris : Study the interaction MyoD/NFATc2 during the myogenesis in mice.” 2013. Web. 28 Feb 2021.
Vancouver:
Daou N. Étude de l’intéraction MyoD/NFATc2 au cours de la myogenèse chez la souris : Study the interaction MyoD/NFATc2 during the myogenesis in mice. [Internet] [Doctoral dissertation]. Université Paris Descartes – Paris V; 2013. [cited 2021 Feb 28].
Available from: http://www.theses.fr/2013PA05T013.
Council of Science Editors:
Daou N. Étude de l’intéraction MyoD/NFATc2 au cours de la myogenèse chez la souris : Study the interaction MyoD/NFATc2 during the myogenesis in mice. [Doctoral Dissertation]. Université Paris Descartes – Paris V; 2013. Available from: http://www.theses.fr/2013PA05T013
University of Colorado
19.
Hausburg, Melissa Ann.
Tristetraprolin Regulation of MyoD mRNA Stability Commits Quiescent Adult Muscle Stem Cells to Myogenesis.
Degree: PhD, 2010, University of Colorado
URL: https://scholar.colorado.edu/mcdb_gradetds/3
► In animals, tissue maintenance, plasticity and repair rely on adult stem cells which have been identified in nearly all tissues. Many adult stem cells…
(more)
▼ In animals, tissue maintenance, plasticity and repair rely on adult stem cells which have been identified in nearly all tissues. Many adult stem cells are typically quiescent and only activate when required for maintenance and repair of adult tissues. Within hours of activation skeletal muscle stem cells called satellite cells begin to express
MyoD, a muscle-specific transcription factor that functions as a master regulator, committing satellite cells to myogenesis. The earliest detectable event in satellite cells following muscle injury is phosphorylation of p38α/β MAPKs, which is required for
MyoD induction and cell-cycle entry. Loss of Syndecan-4, a component of the satellite cell niche disrupts p38α/β MAPK activation and severely delays
MyoD induction. We performed a microarray gene chip experiment to identify genes expressed during satellite cell activation. We identified differentially expressed genes by subtracting genes changing in Sdc4-/- satellite cells from those changing in WT satellite cells following 12h of muscle injury. Unexpectedly, we observed that 70% of RNA-binding proteins (RNA-BPs) decreased in activated satellite cells. Expression levels of the Tristetraprolin (TTP) family of RNA-BPs declined dramatically as satellite cells activated. The TTP family is known to direct mRNA decay and we identified the 3‘UTR of
MyoD as a direct TTP target. Furthermore, p38α/β MAPK signaling inhibits TTP-mediated mRNA decay in satellite cells. HuR, an RNA-BP that is induced during satellite cell activation is known to stabilize
MyoD mRNA. The coordinate inhibition of TTP and induction of HuR may together function as a feed-forward loop to commit satellite cells to myogenesis by rapid induction of
MyoD. A similar feed-forward circuit could operate in other stem cell systems, implicating that post-transcriptional regulation of mRNA could play a major role in regulating adult stem cells to maintain and repair adult tissues.
Advisors/Committee Members: Bradley B. Olwin, Corrella Detweiler, Leslie A. Leinwand.
Subjects/Keywords: MyoD; RNA decay; satellite cell; skeletal muscle; stem cell; Tristetraprolin; Other Cell and Developmental Biology
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Hausburg, M. A. (2010). Tristetraprolin Regulation of MyoD mRNA Stability Commits Quiescent Adult Muscle Stem Cells to Myogenesis. (Doctoral Dissertation). University of Colorado. Retrieved from https://scholar.colorado.edu/mcdb_gradetds/3
Chicago Manual of Style (16th Edition):
Hausburg, Melissa Ann. “Tristetraprolin Regulation of MyoD mRNA Stability Commits Quiescent Adult Muscle Stem Cells to Myogenesis.” 2010. Doctoral Dissertation, University of Colorado. Accessed February 28, 2021.
https://scholar.colorado.edu/mcdb_gradetds/3.
MLA Handbook (7th Edition):
Hausburg, Melissa Ann. “Tristetraprolin Regulation of MyoD mRNA Stability Commits Quiescent Adult Muscle Stem Cells to Myogenesis.” 2010. Web. 28 Feb 2021.
Vancouver:
Hausburg MA. Tristetraprolin Regulation of MyoD mRNA Stability Commits Quiescent Adult Muscle Stem Cells to Myogenesis. [Internet] [Doctoral dissertation]. University of Colorado; 2010. [cited 2021 Feb 28].
Available from: https://scholar.colorado.edu/mcdb_gradetds/3.
Council of Science Editors:
Hausburg MA. Tristetraprolin Regulation of MyoD mRNA Stability Commits Quiescent Adult Muscle Stem Cells to Myogenesis. [Doctoral Dissertation]. University of Colorado; 2010. Available from: https://scholar.colorado.edu/mcdb_gradetds/3
University of Washington
20.
Feng, Qing.
Functional roles of nonsense-mediated decay in a human muscular dystrophy and myogenesis.
Degree: PhD, 2017, University of Washington
URL: http://hdl.handle.net/1773/40264
► Multiple layers of regulation occur in mRNA life cycle, from RNA processing to translation to degradation. These multi-step processes benefit the organism to achieve genomic…
(more)
▼ Multiple layers of regulation occur in mRNA life cycle, from RNA processing to translation to degradation. These multi-step processes benefit the organism to achieve genomic complexity, while risking it with increasing likelihood that errors can be introduced along the way. To maintain mRNA fidelity, cells evoke quality control mechanisms, including nonsense-mediated decay (NMD), which degrades mRNAs undergoing prematurely terminated translation. While efficient degradation of undesired gene products seem necessary, NMD efficiency is highly variable between cell types, in diseased or healthy conditions, raising the question: Is this variation in NMD efficiency simply a consequence of, or an unknown contributor to the difference in cell phenotypes? To address this question, I compared variation in NMD in muscular dystrophy and myogenesis models, and identified previously unknown regulatory roles of NMD pathway/factor: 1. A feedback loop between compromised NMD and the disease gene DUX4 in a human muscular dystrophy (Feng et al., eLife, 2015). DUX4 is a transcription factor, whose mis-expression in skeletal muscle causes apoptosis and facioscapulohumeral muscular dystrophy (FSHD). In order to understand the mechanism(s) of DUX4 toxicity in muscle, we performed RNAseq analysis, and found DUX4 induces profound NMD inhibition. As a result of this, RNAs normally degraded by NMD accumulate in DUX4 expressing cells, including DUX4 mRNA itself. We thus found that inhibition of NMD by DUX4 protein stabilizes DUX4 mRNA through a double-negative feedback loop (Figure 1). We also found that DUX4 induces NMD inhibition by, at least partially, triggering proteolytic degradation of UPF1, a central component of the NMD machinery. In this study, we illustrated an unexpected mode of autoregulatory behavior of DUX4, with implications for FSHD pathogenesis, and identified a previously unknown mechanism of proteolytic regulation of the NMD pathway. 2. NMD factor UPF1 in regulating myogenesis via its E3 ubiquitin ligase activity (Feng et al., under review). During muscle differentiation, NMD efficiency also attenuates. In order to understand whether NMD plays a regulatory role in myogenesis, we genetically perturbed the level of UPF1, the key RNA helicase in mediating NMD. We found ectopically suppressing UPF1 accelerates myogenesis, while increasing UPF1 levels slows myogenesis. Surprisingly, we found UPF1 represses myogenesis by promoting the decay of
MYOD protein, a transcription factor that is a master regulator of myogenesis, while leaving
MYOD mRNA stability unaffected. Finally, we found UPF1 acts as an E3 ligase via its RING domain to promote
MYOD protein ubiquitination and degradation (Figure 2). In this study, we characterized a regulatory role for UPF1 in myogenesis, and demonstrated that UPF1 provides a mechanistic link between the RNA and protein decay machineries in human cells. To sum up, in my thesis research, we found that NMD is a regulatory (rather than constitutive) mechanism, the magnitude of which can be tuned to…
Advisors/Committee Members: Bradley, Robert K. (advisor).
Subjects/Keywords: DUX4; E3 ligase; FSHD; MYOD; NMD; UPF1; Molecular biology; Cellular biology; Biochemistry; Molecular and cellular biology
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Feng, Q. (2017). Functional roles of nonsense-mediated decay in a human muscular dystrophy and myogenesis. (Doctoral Dissertation). University of Washington. Retrieved from http://hdl.handle.net/1773/40264
Chicago Manual of Style (16th Edition):
Feng, Qing. “Functional roles of nonsense-mediated decay in a human muscular dystrophy and myogenesis.” 2017. Doctoral Dissertation, University of Washington. Accessed February 28, 2021.
http://hdl.handle.net/1773/40264.
MLA Handbook (7th Edition):
Feng, Qing. “Functional roles of nonsense-mediated decay in a human muscular dystrophy and myogenesis.” 2017. Web. 28 Feb 2021.
Vancouver:
Feng Q. Functional roles of nonsense-mediated decay in a human muscular dystrophy and myogenesis. [Internet] [Doctoral dissertation]. University of Washington; 2017. [cited 2021 Feb 28].
Available from: http://hdl.handle.net/1773/40264.
Council of Science Editors:
Feng Q. Functional roles of nonsense-mediated decay in a human muscular dystrophy and myogenesis. [Doctoral Dissertation]. University of Washington; 2017. Available from: http://hdl.handle.net/1773/40264
21.
Bourajjaj, M.
Nuclear Factor of Activated T cells (NFAT): key regulator of cardiac hypertrophy and skeletal muscle adaptation.
Degree: 2008, University Utrecht
URL: https://dspace.library.uu.nl/handle/1874/29300
;
URN:NBN:NL:UI:10-1874-29300
;
urn:isbn:978-90-7867-5426
;
URN:NBN:NL:UI:10-1874-29300
;
https://dspace.library.uu.nl/handle/1874/29300
► Despite significant progress in the prevention and treatment of cardiovascular diseases, heart failure is still a leading cause of morbidity and mortality in industrial countries.…
(more)
▼ Despite significant progress in the prevention and treatment of cardiovascular diseases, heart failure is still a leading cause of morbidity and mortality in industrial countries. Sustained cardiac hypertrophy, which is defined as an increase in heart size resulting from an increase in cardiomyocyte cell volume, has been recognized as the single most important risk factor for heart failure development. Cardiac hypertrophy can be initiated by a wide array of (neuro/humoral) growth factors in response to increased workload, injury, or intrinsic defects in contractile performance. To understand the molecular determinants of the hypertrophic response and to achieve future rational drug design to treat heart failure, investigation currently focuses on identifying and characterizing intracellular signal transduction pathways in the heart. The experiments presented in this thesis focus on a signaling pathway which plays a role in the hypertrophic transcriptional response of the myocyte. This signaling route employs the Ca2+-calmodulin-dependent phosphatase calcineurin and its immediate downstream transcriptional effector Nuclear Factor of Activated T-cells (NFAT), and further focuses on the immediate downstream NFAT target genes in cardiac muscle.
Subjects/Keywords: cardiac hypertrophy; heart failure; calcineurin; NFAT; myogenesis; MyoD
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Bourajjaj, M. (2008). Nuclear Factor of Activated T cells (NFAT): key regulator of cardiac hypertrophy and skeletal muscle adaptation. (Doctoral Dissertation). University Utrecht. Retrieved from https://dspace.library.uu.nl/handle/1874/29300 ; URN:NBN:NL:UI:10-1874-29300 ; urn:isbn:978-90-7867-5426 ; URN:NBN:NL:UI:10-1874-29300 ; https://dspace.library.uu.nl/handle/1874/29300
Chicago Manual of Style (16th Edition):
Bourajjaj, M. “Nuclear Factor of Activated T cells (NFAT): key regulator of cardiac hypertrophy and skeletal muscle adaptation.” 2008. Doctoral Dissertation, University Utrecht. Accessed February 28, 2021.
https://dspace.library.uu.nl/handle/1874/29300 ; URN:NBN:NL:UI:10-1874-29300 ; urn:isbn:978-90-7867-5426 ; URN:NBN:NL:UI:10-1874-29300 ; https://dspace.library.uu.nl/handle/1874/29300.
MLA Handbook (7th Edition):
Bourajjaj, M. “Nuclear Factor of Activated T cells (NFAT): key regulator of cardiac hypertrophy and skeletal muscle adaptation.” 2008. Web. 28 Feb 2021.
Vancouver:
Bourajjaj M. Nuclear Factor of Activated T cells (NFAT): key regulator of cardiac hypertrophy and skeletal muscle adaptation. [Internet] [Doctoral dissertation]. University Utrecht; 2008. [cited 2021 Feb 28].
Available from: https://dspace.library.uu.nl/handle/1874/29300 ; URN:NBN:NL:UI:10-1874-29300 ; urn:isbn:978-90-7867-5426 ; URN:NBN:NL:UI:10-1874-29300 ; https://dspace.library.uu.nl/handle/1874/29300.
Council of Science Editors:
Bourajjaj M. Nuclear Factor of Activated T cells (NFAT): key regulator of cardiac hypertrophy and skeletal muscle adaptation. [Doctoral Dissertation]. University Utrecht; 2008. Available from: https://dspace.library.uu.nl/handle/1874/29300 ; URN:NBN:NL:UI:10-1874-29300 ; urn:isbn:978-90-7867-5426 ; URN:NBN:NL:UI:10-1874-29300 ; https://dspace.library.uu.nl/handle/1874/29300
Cleveland State University
22.
Harford, Terri J.
Regulation of Apoptosis by the Muscle Regulatory
Transcription Factor MyoD.
Degree: PhD, College of Science, 2009, Cleveland State University
URL: http://rave.ohiolink.edu/etdc/view?acc_num=csu1265812933
► We have previously reported that the level of MyoD expression correlates with the level of apoptosis that occurs in a subpopulation of skeletal myoblasts induced…
(more)
▼ We have previously reported that the level of
MyoD
expression correlates with the level of apoptosis that occurs in a
subpopulation of skeletal myoblasts induced to differentiate by
serum withdrawal. Herein we document that
MyoD expression dictates
the apoptotic threshold in myoblasts and fibroblasts in response to
a variety of apoptotic stimuli. Specifically, re-expression of
MyoD
inskeletal myoblasts rendered defective for both differentiation
and apoptosis by the expression of oncogenic Ras restores their
ability to undergo bothdifferentiation and apoptosis in response to
serum withdrawal. Further, using a fibroblast cell line expressing
an estrogen receptor:
MyoD fusion protein, we havedetermined that
addition of estrogen sensitizes these fibroblasts to apoptosis
induced by serum withdrawal, or by treatment with etoposide or
thapsigargin. RNAi mediated silencing of
MyoD in either 23A2 or
C2C12 myoblasts rendersthese cells resistant to apoptosis induced
by serum withdrawal, or by treatment with etoposide or
thapsigargin. Finally,
MyoD mediated regulation of the apoptotic
response to these various stimuli correlates with the level of
induction of the pro-apoptotic Bcl-2 family member
PUMA.
Advisors/Committee Members: Weyman, Crystal (Advisor).
Subjects/Keywords: Cellular Biology; Molecular Biology; MyoD; PUMA; apoptosis
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Harford, T. J. (2009). Regulation of Apoptosis by the Muscle Regulatory
Transcription Factor MyoD. (Doctoral Dissertation). Cleveland State University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=csu1265812933
Chicago Manual of Style (16th Edition):
Harford, Terri J. “Regulation of Apoptosis by the Muscle Regulatory
Transcription Factor MyoD.” 2009. Doctoral Dissertation, Cleveland State University. Accessed February 28, 2021.
http://rave.ohiolink.edu/etdc/view?acc_num=csu1265812933.
MLA Handbook (7th Edition):
Harford, Terri J. “Regulation of Apoptosis by the Muscle Regulatory
Transcription Factor MyoD.” 2009. Web. 28 Feb 2021.
Vancouver:
Harford TJ. Regulation of Apoptosis by the Muscle Regulatory
Transcription Factor MyoD. [Internet] [Doctoral dissertation]. Cleveland State University; 2009. [cited 2021 Feb 28].
Available from: http://rave.ohiolink.edu/etdc/view?acc_num=csu1265812933.
Council of Science Editors:
Harford TJ. Regulation of Apoptosis by the Muscle Regulatory
Transcription Factor MyoD. [Doctoral Dissertation]. Cleveland State University; 2009. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=csu1265812933
23.
Bourajjaj, M.
Nuclear Factor of Activated T cells (NFAT): key regulator of cardiac hypertrophy and skeletal muscle adaptation.
Degree: 2008, University Utrecht
URL: https://dspace.library.uu.nl/handle/1874/29300
;
URN:NBN:NL:UI:10-1874-29300
;
1874/29300
;
urn:isbn:9789078675426
;
URN:NBN:NL:UI:10-1874-29300
;
https://dspace.library.uu.nl/handle/1874/29300
► Despite significant progress in the prevention and treatment of cardiovascular diseases, heart failure is still a leading cause of morbidity and mortality in industrial countries.…
(more)
▼ Despite significant progress in the prevention and treatment of cardiovascular diseases, heart failure is still a leading cause of morbidity and mortality in industrial countries. Sustained cardiac hypertrophy, which is defined as an increase in heart size resulting from an increase in cardiomyocyte cell volume, has been recognized as the single most important risk factor for heart failure development. Cardiac hypertrophy can be initiated by a wide array of (neuro/humoral) growth factors in response to increased workload, injury, or intrinsic defects in contractile performance. To understand the molecular determinants of the hypertrophic response and to achieve future rational drug design to treat heart failure, investigation currently focuses on identifying and characterizing intracellular signal transduction pathways in the heart. The experiments presented in this thesis focus on a signaling pathway which plays a role in the hypertrophic transcriptional response of the myocyte. This signaling route employs the Ca2+-calmodulin-dependent phosphatase calcineurin and its immediate downstream transcriptional effector Nuclear Factor of Activated T-cells (NFAT), and further focuses on the immediate downstream NFAT target genes in cardiac muscle.
Subjects/Keywords: cardiac hypertrophy; heart failure; calcineurin; NFAT; myogenesis; MyoD
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Bourajjaj, M. (2008). Nuclear Factor of Activated T cells (NFAT): key regulator of cardiac hypertrophy and skeletal muscle adaptation. (Doctoral Dissertation). University Utrecht. Retrieved from https://dspace.library.uu.nl/handle/1874/29300 ; URN:NBN:NL:UI:10-1874-29300 ; 1874/29300 ; urn:isbn:9789078675426 ; URN:NBN:NL:UI:10-1874-29300 ; https://dspace.library.uu.nl/handle/1874/29300
Chicago Manual of Style (16th Edition):
Bourajjaj, M. “Nuclear Factor of Activated T cells (NFAT): key regulator of cardiac hypertrophy and skeletal muscle adaptation.” 2008. Doctoral Dissertation, University Utrecht. Accessed February 28, 2021.
https://dspace.library.uu.nl/handle/1874/29300 ; URN:NBN:NL:UI:10-1874-29300 ; 1874/29300 ; urn:isbn:9789078675426 ; URN:NBN:NL:UI:10-1874-29300 ; https://dspace.library.uu.nl/handle/1874/29300.
MLA Handbook (7th Edition):
Bourajjaj, M. “Nuclear Factor of Activated T cells (NFAT): key regulator of cardiac hypertrophy and skeletal muscle adaptation.” 2008. Web. 28 Feb 2021.
Vancouver:
Bourajjaj M. Nuclear Factor of Activated T cells (NFAT): key regulator of cardiac hypertrophy and skeletal muscle adaptation. [Internet] [Doctoral dissertation]. University Utrecht; 2008. [cited 2021 Feb 28].
Available from: https://dspace.library.uu.nl/handle/1874/29300 ; URN:NBN:NL:UI:10-1874-29300 ; 1874/29300 ; urn:isbn:9789078675426 ; URN:NBN:NL:UI:10-1874-29300 ; https://dspace.library.uu.nl/handle/1874/29300.
Council of Science Editors:
Bourajjaj M. Nuclear Factor of Activated T cells (NFAT): key regulator of cardiac hypertrophy and skeletal muscle adaptation. [Doctoral Dissertation]. University Utrecht; 2008. Available from: https://dspace.library.uu.nl/handle/1874/29300 ; URN:NBN:NL:UI:10-1874-29300 ; 1874/29300 ; urn:isbn:9789078675426 ; URN:NBN:NL:UI:10-1874-29300 ; https://dspace.library.uu.nl/handle/1874/29300
24.
Moraes, Luis Henrique Rapucci.
A reinervação do músculo extensor longo dos dedos (EDL) de ratos (rattus norvegicus) seria influenciada pelo uso do laser de baixa potência e do tecido adiposo na técnica de tubulização?.
Degree: Mestrado, Biologia Oral, 2009, University of São Paulo
URL: http://www.teses.usp.br/teses/disponiveis/25/25142/tde-18082010-090713/
;
► Lesões nervosas periféricas com alterações morfofuncionais são de grande importância clínica, porque pode prejudicar a função, comprometendo a sensibilidade e/ou a motricidade do órgão alvo.…
(more)
▼ Lesões nervosas periféricas com alterações morfofuncionais são de grande importância clínica, porque pode prejudicar a função, comprometendo a sensibilidade e/ou a motricidade do órgão alvo. Quando o nervo é lesado, o indivíduo torna-se impossibilitado de realizar suas atividades, seja profissional ou pessoal, e a partir do acidente esta situação se agrava ainda mais, pois tem início uma trajetória de sofrimento e humilhações decorrentes do tipo de assistência que passa a receber, tendo em vista, ainda, a fragilidade emocional e o abatimento moral de que passa a ser vítima. Na tentativa de reparo de lesões graves de nervos periféricos, várias técnicas têm sido utilizada, mas algumas com prejuízos funcionais para outras área do corpo, como por exemplo, quando se usa outro nervo no enxerto. Considerando que enxertos venosos tem tido bons resultados na capacidade regenerativa das fibras nervosas, e como elas são encontradas em abundância e em locais de fácil acesso cirúrgico, pensou-se em verificar se o tecido adiposo e o laser de baixa potência alterariam os resultados da reinervação, por tubulização, em músculos de contração rápida (EDL). Para isso foi utilizado 84 ratos (Rattus norvegicus) da linhagem wistar, machos, que foram divididos em 12 grupos (oito experimentais e quatro controles). Nos grupos experimentais (GE) foi utilizada tubulização de veia preenchida, ou não de tecido adiposo (GEVV e GEVG, respectivamente), com e sem tratamento de laser (GEVVL e GEVGL, respectivamente). Os grupos controles (GC) receberam os nomes de positivos (GCP) quando os animais não sofreram intervenção cirúrgica, e negativos (GCN) quando os animais foram submetidos à desnervação do nervo ciático. Todos os grupos tiveram os seus animais sacrificados em dois períodos, 45 e 150 dias, após o início do experimento. A certificação da recuperação foi feita por meio da análise dos músculos inervados por ele (EDL), comparando-os com os respectivos grupos controles. Técnicas de microscopia, Imunofluorescência (MyoD e miogenina), apoptose (Tunel), morfométricas e análise funcional do ciático, foram empregadas nesta investigação. Os resultados mostraram que aos 45 dias pós desnervação os dados dos grupos experimentais estavam mais próximos do grupo controle negativo, mas aos 150 dias eles estavam mais próximos aos do grupo controle positivo. Baseado nos dados obtidos pode-se concluir que o uso de tecido adiposo e do laser de baixa potência na técnica de tubulização do nervo ciático interferem na recuperação do músculo EDL desnervado.
The peripheral nerves injuries with morphofunctional alterations, have great clinical importance because could prejudice the function, committing the sensibility and/or the motricity of target organ. When nerve is damage, the individual becomes disabled to realize yours activities, either professional or personal, in the post accident periods, this situation aggravates each more, therefore initiate a trajectory of suffering and distressing despite of the kind of assistance that this person receives, in view of…
Advisors/Committee Members: Andreo, Jesus Carlos.
Subjects/Keywords: Análise funcional do ciático; Apoptose; Apoptosis; m- ATPase; m-ATPase; Miogenin; Miogenina; Muscle extensor digitorius longus; Músculo extensor longo dos dedos; MyoD; Myod; Sciatic functional analysis; Técnica de tubulização; Tubulization techniques
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Moraes, L. H. R. (2009). A reinervação do músculo extensor longo dos dedos (EDL) de ratos (rattus norvegicus) seria influenciada pelo uso do laser de baixa potência e do tecido adiposo na técnica de tubulização?. (Masters Thesis). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/25/25142/tde-18082010-090713/ ;
Chicago Manual of Style (16th Edition):
Moraes, Luis Henrique Rapucci. “A reinervação do músculo extensor longo dos dedos (EDL) de ratos (rattus norvegicus) seria influenciada pelo uso do laser de baixa potência e do tecido adiposo na técnica de tubulização?.” 2009. Masters Thesis, University of São Paulo. Accessed February 28, 2021.
http://www.teses.usp.br/teses/disponiveis/25/25142/tde-18082010-090713/ ;.
MLA Handbook (7th Edition):
Moraes, Luis Henrique Rapucci. “A reinervação do músculo extensor longo dos dedos (EDL) de ratos (rattus norvegicus) seria influenciada pelo uso do laser de baixa potência e do tecido adiposo na técnica de tubulização?.” 2009. Web. 28 Feb 2021.
Vancouver:
Moraes LHR. A reinervação do músculo extensor longo dos dedos (EDL) de ratos (rattus norvegicus) seria influenciada pelo uso do laser de baixa potência e do tecido adiposo na técnica de tubulização?. [Internet] [Masters thesis]. University of São Paulo; 2009. [cited 2021 Feb 28].
Available from: http://www.teses.usp.br/teses/disponiveis/25/25142/tde-18082010-090713/ ;.
Council of Science Editors:
Moraes LHR. A reinervação do músculo extensor longo dos dedos (EDL) de ratos (rattus norvegicus) seria influenciada pelo uso do laser de baixa potência e do tecido adiposo na técnica de tubulização?. [Masters Thesis]. University of São Paulo; 2009. Available from: http://www.teses.usp.br/teses/disponiveis/25/25142/tde-18082010-090713/ ;
25.
Natalia Camargo Rodrigues.
Ação da laserterapia de baixa intensidade (830nm) na regeneração muscular de ratos idosos.
Degree: 2009, Universidade Federal de São Carlos
URL: http://www.bdtd.ufscar.br/htdocs/tedeSimplificado//tde_busca/arquivo.php?codArquivo=2415
► Os idosos passam por continuas mudanças físicas, principalmente músculo-esqueléticas, como sarcopenia, alterações no sistema nervoso central e periférico, hipoperfusão sanguínea, alterações regenerativas contribuindo para atrofia…
(more)
▼ Os idosos passam por continuas mudanças físicas, principalmente músculo-esqueléticas, como sarcopenia, alterações no sistema nervoso central e periférico, hipoperfusão sanguínea, alterações regenerativas contribuindo para atrofia e fraqueza muscular, prejudicando as atividades de vida diárias (AVDs). O processo regenerativo ocorre pela determinação, proliferação, diferenciação das células satélites através da ativação do programa genético músculo-específico, que é regulado por fatores de transcrição específicos, conhecidos como fatores regulatórios miogênicos (FRMs). Porém no idoso por causa das alterações músculo-esqueléticas a ativação dos FRMs são ineficientes, prejudicando o processo de regeneração. Entretanto, recentes achados mostraram resultados muito promissores da laser terapia de baixa intensidade (LTBI) na regeneração muscular, mas os efeitos desta terapia quando associado ao envelhecimento continuam desconhecidos. Este projeto tem por objetivo avaliar os efeitos da (LTBI), λ=830nm, no músculo tibial de ratos idosos após criolesão. Foram utilizados 56 ratos machos Wistar, divididos aleatoriamente em 4 grupos (n=7) de ratos jovens de 3 meses e 4 grupos (n=7) de ratos idosos de 10 meses; subdivididos em: grupos controle (C), grupos em que o músculo tibial anterior direito (TAD) foi apenas irradiado (I), grupos em que o TAD foi submetido à criolesão (CL) e grupos onde o TAD foi submetido à criolesão e a irradiação (LI). O tratamento com o laser modelo da DMC, classe 3B, energia de 0,87 J, foi realizado a cada 24 h, durante cinco dias consecutivos, com a primeira aplicação 24 horas após a indução da lesão. No sexto dia pós lesão, com os animais vivos e anestesiados, o músculo TAD foi cuidadosamente dissecado e retirado, e logo depois os animais foram eutanaziados. Realizou-se analises histológicas da área da lesão com Azul de Toluidina e contagem dos capilares sanguíneos com Hematoxilina-eosina. Por meio da análise por RT-PCR, foi possível analisar a expressão dos genes MyoD e VEGF. Os resultados mostraram que houve aumento significativo (p<0,05) da expressão gênica da MyoD, do VEGF e da contagem de capilares sanguíneos mais proeminentes nos grupos idosos lesados e irradiados do que no grupo jovem. Provavelmente a LTBI aumentou a maturação das células satélites em mioblastos e miotubos, melhorando o processo regenerativo dos ratos idosos irradiados.
The elderly still go through physical changes, especially musculoskeletal disorders such as sarcopenia, changes in central and peripheral nervous system, blood hypoperfusion, regenerative changes contributing to atrophy and muscle weakness, undermining the activities of daily living (AVL). The regenerative process happens about the determination, proliferation and differentiation of satellite cells through activation of muscle-specific genetic program, which is regulated by specific transcription factors, known as myogenic regulatory factors (MRFs). But in the elderly because of changes in skeletal muscle-activation of MRFs are inefficient, hindering the…
Advisors/Committee Members: Nivaldo Antonio Parizotto.
Subjects/Keywords: Biotecnologia; Laserterapia; Regeneração muscular; Ratos idosos; MyoD; VEGF (Fator de Crescimento de Endotélio Vascular); Terapia laser de baixa intensidade (LTBI); Outros; Low laser therapy (LLT); Muscle regeneration; Aged rats
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Rodrigues, N. C. (2009). Ação da laserterapia de baixa intensidade (830nm) na regeneração muscular de ratos idosos. (Thesis). Universidade Federal de São Carlos. Retrieved from http://www.bdtd.ufscar.br/htdocs/tedeSimplificado//tde_busca/arquivo.php?codArquivo=2415
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Rodrigues, Natalia Camargo. “Ação da laserterapia de baixa intensidade (830nm) na regeneração muscular de ratos idosos.” 2009. Thesis, Universidade Federal de São Carlos. Accessed February 28, 2021.
http://www.bdtd.ufscar.br/htdocs/tedeSimplificado//tde_busca/arquivo.php?codArquivo=2415.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Rodrigues, Natalia Camargo. “Ação da laserterapia de baixa intensidade (830nm) na regeneração muscular de ratos idosos.” 2009. Web. 28 Feb 2021.
Vancouver:
Rodrigues NC. Ação da laserterapia de baixa intensidade (830nm) na regeneração muscular de ratos idosos. [Internet] [Thesis]. Universidade Federal de São Carlos; 2009. [cited 2021 Feb 28].
Available from: http://www.bdtd.ufscar.br/htdocs/tedeSimplificado//tde_busca/arquivo.php?codArquivo=2415.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Rodrigues NC. Ação da laserterapia de baixa intensidade (830nm) na regeneração muscular de ratos idosos. [Thesis]. Universidade Federal de São Carlos; 2009. Available from: http://www.bdtd.ufscar.br/htdocs/tedeSimplificado//tde_busca/arquivo.php?codArquivo=2415
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
26.
Uliana Sbeguen Stotzer.
Efeitos do treinamento resistido associado com decanoato de nandrolona sobre a expressão gênica de moduladores de vias de hipertrofia e atrofia do músculo esquelético.
Degree: 2009, Universidade Federal de São Carlos
URL: http://www.bdtd.ufscar.br/htdocs/tedeSimplificado//tde_busca/arquivo.php?codArquivo=2914
► O uso de esteróides anabólicos androgênicos (EAA) é disseminado entre atletas e não atletas que desejam melhorar o desempenho ou a aparência física. Os EAA…
(more)
▼ O uso de esteróides anabólicos androgênicos (EAA) é disseminado entre atletas e não atletas que desejam melhorar o desempenho ou a aparência física. Os EAA agem sobre as células satélites no músculo esquelético, que são as principais precursoras do músculo esquelético, sendo essenciais tanto para crescimento quanto para reparo muscular. Quando são ativadas, na presença de diversos fatores, incluindo o fator D de diferenciação miogênica (MyoD), elas podem se proliferar e diferenciar-se em novas miofibrilas ou mionúcleos, resultando em maior síntese proteica. Por outro lado, a miostatina é capaz de inibir essa progressão do ciclo celular. Uma maior expressão de ubiquitinas de ligação, Atrogina-1 e muscle ring finger protein 1(MuRF-1), resulta em aumentada degradação muscular. Entender os mecanismos de ação dos EAA no músculo esquelético é essencial para uma melhor compreensão da fisiologia muscular sob a ação dos EAA. O objetivo desse estudo foi investigar os efeitos do treinamento pliométrico aquático com sobrecarga associado a doses suprafisiológicas de EAA sobre a expressão de moduladores de vias de hipertrofia e atrofia do músculo esquelético. Ratos Wistar foram agrupados em não treinados (S), treinados (T), S tratados com EAA (E), e T tratados com EAA (TE). Os grupos que treinaram realizaram saltos na água: quatro séries de 10 saltos com 30 segundos de intervalo entre as séries, 5 vezes por semana durante 7 semanas, com uma sobrecarga progressiva de 50 a 80% do peso corporal. Decanoato de nandrolona (5 mg/kg) foi injetado subcutaneamente duas vezes por semana. Imediatamente após a última sessão os animais foram mortos. A expressão gênica de miostatina, MyoD, Atrogina-1 e MuRF-1 do músculo gastrocnêmio foi determinada por transcriptase reversa-reação em cadeia da polimerase (RT-PCR) em tempo real. O treinamento não alterou a expressão de nenhum dos genes estudados, enquanto sua associação com o EAA aumentou a expressão gênica de atrogina-1 e reduziu de miostatina. A expressão de MyoD e MuRF-1 não foi alterada pelo EAA. Os resultados mostraram que tanto a miostatina quando a atrogina-1, importantes genes relacionados tanto a progressão do ciclo celular quanto a degradação de proteínas no músculo esquelético, são sensíveis ao EAA.
Androgenic-anabolic steroids (AAS) are spread among athletes and no athletes in order to improve performance or physical appearance. AAS targets the satellite cells in skeletal muscles, which are the major precursors of the skeletal muscle, and are essential for muscle growth and repair. When activated, in the presence of several factors, including myogenic differentiation factor D (MyoD), they proliferate and differentiate into new myofibers or myonuclei, resulting in increased protein synthesis. On the other hand, myostatin is able to inhibit cell cycle progression. Up-regulation of the expression of ubiquitin ligases, Atrogin-1 and muscle ring finger protein 1 (MuRF-1), results in increased muscle degradation. The understanding of AAS mechanism of action in skeletal muscle is critical…
Advisors/Committee Members: Heloísa Sobreiro Selistre de Araujo.
Subjects/Keywords: MuRF-1; Atrogina-1; MyoD; Treinamento pliométrico Aquático; Músculo gatrocnêmio; Ciclo celular; Esteróides anabólicos; Fisiologia do exercício físico; FISIOLOGIA; Aquatic plyometric training; Androgenic-anabolic steroids; Myostatin
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Stotzer, U. S. (2009). Efeitos do treinamento resistido associado com decanoato de nandrolona sobre a expressão gênica de moduladores de vias de hipertrofia e atrofia do músculo esquelético. (Thesis). Universidade Federal de São Carlos. Retrieved from http://www.bdtd.ufscar.br/htdocs/tedeSimplificado//tde_busca/arquivo.php?codArquivo=2914
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Stotzer, Uliana Sbeguen. “Efeitos do treinamento resistido associado com decanoato de nandrolona sobre a expressão gênica de moduladores de vias de hipertrofia e atrofia do músculo esquelético.” 2009. Thesis, Universidade Federal de São Carlos. Accessed February 28, 2021.
http://www.bdtd.ufscar.br/htdocs/tedeSimplificado//tde_busca/arquivo.php?codArquivo=2914.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Stotzer, Uliana Sbeguen. “Efeitos do treinamento resistido associado com decanoato de nandrolona sobre a expressão gênica de moduladores de vias de hipertrofia e atrofia do músculo esquelético.” 2009. Web. 28 Feb 2021.
Vancouver:
Stotzer US. Efeitos do treinamento resistido associado com decanoato de nandrolona sobre a expressão gênica de moduladores de vias de hipertrofia e atrofia do músculo esquelético. [Internet] [Thesis]. Universidade Federal de São Carlos; 2009. [cited 2021 Feb 28].
Available from: http://www.bdtd.ufscar.br/htdocs/tedeSimplificado//tde_busca/arquivo.php?codArquivo=2914.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Stotzer US. Efeitos do treinamento resistido associado com decanoato de nandrolona sobre a expressão gênica de moduladores de vias de hipertrofia e atrofia do músculo esquelético. [Thesis]. Universidade Federal de São Carlos; 2009. Available from: http://www.bdtd.ufscar.br/htdocs/tedeSimplificado//tde_busca/arquivo.php?codArquivo=2914
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Université Laval
27.
B-Huot, Nicolas.
Un adenovirus exprimant MyoD induit la myogenèse des
cellules souches embryonnaires humaines.
Degree: 2009, Université Laval
URL: http://hdl.handle.net/20.500.11794/20682
► Avec leurs caractéristiques d'auto-renouvellement illimité et de pluripotence, les cellules souches embryonnaires humaines (hESC) représentent une source infinie de cellules pour la thérapie cellulaire de…
(more)
▼ Avec leurs caractéristiques d'auto-renouvellement
illimité et de pluripotence, les cellules souches embryonnaires
humaines (hESC) représentent une source infinie de cellules pour la
thérapie cellulaire de maladies, telle que la dystrophie musculaire
de Duchenne. Des études ont démontré que les hESC pouvaient être
différenciées en cellules musculaires squelettiques, mais les
techniques employées sont longues et inefficaces. Ce mémoire décrit
un nouveau protocole de différenciation des hESC en cellules
musculaires squelettiques à l'aide d'un adénovirus exprimant le
gène
MyoD sous le contrôle du promoteur CAO (Ad.CAO-
MyoD).
L'efficacité de ce virus pour induire la myogenèse des hESC a été
mise en évidence par la présence de divers marqueurs myogéniques.
Ensuite, le potentiel de fusion de ces cellules a été illustré par
le marquage de la MyHC et par l'observation de quelques myotubes.
Ces résultats préliminaires semblent indiquer que l'Ad.CAO-
MyoD est
un outil prometteur pour différencier les hESC en cellules
musculaires squelettiques.
Advisors/Committee Members: Tremblay, Jacques-P..
Subjects/Keywords: Muscle strié – Régénération; Protéine MyoD; Adénovirus; Myogénèse; Cellules souches embryonnaires
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
B-Huot, N. (2009). Un adenovirus exprimant MyoD induit la myogenèse des
cellules souches embryonnaires humaines. (Thesis). Université Laval. Retrieved from http://hdl.handle.net/20.500.11794/20682
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
B-Huot, Nicolas. “Un adenovirus exprimant MyoD induit la myogenèse des
cellules souches embryonnaires humaines.” 2009. Thesis, Université Laval. Accessed February 28, 2021.
http://hdl.handle.net/20.500.11794/20682.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
B-Huot, Nicolas. “Un adenovirus exprimant MyoD induit la myogenèse des
cellules souches embryonnaires humaines.” 2009. Web. 28 Feb 2021.
Vancouver:
B-Huot N. Un adenovirus exprimant MyoD induit la myogenèse des
cellules souches embryonnaires humaines. [Internet] [Thesis]. Université Laval; 2009. [cited 2021 Feb 28].
Available from: http://hdl.handle.net/20.500.11794/20682.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
B-Huot N. Un adenovirus exprimant MyoD induit la myogenèse des
cellules souches embryonnaires humaines. [Thesis]. Université Laval; 2009. Available from: http://hdl.handle.net/20.500.11794/20682
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
28.
Faralli, Hervé.
Tshz3 un marqueur des cellules satellites : une étude de sa fonction dans la régulation de la myogenèse chez la souris : Tshz3 a marker of Satellite cells : study of his role in the regulation of mouse myogenesis.
Degree: Docteur es, Biologie des eucaryotes, 2010, Aix-Marseille 2
URL: http://www.theses.fr/2010AIX22045
► L’unité cellulaire du muscle squelettique est la myofibre, un syncytium hautement spécialisé générant la contraction musculaire. Au cours de la croissance et de la régénération…
(more)
▼ L’unité cellulaire du muscle squelettique est la myofibre, un syncytium hautement spécialisé générant la contraction musculaire. Au cours de la croissance et de la régénération musculaire, les cellules satellites quiescentes (cellules souches) du muscle squelettique adulte sont activées, prolifèrent puis fusionnent formant de nouvelles fibres. A l’aide d’un modèle murin de régénération et de cultures primaires, j’ai identifié TSHZ3 comme un nouveau marqueur des cellules satellites quiescentes et activées. Dans la lignée cellulaire C2C12, j’ai mis en évidence un effet répresseur spécifique de Tshz3 sur la différenciation myogénique. L’entrée des myoblastes dans la voie de différenciation terminale est déclenchée par le facteur Myogenin (MYOG). L’activation de la transcription du gène myogenin (Myog) est dépendante du facteur MYOD et fait intervenir le complexe de remodelage de la chromatine SWI/SNF. In vitro, TSHZ3 interagit avec BAF57 une sous unité du complexe SWI/SNF. TSHZ3 réprime l’activation dépendante de MYOD sur le promoteur proximal de Myog et cette répression dépend en partie de la présence de BAF57. L’activité répressive et la cinétique d’expression de Tshz3, indique que TSHZ3 pourrait empêcher l’activation prématurée du promoteur Myog lors de la prolifération des cellules satellites activées. TSHZ3 pourrait ainsi participer aux mécanismes de régulation permettant de contrôler l’équilibre entre prolifération, différenciation et renouvellement des progéniteurs myogéniques.
Skeletal muscles are made of several units called myofibers, a syncitium into which muscular contraction is generated. During the muscle growth and repair, the quiescent Satellite Cells (SCs; adult stem cells) become activated, proliferate and differentiate to form new multinucleated myofibers. In animal model and primary culture, I found that, Tshz3 was strongly expressed in the quiescent and activated satellite cells.In C2C12 myoblast cells, I showed a specific repressive effect of TSHZ3 on the myogenic differentiation. The terminal differentiation of the myoblastes is trigger by Myogenin (Myog). The transcriptional activation of Myog promoter involves MYOD and the SWI/SNF remodelling complex. In vitro, I showed that TSHZ3 interacts with BAF57, a subunit of the SWI/SNF complex. TSHZ3 represses the MYOD-dependant activation on the Myog promoter. This specific repression involves in part BAF57.The repressive activity of and the temporal dynamic of expression of Tshz3, indicated that TSHZ3 potentially is required to impede the premature activation of the Myog promotor during the SCs proliferation. These results suggest that TSHZ3 plays important roles in the molecular mechanisms operating in activated SCs when there are poised between proliferation, differentiation and self renewal of muscular progenitors.
Advisors/Committee Members: Fasano, Laurent (thesis director), Caubit, Xavier (thesis director).
Subjects/Keywords: Muscle squelettique; Cellules satellites; Développement; Régénération; Tshz3; MyoD; Myog; Baf57; Swi/snf
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Faralli, H. (2010). Tshz3 un marqueur des cellules satellites : une étude de sa fonction dans la régulation de la myogenèse chez la souris : Tshz3 a marker of Satellite cells : study of his role in the regulation of mouse myogenesis. (Doctoral Dissertation). Aix-Marseille 2. Retrieved from http://www.theses.fr/2010AIX22045
Chicago Manual of Style (16th Edition):
Faralli, Hervé. “Tshz3 un marqueur des cellules satellites : une étude de sa fonction dans la régulation de la myogenèse chez la souris : Tshz3 a marker of Satellite cells : study of his role in the regulation of mouse myogenesis.” 2010. Doctoral Dissertation, Aix-Marseille 2. Accessed February 28, 2021.
http://www.theses.fr/2010AIX22045.
MLA Handbook (7th Edition):
Faralli, Hervé. “Tshz3 un marqueur des cellules satellites : une étude de sa fonction dans la régulation de la myogenèse chez la souris : Tshz3 a marker of Satellite cells : study of his role in the regulation of mouse myogenesis.” 2010. Web. 28 Feb 2021.
Vancouver:
Faralli H. Tshz3 un marqueur des cellules satellites : une étude de sa fonction dans la régulation de la myogenèse chez la souris : Tshz3 a marker of Satellite cells : study of his role in the regulation of mouse myogenesis. [Internet] [Doctoral dissertation]. Aix-Marseille 2; 2010. [cited 2021 Feb 28].
Available from: http://www.theses.fr/2010AIX22045.
Council of Science Editors:
Faralli H. Tshz3 un marqueur des cellules satellites : une étude de sa fonction dans la régulation de la myogenèse chez la souris : Tshz3 a marker of Satellite cells : study of his role in the regulation of mouse myogenesis. [Doctoral Dissertation]. Aix-Marseille 2; 2010. Available from: http://www.theses.fr/2010AIX22045
29.
Teng, Allen C. T.
Transcriptional Control of Metabolism and the Response to Ischemia in Muscle
.
Degree: 2011, University of Ottawa
URL: http://hdl.handle.net/10393/20479
► Skeletal muscle is one of the largest tissues in humans and provides many pivotal functions to support life. Abnormality in skeletal muscle functions can lead…
(more)
▼ Skeletal muscle is one of the largest tissues in humans and provides many pivotal functions to support life. Abnormality in skeletal muscle functions can lead to disease. For example, insulin resistance in skeletal muscle leads to type II diabetes. The underlying mechanisms that control energy balance in skeletal muscle remain largely elusive, especially at the genetic level. Here in the second chapter, I showed that MyoD mediated the transcriptional regulation of ACSL5, a mitochondrial protein, in C2C12 myoblasts via two E-box elements. A SNP rs2419621 (T) created a de novo E-box that together with the two pre-existing proximal E-boxes strongly enhances ACSL5 expression in both CV1 and C2C12 cells. In the third chapter, I identified a novel VGLL4-interacting protein IRF2BP2 and verified the interaction with co-immunoprecipitation and mammalian two-hybrid assays. Functionally, overexpression of IRF2BP2 and transcription factor TEAD1 activates mouse VEGF-A promoter in CV1 cells and enhances the biosynthesis of VEGF-A in C2C12 myoblasts. In vivo studies showed that ischemia induced the expression of IRF2BP2 by more than three fold, suggesting that IRF2BP2 could play a pivotal role during tissue ischemia. IRF2BP2 is a nuclear protein in both mouse cardiac myocytes and C2C12 myoblasts as demonstrated by immunohistochemistry and immunocytochemistry, respectively. Therefore, I sought to delineate the mechanism for the nuclear shuttling of IRF2BP2 in the fourth chapter. With various DNA alternations, I mapped the NLS to an evolutionarily conserved sequence 354ARKRKPSP361 in IRF2BP2. Deletion of the positively charged amino acids resulted in the abolishment of the NLS signal. Next, I showed that phosphorylation of serine 360 (S360) mediates the nuclear import of the protein. Whereas an alanine substitution (S360A) at the site resulted in perinuclear accumulation of the protein, an aspartic acid substitution (S360D) forced the nuclear accumulation. Nevertheless, the forced accumulation of the S360D mutant did not enhance the activation of VEGF-A promoter in CV1 cells as did the wild-type protein. My studies revealed two novel mechanisms by which skeletal muscle could harvest energy, thus providing new insight into the energy metabolism in skeletal muscle
Subjects/Keywords: VEGF-A;
Angiogenesis;
Skeletal Muscle;
TEAD1;
IRF2BP2;
MyoD;
ACSL5
…Figure 2. The ACSL5 rs2419621 (T) allele is a functional MyoD binding site….. …37… …Figure 3. MyoD differentially activates the ACSL5 promoter according to the rs2419621
genotype…
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Teng, A. C. T. (2011). Transcriptional Control of Metabolism and the Response to Ischemia in Muscle
. (Thesis). University of Ottawa. Retrieved from http://hdl.handle.net/10393/20479
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Teng, Allen C T. “Transcriptional Control of Metabolism and the Response to Ischemia in Muscle
.” 2011. Thesis, University of Ottawa. Accessed February 28, 2021.
http://hdl.handle.net/10393/20479.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Teng, Allen C T. “Transcriptional Control of Metabolism and the Response to Ischemia in Muscle
.” 2011. Web. 28 Feb 2021.
Vancouver:
Teng ACT. Transcriptional Control of Metabolism and the Response to Ischemia in Muscle
. [Internet] [Thesis]. University of Ottawa; 2011. [cited 2021 Feb 28].
Available from: http://hdl.handle.net/10393/20479.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Teng ACT. Transcriptional Control of Metabolism and the Response to Ischemia in Muscle
. [Thesis]. University of Ottawa; 2011. Available from: http://hdl.handle.net/10393/20479
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Universitat de Barcelona
30.
Pedraza González, Neus.
Estudi de la regulació transcripcional del gen de la proteïna desacobladora UCP3.
Degree: Departament de Bioquímica i Biologia Molecular (Divisió III), 2004, Universitat de Barcelona
URL: http://hdl.handle.net/10803/2987
► <i>UCP3</i> gene is mainly expressed in skeletal muscle and brown adipose tissue in rodents, and almost exclusively in skeletal muscle in humans. The gene is…
(more)
▼ <i>UCP3</i> gene is mainly expressed in skeletal muscle and brown adipose tissue in rodents, and almost exclusively in skeletal muscle in humans. The gene is activated in response to different stimulus, such as retinoic acid, fatty acids and thyroid hormones. In the present study we investigate the molecular mechanisms responsible for <i>UCP3</i> gene expression in skeletal muscle and for the retinoic acid, fatty acids and thyroid hormones-dependent activation. Studying <i>UCP3</i> gene regulation <i>in vivo</i> has allowed to establish the importance of some of these mechanisms in a physiological context. In agreement with the specific expression of human <i>UCP3</i> in muscle, the myogenic transcription factor
MyoD is needed for <i>UCP3</i> promoter basal activity.
MyoD regulates the expression of the human <i>UCP3</i> gene through Ebox-like sequences near the initiation transcription site (-29/-9). Moreover,
MyoD is necessary for retinoic acid, fatty acid or thyroid hormone-dependent activation of the <i>UCP3</i> promoter. Retinoic acid, a transcriptional activator of <i>UCP1</i> and <i>UCP2</i> gene expression, activates <i>UCP3</i> gene expression in differentiated skeletal muscle cells. Human <i>UCP3</i> gene response to retinoic acid is mediated by retinoic acid receptors (RAR-RXR) through a hormone response element DR1 (AGGTTTcAGGTCA) located in the proximal region of the promoter (-71/-59). In addition, <i>UCP3</i> gene activation by fatty acids is achieved by PPAR-alpha or PPAR-delta (peroxisome proliferator activated receptor) through the previously described DR1, <i>in vitro</i> and <i>in vivo</i>. Studies in PPAR-alpha-KO mice has revealed that PPAR-alpha is differentially required for <i>UCP3</i> gene expression, depending on tissues (heart or skeletal muscle) and development stages (newborns and adults). Finally, thyroid hormones activate human and mouse <i>UCP3</i> gene expression <i>in vivo</i> and <i>in vitro</i>. This activation is mediated by thyroid hormone receptor (TR) through the DNA region that contains the DR1 element, in both human and mouse <i>UCP3</i> promoter. In conclusion, the DR1 element located in the proximal region of <i>UCP3</i> gene promoter is a multihormonal response element able to mediate retinoic acid, thyroid hormone and fatty acid-dependent activation of <i>UCP3</i> gene. In the future, it should be interesting to study the relationship between these signalling pathways <i>in vivo</i>.
Advisors/Committee Members: [email protected] (authoremail), true (authoremailshow), Villarroya i Gombau, Francesc (codirector), Solanas Garcia, Gemma (codirector).
Subjects/Keywords: Cèl·lules musculars; Factor de transcripció miogènic MyoD; Proteïnes; Ciències Experimentals i Matemàtiques; 575
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Pedraza González, N. (2004). Estudi de la regulació transcripcional del gen de la proteïna desacobladora UCP3. (Thesis). Universitat de Barcelona. Retrieved from http://hdl.handle.net/10803/2987
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Pedraza González, Neus. “Estudi de la regulació transcripcional del gen de la proteïna desacobladora UCP3.” 2004. Thesis, Universitat de Barcelona. Accessed February 28, 2021.
http://hdl.handle.net/10803/2987.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Pedraza González, Neus. “Estudi de la regulació transcripcional del gen de la proteïna desacobladora UCP3.” 2004. Web. 28 Feb 2021.
Vancouver:
Pedraza González N. Estudi de la regulació transcripcional del gen de la proteïna desacobladora UCP3. [Internet] [Thesis]. Universitat de Barcelona; 2004. [cited 2021 Feb 28].
Available from: http://hdl.handle.net/10803/2987.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Pedraza González N. Estudi de la regulació transcripcional del gen de la proteïna desacobladora UCP3. [Thesis]. Universitat de Barcelona; 2004. Available from: http://hdl.handle.net/10803/2987
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
◁ [1] [2] ▶
. 
Open Access Theses and Dissertations
