subject:(LC3)

NSYSU

1. Lin, Yu-jen. Study of autophagy and cell toxicity in natural product AN30 treated oral cancer cells.

Degree: Master, Institute of Biomedical Sciences, 2015, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0415115-160136

► AN30 is extracted from stem and leaves of Thelypteris torresiana. Recently, select killing cancer cells through apoptosis and other mechanisms are proved to increase the… (more)

Subjects/Keywords: AN30; starvation; autophagy; LC3; oral cancer; chloroquine

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Lin, Y. (2015). Study of autophagy and cell toxicity in natural product AN30 treated oral cancer cells. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0415115-160136

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Lin, Yu-jen. “Study of autophagy and cell toxicity in natural product AN30 treated oral cancer cells.” 2015. Thesis, NSYSU. Accessed April 12, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0415115-160136.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Lin, Yu-jen. “Study of autophagy and cell toxicity in natural product AN30 treated oral cancer cells.” 2015. Web. 12 Apr 2021.

Vancouver:

Lin Y. Study of autophagy and cell toxicity in natural product AN30 treated oral cancer cells. [Internet] [Thesis]. NSYSU; 2015. [cited 2021 Apr 12]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0415115-160136.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Lin Y. Study of autophagy and cell toxicity in natural product AN30 treated oral cancer cells. [Thesis]. NSYSU; 2015. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0415115-160136

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Adelaide

2. Ganesan, Swamynathan. Analysing the role of autophagy in Alzheimer’s disease pathogenesis using the zebrafish model system.

Degree: 2015, University of Adelaide

URL: http://hdl.handle.net/2440/101649

► Alzheimer’s disease (AD) is the most common form of dementia and is characterized by the formation of neuritic plaques and neurofibrillary tangles in the brain.… (more)

▼ Alzheimer’s disease (AD) is the most common form of dementia and is characterized by the formation of neuritic plaques and neurofibrillary tangles in the brain. The plaques are composed of β-amyloid peptides resulting from the cleavage of the Amyloid Precursor Protein (AβPP) by β-secretase and then by γ-secretase. Failure in clearance of these peptides results in the formation of these senile plaques. Autophagy is a degradative pathway in cells responsible for protein clearance and its dysfunction has been implicated in AD pathogenesis. Moreover, the PRESENILINs which are central in AβPP processing also have functional roles in autophagy. Other contributing factors of AD progression such as hypoxia, ER stress, and mitochondrial dysfunction are also related to autophagy. Zebrafish embryos are a suitable system in which to monitor autophagy and investigate its implications for AD pathogenesis. Assays to monitor autophagy can be carried out efficiently in zebrafish embryos. In Chapter II of this thesis, we identified the zebrafish orthologues of the mammalian MAP1LC3 gene family which is comprised of important proteins involved in autophagy. We identified two genes namely map1lc3a and map1lc3b through phylogeny and conserved synteny analysis. Using the LC3 immunoblot assay, we validated that the LC3II/LC3I ratio is significantly increased in the presence of rapamycin and sodium azide with chloroquine. This was used to confirm that hypoxia induces autophagy in 72 hpf zebrafish larvae. Similarly, results of qPCR assays also showed increased map1lc3a transcript levels in the presence of both rapamycin and sodium azide. However transcript levels of map1lc3b were reduced under these same conditions. In Chapter III of this thesis, we used the LC3 immunoblot assay to monitor the effects of truncations of PRESENILIN proteins on autophagy. PRESENILINs are critical for the autophagy pathway but in our study, truncations of PRESENILIN proteins (zPsen1Δ4 and zPsen2Δ4) do not affect autophagy in zebrafish larvae. We also showed that rapamycin has the ability to induce autophagy in explanted zebrafish adult brains. In Chapter IV, we tested a chemical, Latrepirdine, to see whether it can induce autophagy in zebrafish larvae. Using the LC3 immunoblot assay and TEM analysis we showed that Latrepirdine at a 5μM concentration can induce autophagy in zebrafish larvae. As a continuation, in Chapter V, we tested two Latrepirdine-related drugs (Harmol and P7C3) on zebrafish larvae to observe whether they show similar effects. Both these drugs did not appear to have an effect on autophagy or apoptosis in 72 hpf zebrafish larvae. In Chapter VI we developed a novel assay based on poly-glutamine repeats fused to GFP (polyQ80-GFP) to monitor autophagy. Using this assay we showed that polyQ degradation in cells occur in an autophagy-dependent manner. This assay will be a useful tool to monitor autophagy in zebrafish larvae in future. In conclusion, zebrafish serves as an excellent tool to analyze autophagy. Various assays to monitor autophagy can… Advisors/Committee Members: Lardelli, Michael Trent (advisor), Richards, Robert Ian (advisor), School of Biological Sciences (school).

Subjects/Keywords: Alzheimer's disease; autophagy; zebrafish; Presenilin; LC3

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Ganesan, S. (2015). Analysing the role of autophagy in Alzheimer’s disease pathogenesis using the zebrafish model system. (Thesis). University of Adelaide. Retrieved from http://hdl.handle.net/2440/101649

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Ganesan, Swamynathan. “Analysing the role of autophagy in Alzheimer’s disease pathogenesis using the zebrafish model system.” 2015. Thesis, University of Adelaide. Accessed April 12, 2021. http://hdl.handle.net/2440/101649.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Ganesan, Swamynathan. “Analysing the role of autophagy in Alzheimer’s disease pathogenesis using the zebrafish model system.” 2015. Web. 12 Apr 2021.

Vancouver:

Ganesan S. Analysing the role of autophagy in Alzheimer’s disease pathogenesis using the zebrafish model system. [Internet] [Thesis]. University of Adelaide; 2015. [cited 2021 Apr 12]. Available from: http://hdl.handle.net/2440/101649.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Ganesan S. Analysing the role of autophagy in Alzheimer’s disease pathogenesis using the zebrafish model system. [Thesis]. University of Adelaide; 2015. Available from: http://hdl.handle.net/2440/101649

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of New South Wales

3. Nguyen, Quang Dieu. Durability properties of low-carbon concrete incorporating alternative supplementary cementitious materials and manufactured aggregate.

Degree: Civil & Environmental Engineering, 2020, University of New South Wales

URL: http://handle.unsw.edu.au/1959.4/65033

► The demand for concrete has been overwhelming nowadays due to globally booming economy and population, which induces environmental and social issues including the increase in… (more)

▼ The demand for concrete has been overwhelming nowadays due to globally booming economy and population, which induces environmental and social issues including the increase in anthropogenic CO2 emission from cement production and natural sand rarefaction by excessive exploitations. A new supplementary cementitious material (SCM) known as a combination of flash calcined clay and limestone has been promoted as promising alternatives to fulfil the development of sustainable concrete. Ferronickel slag sand is also a potential option to replace natural sand in concrete. However, performance in terms of durability is always a concern for the industry delaying the widespread adoption of new low-carbon concrete. This study aims to investigate the durability performance of concrete containing flash calcined clay, limestone as binder replacement (LC3 concrete) and ferronickel slag as natural fine aggregate replacement (FNS concrete). The influence of flash calcined clay, limestone and ferronickel slag on the deterioration of concrete structure including alkali-silica reaction (ASR), reinforcement corrosion in initial and propagation phases were evaluated. The variation of mechanical, physical and durability properties of LC3 concrete with various amounts of calcined clay and limestone and FNS concrete with fly ash as SCM was investigated. The performance of both LC3 and FNS concretes in the initial phase of reinforcement corrosion relating to carbonation and chloride diffusion resistance was investigated through accelerated and natural test protocols. The propagation stage of rebar corrosion of LC3 concrete was monitored and the electrochemical testing methods developed for Ordinary Portland Cement (OPC) concrete were validated for LC3 concrete. The mitigation effect on ASR expansion of flash calcined clay and limestone was systematically evaluated using the accelerated mortar bar test, scanning electron microscopy (SEM) analysis and model reactant experiments. The expansion due to ASR of FNS concrete which is the major concern to adopt manufactured sand into concrete industry was monitored and evaluated by using concrete prism test (CPT) and SEM. Results show that the use of flash calcined clay, limestone and ferronickel slag sand in concrete not only allows to produce low-carbon concretes but also to enhance the durability performance, except for carbonation penetration in LC3 concrete. Advisors/Committee Members: Castel , Arnaud , UNSW, Kim, Taehwan, UNSW.

Subjects/Keywords: Limestone; LC3; Calcined clay; Ferronickel slag; Durability

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Nguyen, Q. D. (2020). Durability properties of low-carbon concrete incorporating alternative supplementary cementitious materials and manufactured aggregate. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/65033

Chicago Manual of Style (16^th Edition):

Nguyen, Quang Dieu. “Durability properties of low-carbon concrete incorporating alternative supplementary cementitious materials and manufactured aggregate.” 2020. Doctoral Dissertation, University of New South Wales. Accessed April 12, 2021. http://handle.unsw.edu.au/1959.4/65033.

MLA Handbook (7^th Edition):

Nguyen, Quang Dieu. “Durability properties of low-carbon concrete incorporating alternative supplementary cementitious materials and manufactured aggregate.” 2020. Web. 12 Apr 2021.

Vancouver:

Nguyen QD. Durability properties of low-carbon concrete incorporating alternative supplementary cementitious materials and manufactured aggregate. [Internet] [Doctoral dissertation]. University of New South Wales; 2020. [cited 2021 Apr 12]. Available from: http://handle.unsw.edu.au/1959.4/65033.

Council of Science Editors:

Nguyen QD. Durability properties of low-carbon concrete incorporating alternative supplementary cementitious materials and manufactured aggregate. [Doctoral Dissertation]. University of New South Wales; 2020. Available from: http://handle.unsw.edu.au/1959.4/65033

4. Jenzer, Céline. Physiopathologie de l’autophagie au cours du développement embryonnaire chez Caenorhabditis elegans : Physiology of autophagy during embryonic development in Caenorhabditis elegans.

Degree: Docteur es, Sciences de la vie et de la santé, 2016, Université Paris-Saclay (ComUE)

URL: http://www.theses.fr/2016SACLS201

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La macroautophagie est un processus cellulaire qui permet la dégradation et le recyclage de constituants cytoplasmiques par formation de vésicules à double membrane, les autophagosomes… (more)

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La macroautophagie est un processus cellulaire qui permet la dégradation et le recyclage de constituants cytoplasmiques par formation de vésicules à double membrane, les autophagosomes qui fusionnent ensuite avec les lysosomes. Ce processus intervient dans divers processus physiologiques tels que le développement, la longévité, la mort cellulaire et dans des pathologies humaines comme des cancers ou maladies neurodégénératives. Mes travaux de thèse ont révélé l’existence de rôles séquentiels et spécifiques des protéines autophagiques, LGG-1 et LGG-2, homologues d’Atg8/LC3 chez le nématode Caenorhabditis elegans. Cette étude a été réalisée dans l’embryon précoce sur une population particulière d’autophagosomes responsables d’un processus physiologique stéréotypé : la dégradation des mitochondries paternelles au moment de la fécondation. Nous avons montré que LGG-1 est recruté au niveau des autophagosomes précoces et permet le recrutement de LGG-2 qui intervient plus tardivement dans le processus autophagique pour permettre la fusion des autophagosomes avec les lysosomes. De plus, la fonction de LGG-1 peut être complémentée par son homologue humain témoignant de l’intérêt du système modèle C. elegans pour l’analyse des homologues d’Atg8.Par ailleurs, des études récentes ont démontré que la protéine autophagique LC3 était recrutée au cours de la phagocytose des corps apoptotiques. Ce processus a été appelé LAP pour LC3-associated phagocytosis. Par des approches génétiques et cellulaires, utilisant la microscopie optique et électronique, j’ai montré qu’il existait une implication différente de protéines autophagiques LGG-1 et LGG-2 dans la dégradation des corps apoptotiques chez C. elegans. La protéine LGG-2, spécifiquement, joue un rôle dans la cellule phagocytaire afin de dégrader le corps apoptotique. Ces travaux suggèrent également une implication de l’autophagie dans le corps apoptotique pour permettre la phagocytose.

Macroautophagy is a major ubiquitous catabolic process which allows the bulk degradation and recycling of cytoplasmic constituents by formation of double membrane vesicles called autophagosomes which then fuse with lysosomes. This process is involved in a large variety of physiological processes such as development, anti-aging, cell death and in human pathologies like cancers or neurodegenerative diseases. My thesis work revealed the existence of sequential and specific roles of autophagic proteins LGG-1 and LGG-2, homologs of Atg8/LC3 in Caenorhabditis elegans. In this study, we focused on a particular population of autophagosomes involved in a physiological process in early embryos: the degradation of paternal mitochondria during fertilization. We showed that LGG-1 is recruited at the early autophagosomes and allows LGG -2 recruitment which acts later in the autophagic process to allow the fusion of autophagosomes with lysosomes. Moreover, the function of LGG -1 can be complemented with its human homologs revealing the interest of the C. elegans model system for analyzing Atg8…

Advisors/Committee Members: Legouis, Renaud (thesis director).

Subjects/Keywords: Autophagie; Apoptose; Caenorhabditis elegans; Atg8; LC3; Autophagy; Apoptosis; Caenorhabditis elegans; Atg8; LC3

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Jenzer, C. (2016). Physiopathologie de l’autophagie au cours du développement embryonnaire chez Caenorhabditis elegans : Physiology of autophagy during embryonic development in Caenorhabditis elegans. (Doctoral Dissertation). Université Paris-Saclay (ComUE). Retrieved from http://www.theses.fr/2016SACLS201

Chicago Manual of Style (16^th Edition):

Jenzer, Céline. “Physiopathologie de l’autophagie au cours du développement embryonnaire chez Caenorhabditis elegans : Physiology of autophagy during embryonic development in Caenorhabditis elegans.” 2016. Doctoral Dissertation, Université Paris-Saclay (ComUE). Accessed April 12, 2021. http://www.theses.fr/2016SACLS201.

MLA Handbook (7^th Edition):

Jenzer, Céline. “Physiopathologie de l’autophagie au cours du développement embryonnaire chez Caenorhabditis elegans : Physiology of autophagy during embryonic development in Caenorhabditis elegans.” 2016. Web. 12 Apr 2021.

Vancouver:

Jenzer C. Physiopathologie de l’autophagie au cours du développement embryonnaire chez Caenorhabditis elegans : Physiology of autophagy during embryonic development in Caenorhabditis elegans. [Internet] [Doctoral dissertation]. Université Paris-Saclay (ComUE); 2016. [cited 2021 Apr 12]. Available from: http://www.theses.fr/2016SACLS201.

Council of Science Editors:

Jenzer C. Physiopathologie de l’autophagie au cours du développement embryonnaire chez Caenorhabditis elegans : Physiology of autophagy during embryonic development in Caenorhabditis elegans. [Doctoral Dissertation]. Université Paris-Saclay (ComUE); 2016. Available from: http://www.theses.fr/2016SACLS201

5. Borel, Sophie. Etude de l’interaction entre la protéine Vif du VIH-1 et la protéine LC3 impliquée dans le processus autophagique : Study of the interaction between the viral protein Vif and the LC3 protein involved in the autophagic process.

Degree: Docteur es, Biologie Santé, 2012, Université Montpellier I

URL: http://www.theses.fr/2012MON13518

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L'autophagie est un mécanisme de dégradation lysosomale qui joue un rôle important dans l'immunité innée et adaptative. La relation entre le Virus de l'Immunodéficience Humaine… (more)

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L'autophagie est un mécanisme de dégradation lysosomale qui joue un rôle important dans l'immunité innée et adaptative. La relation entre le Virus de l'Immunodéficience Humaine de type 1 (VIH-1) et l'autophagie est complexe. En effet, l'équipe a montré que l'enveloppe virale du VIH-1 (Env), exprimée à la surface des cellules infectées, induit une autophagie massive dans les cellules T CD4 bystanders non infectées. Au contraire, lorsque ces cellules s'infectent de façon productive, l'autophagie est inhibée, suggérant qu'une ou plusieurs protéines virales soient capables de bloquer ce processus. L'objectif de ce travail de thèse a été de rechercher ces protéines virales et leur mécanisme d'action. Un crible double hybride en levure a permis de mettre en évidence que plusieurs protéines du VIH-1 sont capables d'interagir avec des protéines autophagiques (Atg), et plus spécifiquement que la protéine virale Vif (Virion infectivity factor) interagit directement avec la protéine LC3, protéine essentielle au processus autophagique. Cette interaction a été confirmée en système in vitro et in vivo (GST pull-down et immunoprécipitation). Plusieurs mutants des protéines Vif et LC3 ont été réalisés pour déterminer les domaines de liaison. La partie C-terminale de Vif ainsi que la glycine C-terminale de LC3, responsable de la conjugaison au phosphatidylethanolamine (PE), semblent être les domaines impliqués dans cette interaction. Une des principales fonctions de Vif connues est de dégrader, via le protéasome, les facteurs cellulaires APOBEC (Apolipoprotein B mRNA-editing, enzyme-catalytic, polypeptide-like) et en particulier la protéine APOBEC3G (A3G). Les résultats montrent que Vif est impliquée dans le blocage de l'autophagie induite par l'enveloppe indépendamment de son action sur A3G.

Autophagy is a lysosomal degradation pathway involved in the innate and adaptative immunity. The relationship between the Human Immunodeficiency Virus type 1 (HIV-1) and autophagy is complex. The team has demonstrated that autophagy is induced in uninfected CD4 T cells after contact with infected cells expressing HIV-1 envelope glycoproteins (Env), leading to apoptosis. In contrast, when these cells are productively infected, autophagy is repressed, suggesting that one or several viral proteins are able to block this process. The aim of the thesis was to search these viral proteins and to determine their mechanism of action. A two-hybrid screen has revealed that several HIV-1 viral proteins are able to interact with autophagic proteins (Atg). In particular, Vif (Virion infectivity factor) interacts directly with LC3, a protein involved in the formation of autophagosomes. This interaction has been confirmed in vitro and in vivo (GST pull-down and immunoprecipitation). Several mutants of Vif and LC3 have been done to analyze the binding domains. The C-terminal part of Vif and the C-terminal glycine of LC3, responsible for the conjugation to PE, seem to be involved in the interaction between Vif and LC3.Vif plays an important role during HIV-1…

Advisors/Committee Members: Biard-Piechaczyk, Martine (thesis director), Espert, Lucile (thesis director).

Subjects/Keywords: Vih-1; Vif; Lc3; Autophagie; Interactions moléculaires; Hiv-1; Vif; Lc3; Autophagy; Molecular interactions; 616

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Borel, S. (2012). Etude de l’interaction entre la protéine Vif du VIH-1 et la protéine LC3 impliquée dans le processus autophagique : Study of the interaction between the viral protein Vif and the LC3 protein involved in the autophagic process. (Doctoral Dissertation). Université Montpellier I. Retrieved from http://www.theses.fr/2012MON13518

Chicago Manual of Style (16^th Edition):

Borel, Sophie. “Etude de l’interaction entre la protéine Vif du VIH-1 et la protéine LC3 impliquée dans le processus autophagique : Study of the interaction between the viral protein Vif and the LC3 protein involved in the autophagic process.” 2012. Doctoral Dissertation, Université Montpellier I. Accessed April 12, 2021. http://www.theses.fr/2012MON13518.

MLA Handbook (7^th Edition):

Borel, Sophie. “Etude de l’interaction entre la protéine Vif du VIH-1 et la protéine LC3 impliquée dans le processus autophagique : Study of the interaction between the viral protein Vif and the LC3 protein involved in the autophagic process.” 2012. Web. 12 Apr 2021.

Vancouver:

Borel S. Etude de l’interaction entre la protéine Vif du VIH-1 et la protéine LC3 impliquée dans le processus autophagique : Study of the interaction between the viral protein Vif and the LC3 protein involved in the autophagic process. [Internet] [Doctoral dissertation]. Université Montpellier I; 2012. [cited 2021 Apr 12]. Available from: http://www.theses.fr/2012MON13518.

Council of Science Editors:

Borel S. Etude de l’interaction entre la protéine Vif du VIH-1 et la protéine LC3 impliquée dans le processus autophagique : Study of the interaction between the viral protein Vif and the LC3 protein involved in the autophagic process. [Doctoral Dissertation]. Université Montpellier I; 2012. Available from: http://www.theses.fr/2012MON13518

6. Dias, Beatriz Rocha Simões. Vacúolos parasitóforos induzidos porLeishmania amazonensis e Leishmania major interagem de forma distintacom a via autofágica.

Degree: 2014, Centro de Pesquisas Gonçalo Moniz

URL: https://www.arca.fiocruz.br/handle/icict/8686

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Submitted by Ana Maria Fiscina Sampaio ([email protected]) on 2014-10-29T13:31:11Z No. of bitstreams: 1 Beatriz Rocha Simone Dias Vacúolos....pdf: 43303992 bytes, checksum: 310fce5b6b7557207067a51be3ca3c64 (MD5)

Made available… (more)

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Submitted by Ana Maria Fiscina Sampaio ([email protected]) on 2014-10-29T13:31:11Z No. of bitstreams: 1 Beatriz Rocha Simone Dias Vacúolos....pdf: 43303992 bytes, checksum: 310fce5b6b7557207067a51be3ca3c64 (MD5)

Made available in DSpace on 2014-10-29T13:31:11Z (GMT). No. of bitstreams: 1 Beatriz Rocha Simone Dias Vacúolos....pdf: 43303992 bytes, checksum: 310fce5b6b7557207067a51be3ca3c64 (MD5) Previous issue date: 2014

Fundação Oswaldo Cruz. Centro de Pesquisa Gonçalo Moniz. Salvador, BA, Brasil

A Leishmania é um parasito intracelular obrigatório que vive e se multiplic adentro dos vacúolos parasitóforos em macrófagos no hospedeiro vertebrado. Apesar dos vacúolos induzidos por diferentes espécies de Leishmania apresentarem semelhanças bioquímicas, esses compartimentos apresentam diferenças significativas nos seus tamanhos. Os vacúolos parasitóforos induzidos por Leishmania mexicana e Leishmania amazonensis apresentam grandes dimensões e contêm uma grande quantidade de amastigotas, enquanto que os induzidos por Leishmania major e Leishmania donovani são pequenos e com pouco espaço ao redor das amastigotas. Estudos recentes demonstraram que compartimentos induzidos por microrganismos intracelulares são capazes de interagir com a via autofágica e esta pode controlar ou promover o estabelecimento da infecção a depender da natureza do microrganismo. Até o momento, poucos estudos foram realizados para avaliar o papel da autofagia na biogênese e maturação dos vacúolos parasitóforos induzidos por Leishmania. Recentemente, foi demonstrado que em macrófagos de camundongos BALB/c, a indução de autofagia provoca um aumento na carga parasitária de L. amazonensis, no entanto, não é capaz de aumentar a carga parasitária de L. major. Além disso, estudos indicam que vacúolos parasitóforos de L. mexicana adquirem macromoléculas do citoplasma da célula hospedeira por meio de microautofagia. Uma vez que L. amazonensis integra o mesmo complexo que L. mexicana, nossa hipótese é que vacúolos parasitóforos induzidos por L. amazonensis interagem com a via autofágica.Assim, o presente estudo tem como bjetivo verificar e comparar a participação da autofagia na infecção por L. amazonensis ou L. major em macrófagos murinos. Para este fim, avaliamos quanto a características autofágicas, os vacúolos parasitóforos induzidos por L. amazonensis ou L. major em macrófagos de camundongo CBA e analisamos a influência da superexpressão de LC3 sobre a sobrevivência de L. amazonensis ou L. major em macrófagos infectados. Inicialmente, macrófagos de camundongos CBA foram infectados com L. amazonensis ou L. major e incubados com ysoTracker, marcador de compartimentos lisossomais, ou DQ-BSA, marcador de compartimentos degradativos. Além disso, foi avaliada a presença de LAMP, proteína lisossomal, e LC3, proteína específica de autofagossomo, na membrana destes vacúolos. Em seguida, a co- localização dos parasitos com os vacúolos parasitóforos contendo estes marcadores foi quantificada. Nossos resultados demostraram um maior percentual de…

Advisors/Committee Members: Guedes, Carlos Eduardo Sampaio, Bonfim, Gilberto Cafezeiro, Santos, Théo de Araujo, Silva, Tânia Regina Marques da, Veras, Patrícia Sampaio Tavares.

Subjects/Keywords: Leishmania; Vacúolo parasitóforo; Macrófago; Autofagia; LC3; Leishmania; Parasitophorous vacuole; Macrophage; Autophagy; LC3

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Dias, B. R. S. (2014). Vacúolos parasitóforos induzidos porLeishmania amazonensis e Leishmania major interagem de forma distintacom a via autofágica. (Masters Thesis). Centro de Pesquisas Gonçalo Moniz. Retrieved from https://www.arca.fiocruz.br/handle/icict/8686

Chicago Manual of Style (16^th Edition):

Dias, Beatriz Rocha Simões. “Vacúolos parasitóforos induzidos porLeishmania amazonensis e Leishmania major interagem de forma distintacom a via autofágica.” 2014. Masters Thesis, Centro de Pesquisas Gonçalo Moniz. Accessed April 12, 2021. https://www.arca.fiocruz.br/handle/icict/8686.

MLA Handbook (7^th Edition):

Dias, Beatriz Rocha Simões. “Vacúolos parasitóforos induzidos porLeishmania amazonensis e Leishmania major interagem de forma distintacom a via autofágica.” 2014. Web. 12 Apr 2021.

Vancouver:

Dias BRS. Vacúolos parasitóforos induzidos porLeishmania amazonensis e Leishmania major interagem de forma distintacom a via autofágica. [Internet] [Masters thesis]. Centro de Pesquisas Gonçalo Moniz; 2014. [cited 2021 Apr 12]. Available from: https://www.arca.fiocruz.br/handle/icict/8686.

Council of Science Editors:

Dias BRS. Vacúolos parasitóforos induzidos porLeishmania amazonensis e Leishmania major interagem de forma distintacom a via autofágica. [Masters Thesis]. Centro de Pesquisas Gonçalo Moniz; 2014. Available from: https://www.arca.fiocruz.br/handle/icict/8686

NSYSU

7. CHUNG, HSIU-CHANG. Screening of Antimitotic Drug Combretastatin-A4 Derivatives That Are Capable of Inducing Autophagy in Neuroblastoma SHSY5Y Cell Line.

Degree: Master, Biological Sciences, 2013, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0726113-125155

► Autophagy is a process to clear unwanted protein aggregates and damaged organelles for recycling cellular resources. It is a critical mechanism to maintain cellular homeostasis… (more)

▼ Autophagy is a process to clear unwanted protein aggregates and damaged organelles for recycling cellular resources. It is a critical mechanism to maintain cellular homeostasis for cellular survival when facing environmental stress. Therefore, aberrant autophagy might lead to the diseases such as cancer, pathogen infection and neurodegenerative diseases. Autophagic proecess depends on the fusion of autophagosome with lysosome for the enzymatic degradation of its content. Previous reports indicated the involvement of microtubule in mediating the fusion of autophagosome with either lysosome or late endosome. Therefore, proper dynamic for microtubule formation is critical for autophagic process. Combretastatin A-4 (CA-4) is a useful nature product exhibits anticancer and anti-angiogenesis activity by targeting microtubule formation. However, its clinical use is limited as it exhibits drawbacks such as high toxicity and low water solubility. To improve its clinical use, efforts are ongoing in synthesizing better CA-4 derivatives as anticancer drug candidates. A series of Combretastatin A-4 (CA-4) enediyne derivatives were synthesized by Professor Ming-Jung Wu in the Department of Chemistry of National Sun Yat-Sen University. In this thesis, research was focusing on the analyzing their effects on the microtubule formation in neuroblastoma SHSY5Y and hepatoma Hep3B cell lines by confocal microscopic analysis. The results showed that like CA-4, among 9 enediyne derivatives analyzed, LO-OMeãLO-NH2ãLO-py and HYH10f could inhibit microtubule formation using dosage of their individual IC50. The results of flow cytometric cell cycle analysis showed that LO-OMeãLO-NH2 and HYH10f also had antimitotic effect in that they caused G2/M arrest of SHSY5Y cells. Whereas, the derivatives CPC14c, CPC20a, CPC15a, CPC19a and HYH10a had no effects on microtubule formation or cell cycle arrest. These results indicated the modification or replacement of different function groups might affect their activities differentially. We further investigated the effects of these CA-4 enediyne derivatives on the autophagic process by monitoring the level of two autophagic marker proteins LC3-II and p62 using western blot analysis. Our results showed that like CA-4, LO-OMe, LO-NH2 and CPC15a could lead to the increase of both LC3-II and p62. Compound HYH10f could increase LC3-II level, but not on the level of p62. The rest of the derivative compounds had no effects on the level of both LC3-II and p62. Our results again showed that functional modification might affects autophagic process differentially. The detail signaling mediating their effects on autophagy awaits further investigation. Understanding the molecular mechanism underlies might be helpful in evaluation of their use as therapeutic agents for cancer or neurodegenerative diseases. Advisors/Committee Members: Ming-Jung Wu (chair), Hsu, Ching-Mei (chair), Jiin-Tsuey Cheng (committee member).

Subjects/Keywords: Combrestastatin A-4; autophagy; LC3-II; p62; mitosis

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APA (6^th Edition):

CHUNG, H. (2013). Screening of Antimitotic Drug Combretastatin-A4 Derivatives That Are Capable of Inducing Autophagy in Neuroblastoma SHSY5Y Cell Line. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0726113-125155

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

CHUNG, HSIU-CHANG. “Screening of Antimitotic Drug Combretastatin-A4 Derivatives That Are Capable of Inducing Autophagy in Neuroblastoma SHSY5Y Cell Line.” 2013. Thesis, NSYSU. Accessed April 12, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0726113-125155.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

CHUNG, HSIU-CHANG. “Screening of Antimitotic Drug Combretastatin-A4 Derivatives That Are Capable of Inducing Autophagy in Neuroblastoma SHSY5Y Cell Line.” 2013. Web. 12 Apr 2021.

Vancouver:

CHUNG H. Screening of Antimitotic Drug Combretastatin-A4 Derivatives That Are Capable of Inducing Autophagy in Neuroblastoma SHSY5Y Cell Line. [Internet] [Thesis]. NSYSU; 2013. [cited 2021 Apr 12]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0726113-125155.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

CHUNG H. Screening of Antimitotic Drug Combretastatin-A4 Derivatives That Are Capable of Inducing Autophagy in Neuroblastoma SHSY5Y Cell Line. [Thesis]. NSYSU; 2013. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0726113-125155

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

NSYSU

8. Yeh, Chun-Cheng. The effect of Tumor susceptibility gene 101 on Autophagy Marker MAP1LC3B.

Degree: Master, Biological Sciences, 2012, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0217112-160301

► Deregulation of autophagy plays an important role in the pathogenesis of diseases such as cancer, neuronal degenerative or cardiovascular disease. Autophagy is a process to… (more)

▼ Deregulation of autophagy plays an important role in the pathogenesis of diseases such as cancer, neuronal degenerative or cardiovascular disease. Autophagy is a process to engulf the cytoplasmic contents into autophagosome and deliver them for lysosomal degradation. Its major function is to clear unfolded protein or damage organelles for maintaining proper metabolic homeostasis and normal cell physiological activities. Autophagy and multivesicular bodies, MVBs, cooperate to regulate the turnover of intracellular macromolecule, defective organelles and signaling receptor. Endosomal sorting complex required for transport, ESCRT, is important for the formation of MVBs, which regulates membrane receptor recycling, protein sorting and vesicular trafficking. Tumor Susceptibility Gene 101(TSG101) is a member of ESCRT-I that plays an important role on MVBs formation and maintaining ESCRT function. Previous report indicated that autophagosome accumulation upon deprivation of TSG101, implying possible role of TSG101 during autophagic process. In this study, we observed the increase of TSG101 and autophagic marker proteins, such as LC3-II and ATG upon nutrient starvation. Furthermore, knockdown TSG101 in cervical carcinoma HeLa cell resulted in the elevation of LC3-II, ATG3 and ubiquitinated protein aggregates marker protein p62, which is congruous to other reports. However, in neuroblastoma SH-SY5Y cell, transfection of siRNA led to the decrease of LC-II and ubiquitinated protein level. These results indicated that TSG101 might be critical for autophagy and the maintenance of steady-state level of cellular ubiquitinated proteins. Ectopic upregulatory expression of HA-TSG101 led to the increase of LC3-II in both cell type. The elevation of ATG3 level is also observed in HeLa cell. Therefore, we speculated that TSG101 might be important for the formation of autophagosome, but our data did not exclude the possible role of TSG101 in regulation of the fusion of autophagosome and lysosome, because the increase of ATG3 indicated ectopic HA-TSG101 might facilitate the execution of autophagic flow. In addition, we have established GFP-LC3 expression cell lines. Our imaging data showed the colocalization of TSG101 and GFP-LC3 in both cytoplasm and nucleus that might be an interesting research topic for investigation the role of TSG101 in autophagic pathway. Advisors/Committee Members: Yi-Ren Hong (chair), Jiin-Tsuey Cheng (committee member), Chi-Liang Chern (chair).

Subjects/Keywords: LC3-II; ESCRT; MVBs; Tumor Susceptibility Gene-101; Autophagy

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Yeh, C. (2012). The effect of Tumor susceptibility gene 101 on Autophagy Marker MAP1LC3B. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0217112-160301

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Yeh, Chun-Cheng. “The effect of Tumor susceptibility gene 101 on Autophagy Marker MAP1LC3B.” 2012. Thesis, NSYSU. Accessed April 12, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0217112-160301.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Yeh, Chun-Cheng. “The effect of Tumor susceptibility gene 101 on Autophagy Marker MAP1LC3B.” 2012. Web. 12 Apr 2021.

Vancouver:

Yeh C. The effect of Tumor susceptibility gene 101 on Autophagy Marker MAP1LC3B. [Internet] [Thesis]. NSYSU; 2012. [cited 2021 Apr 12]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0217112-160301.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Yeh C. The effect of Tumor susceptibility gene 101 on Autophagy Marker MAP1LC3B. [Thesis]. NSYSU; 2012. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0217112-160301

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Universiteit Utrecht

9. Nieuwenhuis, J.D.M. Autophagy and Intracellular Pathogens: the Killer, the Victim and the Suspects.

Degree: 2012, Universiteit Utrecht

URL: http://dspace.library.uu.nl:8080/handle/1874/254297

► Until recently, autophagy was viewed as a process primarily involved in controlling intracellular biomass as well as protecting cells against toxic protein aggregates and the… (more)

Subjects/Keywords: autophagy; innate immunity; GAS; Streptococcus pyogenus; Coxiella burnetii; Chlamydia trachomatis; LC3

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Nieuwenhuis, J. D. M. (2012). Autophagy and Intracellular Pathogens: the Killer, the Victim and the Suspects. (Masters Thesis). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/254297

Chicago Manual of Style (16^th Edition):

Nieuwenhuis, J D M. “Autophagy and Intracellular Pathogens: the Killer, the Victim and the Suspects.” 2012. Masters Thesis, Universiteit Utrecht. Accessed April 12, 2021. http://dspace.library.uu.nl:8080/handle/1874/254297.

MLA Handbook (7^th Edition):

Nieuwenhuis, J D M. “Autophagy and Intracellular Pathogens: the Killer, the Victim and the Suspects.” 2012. Web. 12 Apr 2021.

Vancouver:

Nieuwenhuis JDM. Autophagy and Intracellular Pathogens: the Killer, the Victim and the Suspects. [Internet] [Masters thesis]. Universiteit Utrecht; 2012. [cited 2021 Apr 12]. Available from: http://dspace.library.uu.nl:8080/handle/1874/254297.

Council of Science Editors:

Nieuwenhuis JDM. Autophagy and Intracellular Pathogens: the Killer, the Victim and the Suspects. [Masters Thesis]. Universiteit Utrecht; 2012. Available from: http://dspace.library.uu.nl:8080/handle/1874/254297

10. Wilz, Livia Margaret. Regulation of Autophagosome Biogenesis by the Autophagy Specific Class III Phosphatidylinostitol-3 Kinase Complex.

Degree: Molecular & Cell Biology, 2015, University of California – Berkeley

URL: http://www.escholarship.org/uc/item/3r09z33z

► Autophagy is a conserved pathway critical for homeostasis in all eukaryotic cells. Autophagy provides a mechanism for cells to respond to a large variety of… (more)

▼ Autophagy is a conserved pathway critical for homeostasis in all eukaryotic cells. Autophagy provides a mechanism for cells to respond to a large variety of cellular stresses through a vesicle-based degradation process. Most of the gene products and other factors required for the execution of autophagy have been elucidated, but the biochemical reactions by which these components work in concert to engulf cargo in a double membrane vesicle, called an autophagosome, is still unclear. In mammalian cells, the class III phosphatidylinositol 3-kinase complex I (PI3KC3-C1) is essential for early steps in autophagy because it generates a membrane lipid, phosphatidylinositol 3-phosphate (PtdIns3P), that is necessary to recruit downstream autophagy factors to cellular membranes. However, it was not known whether the PI3KC3-C1 also contributes to phagophore formation in other ways. The research described in this dissertation focused on one of the subunits of PI3KC3-C1, Atg14L, which is essential for the complex to initiate autophagy. I used an in vitro reconstitution assay where I added back purified PI3KC3-C1 or various mutant derivatives of the complex to extracts derived from a Cas9-generated Atg14L-deficient cell line. As a biochemical readout for examining the functions of Atg14L, I used a cell-free reaction that reproduces a key early step in autophagosome membrane generation, lipidation of a cytoplasmic protein, LC3. In this assay, I found that Atg14L (and the other subunits of PI3KC3-C1) are required for LC3 lipidation, whereas mutants of the complex that abrogate its catalytic activity and membrane curvature-sensing capability did not support LC3 lipidation. In addition, PI3KC3-C1 activity, through Atg14L and its membrane curvature- sensing motif, is required for efficient membrane recruitment of the downstream PtdIns3P-binding effector, WIPI2, but not for recruitment of Atg16L, a key factor required for LC3 lipidation. In an effort to find other cofactors that may also regulate PI3KC3-C1, I found that NRBF2 binds Atg14L and attenuates its autophagy-stimulating function and, hence, serves as a negative regulator of autophagy. Under fed conditions, however, NRBF2 is phosphorylated; phosphorylation null mutants show elevated autophagy under fed conditions. In another study, I uncovered that Atg14L acts as a vesicle tether that supports vesicle fusion when soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) are incorporated into the vesicle. The fusogenic activity of Atg14L requires oligomerization through conserved cysteine repeats near the N-terminus of Atg14L.

Subjects/Keywords: Biochemistry; Cellular biology; Molecular biology; Atg14; Autophagy; Degradation; LC3; PI3K

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APA (6^th Edition):

Wilz, L. M. (2015). Regulation of Autophagosome Biogenesis by the Autophagy Specific Class III Phosphatidylinostitol-3 Kinase Complex. (Thesis). University of California – Berkeley. Retrieved from http://www.escholarship.org/uc/item/3r09z33z

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Wilz, Livia Margaret. “Regulation of Autophagosome Biogenesis by the Autophagy Specific Class III Phosphatidylinostitol-3 Kinase Complex.” 2015. Thesis, University of California – Berkeley. Accessed April 12, 2021. http://www.escholarship.org/uc/item/3r09z33z.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Wilz, Livia Margaret. “Regulation of Autophagosome Biogenesis by the Autophagy Specific Class III Phosphatidylinostitol-3 Kinase Complex.” 2015. Web. 12 Apr 2021.

Vancouver:

Wilz LM. Regulation of Autophagosome Biogenesis by the Autophagy Specific Class III Phosphatidylinostitol-3 Kinase Complex. [Internet] [Thesis]. University of California – Berkeley; 2015. [cited 2021 Apr 12]. Available from: http://www.escholarship.org/uc/item/3r09z33z.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Wilz LM. Regulation of Autophagosome Biogenesis by the Autophagy Specific Class III Phosphatidylinostitol-3 Kinase Complex. [Thesis]. University of California – Berkeley; 2015. Available from: http://www.escholarship.org/uc/item/3r09z33z

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Toronto

11. Beadman, Stephanie Alexandra. The Effect of RGS4 on Autophagic Flux in Min6 Pancreatic Beta Cells.

Degree: 2015, University of Toronto

URL: http://hdl.handle.net/1807/80177

►

Defective autophagy can lead to dysregulation of metabolic homeostasis. Previous studies in our laboratory have shown that RGS4-overexpressing HEK cells show increased autophagic activity. Herein,… (more)

Subjects/Keywords: Atg12; autophagy; Beclin1; LC3; Min6 cells; mTOR; 0719

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Beadman, S. A. (2015). The Effect of RGS4 on Autophagic Flux in Min6 Pancreatic Beta Cells. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/80177

Chicago Manual of Style (16^th Edition):

Beadman, Stephanie Alexandra. “The Effect of RGS4 on Autophagic Flux in Min6 Pancreatic Beta Cells.” 2015. Masters Thesis, University of Toronto. Accessed April 12, 2021. http://hdl.handle.net/1807/80177.

MLA Handbook (7^th Edition):

Beadman, Stephanie Alexandra. “The Effect of RGS4 on Autophagic Flux in Min6 Pancreatic Beta Cells.” 2015. Web. 12 Apr 2021.

Vancouver:

Beadman SA. The Effect of RGS4 on Autophagic Flux in Min6 Pancreatic Beta Cells. [Internet] [Masters thesis]. University of Toronto; 2015. [cited 2021 Apr 12]. Available from: http://hdl.handle.net/1807/80177.

Council of Science Editors:

Beadman SA. The Effect of RGS4 on Autophagic Flux in Min6 Pancreatic Beta Cells. [Masters Thesis]. University of Toronto; 2015. Available from: http://hdl.handle.net/1807/80177

12. Fletcher, Katherine Anne. Novel mechanisms of Atg16L1 recruitment in non-canonical autophagy.

Degree: PhD, 2019, University of Cambridge

URL: https://www.repository.cam.ac.uk/handle/1810/291925

► Autophagy is a well-studied catabolic process through which cytoplasmic components are targeted for lysosomal degradation by autophagosomes. A key step in this process is the… (more)

▼ Autophagy is a well-studied catabolic process through which cytoplasmic components are targeted for lysosomal degradation by autophagosomes. A key step in this process is the recruitment, processing and lipidation of LC3 to autophagosomes. Recently it has become increasingly apparent that, through the unconventional use of some autophagy related proteins, LC3 can also become lipidated to distinct non-autophagosomal membranes of the endolysosomal system. This process is termed non-canonical autophagy and occurs independently of conventional autophagy initiation signals. Non-canonical autophagy usually occurs after macro endocytic engulfment events such as macropinocytosis, entosis and LC3 associated phagocytosis (LAP). Certain ionophores and lysosomotropic drugs, such as monensin, can also activate this process and promote LC3 lipidation to lysosomes. This project focuses on Atg16L1, an essential autophagy protein that directs the membrane site where LC3 is lipidated. Atg16L1 is relatively well characterised in autophagy but little is known about the mechanisms underlying its role in non-canonical autophagy. This project used a structure/function approach to assess the importance of different domains of Atg16L1 in the context of autophagy versus non-canonical autophagy. I have demonstrated for the first time, that the Atg16L1 C-terminal WD40 domain (CTD) is dispensable for its role in autophagy but essential for LC3 lipidation during non-canonical autophagy. Furthermore, single point mutants were uncovered in the CTD of Atg16L1 that likewise are dispensable for autophagy but fundamental to LC3 lipidation in non-canonical autophagy. These data provide a novel strategy for dissecting canonical and non-canonical autophagy pathways at a molecular level. This project used an existing mouse model with an Atg16L1 truncation (lacking the CTD and nearby residues) and implicated the lack of non canonical autophagy to a defect in MHCII antigen presentation. Furthermore this project has generated new refined Atg16L1 mutant models ablating non-canonical autophagy without affecting canonical autopahgy. In parallel, proteomic analysis was done to provide mechanistic insights into Atg16L1 binding partners in the context of non-canonical autophagy.

Subjects/Keywords: autophagy; non-canonical autophagy; LC3 associated phagocytosis; macropinocytosis

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APA (6^th Edition):

Fletcher, K. A. (2019). Novel mechanisms of Atg16L1 recruitment in non-canonical autophagy. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/291925

Chicago Manual of Style (16^th Edition):

Fletcher, Katherine Anne. “Novel mechanisms of Atg16L1 recruitment in non-canonical autophagy.” 2019. Doctoral Dissertation, University of Cambridge. Accessed April 12, 2021. https://www.repository.cam.ac.uk/handle/1810/291925.

MLA Handbook (7^th Edition):

Fletcher, Katherine Anne. “Novel mechanisms of Atg16L1 recruitment in non-canonical autophagy.” 2019. Web. 12 Apr 2021.

Vancouver:

Fletcher KA. Novel mechanisms of Atg16L1 recruitment in non-canonical autophagy. [Internet] [Doctoral dissertation]. University of Cambridge; 2019. [cited 2021 Apr 12]. Available from: https://www.repository.cam.ac.uk/handle/1810/291925.

Council of Science Editors:

Fletcher KA. Novel mechanisms of Atg16L1 recruitment in non-canonical autophagy. [Doctoral Dissertation]. University of Cambridge; 2019. Available from: https://www.repository.cam.ac.uk/handle/1810/291925

University of Toronto

13. Omary, Zuhra. Understanding the Role of LRBA in Patients with Inflammatory Bowel Disease.

Degree: 2019, University of Toronto

URL: http://hdl.handle.net/1807/98286

►

Pathogenic mutations in LRBA is one of the genetic causes of very early-onset inflammatory bowel disease (IBD). A pediatric patient presented with immunodeficiency with chronic… (more)

Subjects/Keywords: autophagy; ibd; inflammatory bowel disease; lc3; lrba; veoibd; 0487

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APA (6^th Edition):

Omary, Z. (2019). Understanding the Role of LRBA in Patients with Inflammatory Bowel Disease. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/98286

Chicago Manual of Style (16^th Edition):

Omary, Zuhra. “Understanding the Role of LRBA in Patients with Inflammatory Bowel Disease.” 2019. Masters Thesis, University of Toronto. Accessed April 12, 2021. http://hdl.handle.net/1807/98286.

MLA Handbook (7^th Edition):

Omary, Zuhra. “Understanding the Role of LRBA in Patients with Inflammatory Bowel Disease.” 2019. Web. 12 Apr 2021.

Vancouver:

Omary Z. Understanding the Role of LRBA in Patients with Inflammatory Bowel Disease. [Internet] [Masters thesis]. University of Toronto; 2019. [cited 2021 Apr 12]. Available from: http://hdl.handle.net/1807/98286.

Council of Science Editors:

Omary Z. Understanding the Role of LRBA in Patients with Inflammatory Bowel Disease. [Masters Thesis]. University of Toronto; 2019. Available from: http://hdl.handle.net/1807/98286

14. Ligeon, Laure-Anne. Rôle des protéines SNARE au niveau de la vacuole bactérienne durant les phases précoces de l'infection par Yersinia pseudotuberculosis dans un contexte d'autophagie : SNAREs trafficking at bacteria vacuoles during early stages of Yersinia pseudotuberculosis infection in the context of autophagy.

Degree: Docteur es, Biologie cellulaire, 2013, Université Lille II – Droit et Santé

URL: http://www.theses.fr/2013LIL2S043

►

Yersinia pseudotuberculosis appartient à la famille des Enterobacteriaceae et peut être responsable de syndromes articulaires et digestifs. Au cours de la colonisation de l’hôte, une… (more)

▼

Yersinia pseudotuberculosis appartient à la famille des Enterobacteriaceae et peut être responsable de syndromes articulaires et digestifs. Au cours de la colonisation de l’hôte, une minorité des bactéries va, en plus de l’étape de multiplication extracellulaire présenter une phase de réplication intracellulaire dans les macrophages. Une partie des Y. pseudotuberculosis va se répliquer dans les macrophages en usurpant la voie de l’autophagie, afin de créer une niche réplicative au sein des autophagosomes bloqués dans leur maturation. Le trafic membranaire associé à l’infection de Y. pseudotuberculosis reste à ce jour peu caractérisé. Dans un premier temps, nous avons observé que lors de l’infection d’une cellule épithéliale par Y. pseudotuberculosis, la vacuole bactérienne est associée avec le marqueur des autophagosomes, la protéine LC3 mais de façon surprenante cette vacuole ne présente pas deux mais une membrane unique. Par ailleurs, nous avons montré que les protéines SNARE jouent un rôle majeur au cours du trafic intracellulaire de Y. pseudotuberculosis. VAMP3 et VAMP7 sont recrutées de manière séquentielle au niveau de la vacuole de Y. pseudotuberuclosis. VAMP7 va participer au recrutement de LC3 au niveau de la vacuole bactérienne et nous proposons que VAMP3 est un des constituants du check-point permettant l’adressage de la bactérie vers des vacuoles présentant une ou de multiple membranes positives pour LC3. Par la suite, nous nous sommes intéressés à la caractérisation des protéines de la voie autophagique et des endosomes, recrutées au niveau de la vacuole bactérienne à membrane unique et positive pour LC3. Nous avons mis en évidence que les protéines impliquées dans la formation de l’autophagosome et les marqueurs des endosomes précoces sont recrutées au niveau de la vacuole contenant Y. pseudotuberculosis. Cette vacuole positive pour LC3 va en suite acquérir les marqueurs des endosomes tardifs et du lysosome mais n’est pas acidifiée. En outre, nous avons initié des travaux sur un criblage en haut contenu afin d’identifier les partenaires des protéines SNARE et leurs rôles dans le trafic intracellulaire de Y. pseudotuberuclosis. Ces travaux démontrent l’importance de l’analyse de l’ultrastructure des compartiments positifs pour LC3. Ils illustrent comment la bactérie s’adapte à son environnement pour établir sa niche réplicative. Ils présentent enfin l’importance de la régulation de l’autophagie avec la première mise en évidence d’un check-point entre deux voies de compartimentation positives pour LC3 mais morphologiquement différentes.

Yersinia pseudotuberculosis is a member of the Enterobacteriaceae family. In human, Y. pseudotuberculosis infection is responsible for enteric and, in rare cases, erythema nodosum. During host colonization, a minor part of Y. pseudotuberculosis presents an intracellular replication step. Y. pseudotuberculosis can replicate inside macrophages by hijacking the autophagy pathway. The bacteria are able to block autophagosome maturation by acidification impairment, which…

Advisors/Committee Members: Lafont, Franck (thesis director).

Subjects/Keywords: Yersinia pseudotuberculosis; Autophagie; LC3-associated-phagocytosis; SNARE; Trafic membranaire; Membrane traffic

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Ligeon, L. (2013). Rôle des protéines SNARE au niveau de la vacuole bactérienne durant les phases précoces de l'infection par Yersinia pseudotuberculosis dans un contexte d'autophagie : SNAREs trafficking at bacteria vacuoles during early stages of Yersinia pseudotuberculosis infection in the context of autophagy. (Doctoral Dissertation). Université Lille II – Droit et Santé. Retrieved from http://www.theses.fr/2013LIL2S043

Chicago Manual of Style (16^th Edition):

Ligeon, Laure-Anne. “Rôle des protéines SNARE au niveau de la vacuole bactérienne durant les phases précoces de l'infection par Yersinia pseudotuberculosis dans un contexte d'autophagie : SNAREs trafficking at bacteria vacuoles during early stages of Yersinia pseudotuberculosis infection in the context of autophagy.” 2013. Doctoral Dissertation, Université Lille II – Droit et Santé. Accessed April 12, 2021. http://www.theses.fr/2013LIL2S043.

MLA Handbook (7^th Edition):

Ligeon, Laure-Anne. “Rôle des protéines SNARE au niveau de la vacuole bactérienne durant les phases précoces de l'infection par Yersinia pseudotuberculosis dans un contexte d'autophagie : SNAREs trafficking at bacteria vacuoles during early stages of Yersinia pseudotuberculosis infection in the context of autophagy.” 2013. Web. 12 Apr 2021.

Vancouver:

Ligeon L. Rôle des protéines SNARE au niveau de la vacuole bactérienne durant les phases précoces de l'infection par Yersinia pseudotuberculosis dans un contexte d'autophagie : SNAREs trafficking at bacteria vacuoles during early stages of Yersinia pseudotuberculosis infection in the context of autophagy. [Internet] [Doctoral dissertation]. Université Lille II – Droit et Santé 2013. [cited 2021 Apr 12]. Available from: http://www.theses.fr/2013LIL2S043.

Council of Science Editors:

Ligeon L. Rôle des protéines SNARE au niveau de la vacuole bactérienne durant les phases précoces de l'infection par Yersinia pseudotuberculosis dans un contexte d'autophagie : SNAREs trafficking at bacteria vacuoles during early stages of Yersinia pseudotuberculosis infection in the context of autophagy. [Doctoral Dissertation]. Université Lille II – Droit et Santé 2013. Available from: http://www.theses.fr/2013LIL2S043

15. Lima, Taiane Berguermaier de. Autofagia na carcinogênese bucal.

Degree: 2016, Brazil

URL: http://hdl.handle.net/10183/164889

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Autofagia é o processo catabólico que ocorre nos lisossomos, e tem por finalidade degradar os componentes celulares e proteínas que já não são mais funcionantes… (more)

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Autofagia é o processo catabólico que ocorre nos lisossomos, e tem por finalidade degradar os componentes celulares e proteínas que já não são mais funcionantes e, assim manter seu equilíbrio homeostático para sobreviverem adequadamente em condições estressantes. Diante das funções biológicas da autofagia identificadas até hoje, a relação entre autofagia celular e neoplasias está provavelmente entre as mais estudadas, devido ao papel duplo que a autofagia exerce sobre o desenvolvimento do câncer, podendo atuar como um mecanismo supressor de tumor ou, podendo ser um mecanismo fundamental para a sobrevivência de células neoplásicas. No entanto, em lesões potencialmente malignas não se sabe sobre o comportamento do processo autofágico. Dessa forma, nosso estudo se propôs a estudar o comportamento da autofagia em neoplasias e em lesões potencialmente malignas bucais e correlacionar com os parâmetros clínicos e a evolução dessas lesões. Para tal finalidade foi utilizado a técnica de imunoistoquímica para avaliar em amostras de mucosa normal, leucoplasias e carcinomas espinocelulares bucais, o percentual de células positivas para o marcador LC3-II. Foram avaliadas 7 amostras de mucosa bucal normal, 51 leucoplasias e 120 carcinomas espinocelulares. Para a análise de carcinomas espinocelulares foi construído um microarranjo tecidual com 2 cilindros de cada paciente. Observamos o aumento dos níveis de autofagia no carcinoma espinocelular bucal (p<0,001) em relação aos outro grupos, porém sem associação com a evolução e sobrevida desses pacientes. Entre as leucoplasias, observamos maior percentual de células positivas na camada intermediária de leucoplasias 12 displásicas (p=0,0319) e na camada basal de lesões com pior evoluação (p=0,0133). Concluimos que os níveis de autofagia aumentam durante o processo de carcinogênese bucal e estão correlacionados com o pior comportamento das leucoplasias.

Autophagy is a catabolic process to digest the cell components and proteins that are no functional anymore. Autophagy maintains the homeostasis in order to cells survive in stressful conditions. In view of the biological functions of autophagy identified to date, the relationship between cellular autophagy and neoplasia is probably among the most studied, due to the dual role that autophagy exerts on the development of cancer. Cell autophagy can act as a tumor suppressor mechanism, or as a key mechanism for the survival of neoplastic cells. However, it is not known in potentially malignant lesions how the autophagic process is controlled. Therefore, the purpose of this study is to assess the autophagic process in oral cancer and potentially malignant oral lesions and to correlate with clinical parameters and the evolution of these lesions. For this purpose, the immunohistochemical technique was used to evaluate the percentage of cells positive for the LC3-II marker in the normal mucosa, leukoplakia and oral squamous cell carcinoma samples. Seven samples of normal buccal mucosa, 51 leukoplakia and 120 squamous cell carcinomas were…

Advisors/Committee Members: Visioli, Fernanda.

Subjects/Keywords: Autofagia; Leucoplasia bucal; Neoplasias bucais; Oral Cancer; LC3-II; Autophagy; Leukoplakia

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Lima, T. B. d. (2016). Autofagia na carcinogênese bucal. (Masters Thesis). Brazil. Retrieved from http://hdl.handle.net/10183/164889

Chicago Manual of Style (16^th Edition):

Lima, Taiane Berguermaier de. “Autofagia na carcinogênese bucal.” 2016. Masters Thesis, Brazil. Accessed April 12, 2021. http://hdl.handle.net/10183/164889.

MLA Handbook (7^th Edition):

Lima, Taiane Berguermaier de. “Autofagia na carcinogênese bucal.” 2016. Web. 12 Apr 2021.

Vancouver:

Lima TBd. Autofagia na carcinogênese bucal. [Internet] [Masters thesis]. Brazil; 2016. [cited 2021 Apr 12]. Available from: http://hdl.handle.net/10183/164889.

Council of Science Editors:

Lima TBd. Autofagia na carcinogênese bucal. [Masters Thesis]. Brazil; 2016. Available from: http://hdl.handle.net/10183/164889

16. Chakrama, Fatima Zahra. La protéine Gec1/Gabarapl1 : rôle au cours de l'autophagie et expression dans les cellules cancéreuses : Gabarapl1/Gec1 protein : role in the autophagy process and study of its expression in cancer ceIIs.

Degree: Docteur es, Sciences de la vie et de la santé, 2011, Besançon

URL: http://www.theses.fr/2011BESA3007

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Le gène Gec1/Gabarapl1 a été identifié au sein de notre laboratoire comme un gène régulé par les estrogènes. Il appartient à la famille Gabarap incluant… (more)

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Le gène Gec1/Gabarapl1 a été identifié au sein de notre laboratoire comme un gène régulé par les estrogènes. Il appartient à la famille Gabarap incluant les gènes Gabarap, gabarap/2 et Gabarapl3 qui codent des protéines présentant de fortes homologies de séquences. L'étude fonctionnelle de Gabarapl 1 a montré que cette protéine est impliquée dans le transport des récepteurs et particulièrement les récepteurs Gabaₐ et des κ-opioïdes via son interaction avec la tubuline et la protéine NSF. Cependant, il a été décrit que certaines protéines de la famille Atg8 sont impliquées dans l' autophagie, un mécanisme de dégradation et de survie cellulaire, qui se caractérise par la formation de doubles membranes appelées autophagosomes. Les objectifs de mon travail étaient, d'une part, de caractériser le rôle de la protéine GABARAPL1 au cours de !'autophagie et, d'autre part, de caractériser son expression dans des lignées et tissus cancéreux et sa régulation en réponse à des composés anti-cancéreux. Tout d'abord, nous avons montré que Gabarapl1 est clivée par la protéase Atg4B au niveau de sa glycine 116 avant sa conjugaison à des phopholipides. Cette forme modifiée, lipidée, est localisée à la surface des autophagosomes et des lysosomes. Nous avons ensuite montré que Gabarapl1 est faiblement exprimée dans de nombreuses lignées cancéreuses, que son expression est altérée dans les méningiomes et qu'elle est régulée par des inhibiteurs du protéasome. Ces travaux ont montré, pour la première fois, que la protéine Gabarapl1 est associée à des vésicules autophagiques et permettront de poser les hypothèses de nos futurs travaux.

The Gec1 / Gabarapl1 gene was identified in our laboratory as an early estrogen regulated gene. Gabarapl1 belongs to the Gabarap family, also including Gabarap, Gabarapl2 and Gabarapl3 genes, that encode proteins which present high sequence homology with each other. A functional study of the Gabarapl 1 protein showed that this protein is involved in the transport of receptors such as the Gabaₐ and κ-opioid receptors via its interaction with tubulin and NSF. It has been reported that the Atg8 family proteins are involved in autophagy, a mechanism of degradation and cell survival that is charactenzed by the formation of double membranes called autophagosomes. The aims of my research were, firstly, to characterize the role of the Gabarapl1 protein during autophagy and, secondly, to study its expression in cancer cell lines and cancerous tissues and its regulation in response to anti-cancer drugs. First, we showed that Gabarapl1 is cleaved in the cells by the protease Atg4B at its 116 glycine residue prior to its conjugation to phospholipids. This modified form, lipidated, is located on the surface of autophagosomes and lysosomes. We then showed that Gabarapl1 expression is reduced in many cancer cell lines, and that its expression is also altered in meningiomas. Finally, we showed that Gabarapl1 expression is regulated by proteasom€: inhibitors. Thus, our results demonstrated for the first time that the…

Advisors/Committee Members: Jouvenot, Michèle (thesis director), Boyer-Guittaut, Michaël (thesis director).

Subjects/Keywords: GABARAPL1; GABARAP; LC3; Macroautophagie; Tumeurs du sein; Méningiomes; Résistance aux drogues anti-cancéreuses; Protéasome; GABARAPL1; GABARAP; LC3; Macroautophagy; Breast tumors; Meningiomas; Resistance to anti-cancer drugs; Proteasome; 616.9; QZ 210

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Chakrama, F. Z. (2011). La protéine Gec1/Gabarapl1 : rôle au cours de l'autophagie et expression dans les cellules cancéreuses : Gabarapl1/Gec1 protein : role in the autophagy process and study of its expression in cancer ceIIs. (Doctoral Dissertation). Besançon. Retrieved from http://www.theses.fr/2011BESA3007

Chicago Manual of Style (16^th Edition):

Chakrama, Fatima Zahra. “La protéine Gec1/Gabarapl1 : rôle au cours de l'autophagie et expression dans les cellules cancéreuses : Gabarapl1/Gec1 protein : role in the autophagy process and study of its expression in cancer ceIIs.” 2011. Doctoral Dissertation, Besançon. Accessed April 12, 2021. http://www.theses.fr/2011BESA3007.

MLA Handbook (7^th Edition):

Chakrama, Fatima Zahra. “La protéine Gec1/Gabarapl1 : rôle au cours de l'autophagie et expression dans les cellules cancéreuses : Gabarapl1/Gec1 protein : role in the autophagy process and study of its expression in cancer ceIIs.” 2011. Web. 12 Apr 2021.

Vancouver:

Chakrama FZ. La protéine Gec1/Gabarapl1 : rôle au cours de l'autophagie et expression dans les cellules cancéreuses : Gabarapl1/Gec1 protein : role in the autophagy process and study of its expression in cancer ceIIs. [Internet] [Doctoral dissertation]. Besançon; 2011. [cited 2021 Apr 12]. Available from: http://www.theses.fr/2011BESA3007.

Council of Science Editors:

Chakrama FZ. La protéine Gec1/Gabarapl1 : rôle au cours de l'autophagie et expression dans les cellules cancéreuses : Gabarapl1/Gec1 protein : role in the autophagy process and study of its expression in cancer ceIIs. [Doctoral Dissertation]. Besançon; 2011. Available from: http://www.theses.fr/2011BESA3007

Linköping University

17. Westergren, Samuel. Nivåer av det lysosomala systemets proteiner i hjärnvävnad från Alzheimerpatienter.

Degree: Faculty of Health Sciences, 2014, Linköping University

URL: http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-110566

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Alzheimers sjukdom är den vanligaste orsaken till demens och i samband med att befolkningen blir större och allt äldre ökar även antalet patienter. Vid… (more)

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Alzheimers sjukdom är den vanligaste orsaken till demens och i samband med att befolkningen blir större och allt äldre ökar även antalet patienter. Vid sjukdomen sker en hjärnatrofi och de mikroskopiska fynd man ser är extracellulära plack av β-amyloid, intracellulära neurofibriller av fosforylerat tau och förlust av nervcellsutskott, axoner, synapser och dendriter. Några av de tidiga patologiska förändringarna man kan se är störningar i nervcellernas lysosomala system som fyller en viktig roll vid nedbrytning av makromolekyler. I en tidigare studie har man påvisat förhöjda nivåer av proteiner från det lysosomala systemet i cerebrospinalvätska. Syftet med den här studien var att mäta nivåer av det lysosomala systemets proteiner i human hjärnvävnad från patienter med Alzheimer och jämföra dessa med kontrollprover. De sex proteiner som analyserades med Western blot var EEA1, PICALM, LAMP-1, LAMP-2, LC3 och TFEB. Resultaten visar på signifikant ökning i temporala cortex av LAMP-1 och LAMP-2 och en signifikant minskning av LC3 och EEA1 hos patienter med Alzheimers sjukdom. För att kunna dra riktiga slutsatser kring hur de ökade nivåerna i cerebrospinalvätska speglar de olika sjukdomsmekanismerna i hjärnan krävs vidare analyser av fler patientprover samt prover från andra områden i hjärnan.

Alzheimer's disease is the most common cause of dementia, and when the population becomes larger and older also the number of patients increase. A cerebral atrophy and microscopic findings of extracellular plaques of β-amyloid, intracellular neurofibrillary of phosphorylated tau and loss of nerve cell protrusions, axons, synapses and dendrites are seen during the disease. One of the early pathological changes is the disruption of the neuronal lysosomal network that plays an important role in the degradation of macromolecules. In a previous study elevated levels of proteins of the lysosomal network in cerebrospinal fluid from Alzheimer’s disease patients was demonstrated. The purpose of this study was to measure levels of the lysosomal network system in the brain. The six proteins EEA1, PICALM, LAMP-1, LAMP -2, LC3 and TFEB were analyzed in human brain tissue from five Alzheimer's disease cases and five control cases by Western blot. The results show a significant increase in the temporal cortex of LAMP-1 and LAMP -2 and a significant decrease of LC3 and EEA1 in patients with Alzheimer's disease. In order to draw proper conclusions about how the increased levels in cerebrospinal fluid reflect the different disease mechanisms in the brain it requires further analysis of more patient samples and from other areas of the brain.

Subjects/Keywords: Alzheimer’s disease; lysosome; endosome; autophagy; EEA1; PICALM; LAMP-1; LAMP -2; LC3; TFEB; Alzheimers sjukdom; lysosom; endosom; autofagi; EEA1; PICALM; LAMP-1; LAMP -2; LC3; TFEB; Neurology; Neurologi; Neurosciences; Neurovetenskaper

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Westergren, S. (2014). Nivåer av det lysosomala systemets proteiner i hjärnvävnad från Alzheimerpatienter. (Thesis). Linköping University. Retrieved from http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-110566

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Westergren, Samuel. “Nivåer av det lysosomala systemets proteiner i hjärnvävnad från Alzheimerpatienter.” 2014. Thesis, Linköping University. Accessed April 12, 2021. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-110566.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Westergren, Samuel. “Nivåer av det lysosomala systemets proteiner i hjärnvävnad från Alzheimerpatienter.” 2014. Web. 12 Apr 2021.

Vancouver:

Westergren S. Nivåer av det lysosomala systemets proteiner i hjärnvävnad från Alzheimerpatienter. [Internet] [Thesis]. Linköping University; 2014. [cited 2021 Apr 12]. Available from: http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-110566.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Westergren S. Nivåer av det lysosomala systemets proteiner i hjärnvävnad från Alzheimerpatienter. [Thesis]. Linköping University; 2014. Available from: http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-110566

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

18. Graziela Batista da Silva. Remodelamento da matriz extracelular da medula óssea em desnutrição protéica: possível relação da via de AKT com a expressão de fibronectina e metaloproteinases de matriz.

Degree: 2016, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/9/9136/tde-13052016-141240/

► A desnutrição proteica (DP) pode ocasionar alterações na matriz extracelular (MEC) de diferentes órgãos e tecidos, inclusive o hematopoético, com comprometimento funcional. Estudos do nosso… (more)

▼ A desnutrição proteica (DP) pode ocasionar alterações na matriz extracelular (MEC) de diferentes órgãos e tecidos, inclusive o hematopoético, com comprometimento funcional. Estudos do nosso laboratório demonstraram, em modelo murino de DP, aumento da expressão proteica de fibronectina (FN) no estroma medular ósseo in vivo, principalmente na região subendosteal (local de fixação da célula tronco progenitora hemopoética). Já in vitro, no estroma medular ósseo, observou-se tanto o aumento quanto a diminuição de FN e a presença de suas isoformas. Essas alterações de FN parecem estar envolvidas com a hipoplasia da medula óssea (MO) em camundongos desnutridos. As modificações quantitativas de FN podem ser devidas: (i) à ação das metaloproteinases de matriz (MMP) responsáveis pela degradação das proteínas da MEC; (ii) aos inibidores de metaloproteinases (TIMP) que regulam a degradação da MEC; (iii) às alterações transcricionais, reguladas pela via de AKT/mTOR, que controla os splicing alternativos na FN, resultando em isoformas dessa proteína; (iv) a processos pós-transcricionais modulados por LC3, que aumenta a tradução do RNAm de FN. Assim, o objetivo deste estudo foi elucidar os mecanismos que alteram o turnover de FN no estroma medular ósseo em modelo murino de DP. Utilizamos camundongos, C57BL/6J machos, adultos, separados em dois grupos: controle e desnutrido, alimentados, ad libitum, com ração contendo 12% e 2% de proteína, respectivamente. Após cinco semanas de indução à desnutrição os camundongos foram eutanasiados, e coletado o material biológico. Avaliamos: o estado nutricional, o hematológico, a histologia da MO femoral bem como a determinação imunohistoquímica da FN, MMP-2 e MMP-9, determinação da expressão de FN e suas isoformas em células totais da MO, o estabelecimento do estroma medular ósseo in vitro, por 28 e 35 dias de cultivo. A partir das culturas foram avaliadas a expressão de RNAm de FN e suas isoformas, MMP-2, MMP-9, TIMP-1, TIMP-2, AKT, mTOR e LC3α e β, quantificação de MMP-2, MMP-9, TIMP-1, TIMP-2,TNFα, TGFβ e IL-1β e determinação de LC3β e proteínas da via de AKT/mTOR. Não observamos alterações na expressão do RNAm de FN e suas isoformas ex vivo e in vitro, mas um aumento da deposição de FN na MO.Também não observamos modificações na imunolocalização de MMP-2 e MMP-9 na MO e na atividade dessas proteínas no sobrenadante de culturas de células estromais in vitro, mas houve aumento da expressão do RNAm de MMP-9 em 28 dias de cultivo. Não detectamos alterações na expressão de RNAm e na concentração de TIMP-1 e TIMP-2 no sobrenadante das culturas. Houve redução significativa de TNFα e TGFβ no sobrenadante das culturas de 28 dias. Observamos aumento da expressão do RNAm de mTOR em culturas de 28 dias e LC3α e LC3β em 35 dias de células estromais. Encontramos menor fosforilação de PI3K, AKT, PTEN, mTOR e mTOR total e aumento de LC3β em culturas de 28 dias, mas redução de LC3β em 35 dias. Em função dos dados inferimos que a DP conduz a… Advisors/Committee Members: Primavera Borelli Garcia, Edgar Julian Paredes Gamero, Ruy Gastaldoni Jaeger.

Subjects/Keywords: AKT/mTOR; Hemopoese e desnutrição proteica; LC3β;

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Silva, G. B. d. (2016). Remodelamento da matriz extracelular da medula óssea em desnutrição protéica: possível relação da via de AKT com a expressão de fibronectina e metaloproteinases de matriz. (Doctoral Dissertation). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/9/9136/tde-13052016-141240/

Chicago Manual of Style (16^th Edition):

Silva, Graziela Batista da. “Remodelamento da matriz extracelular da medula óssea em desnutrição protéica: possível relação da via de AKT com a expressão de fibronectina e metaloproteinases de matriz.” 2016. Doctoral Dissertation, University of São Paulo. Accessed April 12, 2021. http://www.teses.usp.br/teses/disponiveis/9/9136/tde-13052016-141240/.

MLA Handbook (7^th Edition):

Silva, Graziela Batista da. “Remodelamento da matriz extracelular da medula óssea em desnutrição protéica: possível relação da via de AKT com a expressão de fibronectina e metaloproteinases de matriz.” 2016. Web. 12 Apr 2021.

Vancouver:

Silva GBd. Remodelamento da matriz extracelular da medula óssea em desnutrição protéica: possível relação da via de AKT com a expressão de fibronectina e metaloproteinases de matriz. [Internet] [Doctoral dissertation]. University of São Paulo; 2016. [cited 2021 Apr 12]. Available from: http://www.teses.usp.br/teses/disponiveis/9/9136/tde-13052016-141240/.

Council of Science Editors:

Silva GBd. Remodelamento da matriz extracelular da medula óssea em desnutrição protéica: possível relação da via de AKT com a expressão de fibronectina e metaloproteinases de matriz. [Doctoral Dissertation]. University of São Paulo; 2016. Available from: http://www.teses.usp.br/teses/disponiveis/9/9136/tde-13052016-141240/

NSYSU

19. Zeng, Jun-Yan. New Combretastatin A-4 enediyne derivatives induce Program Cell Death in Neuroblastoma SH-SY5Y cell line.

Degree: Master, Biological Sciences, 2015, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0019115-165758

► Antimitotic drug, combretastatin A-4 (CA-4) is a natural plant extract exhibits powerful anticancer and anti-angiogenesis activity by targeting microtubule formation. CA-4 enediyne derivatives, such as… (more)

Subjects/Keywords: Combretastatin A-4; LO-OMe; LO-NH2; PARP; Caspase-3; Apoptosis; Autophagy; p62; LC3

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Zeng, J. (2015). New Combretastatin A-4 enediyne derivatives induce Program Cell Death in Neuroblastoma SH-SY5Y cell line. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0019115-165758

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Zeng, Jun-Yan. “New Combretastatin A-4 enediyne derivatives induce Program Cell Death in Neuroblastoma SH-SY5Y cell line.” 2015. Thesis, NSYSU. Accessed April 12, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0019115-165758.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Zeng, Jun-Yan. “New Combretastatin A-4 enediyne derivatives induce Program Cell Death in Neuroblastoma SH-SY5Y cell line.” 2015. Web. 12 Apr 2021.

Vancouver:

Zeng J. New Combretastatin A-4 enediyne derivatives induce Program Cell Death in Neuroblastoma SH-SY5Y cell line. [Internet] [Thesis]. NSYSU; 2015. [cited 2021 Apr 12]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0019115-165758.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Zeng J. New Combretastatin A-4 enediyne derivatives induce Program Cell Death in Neuroblastoma SH-SY5Y cell line. [Thesis]. NSYSU; 2015. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0019115-165758

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Freie Universität Berlin

20. Milojkovic, Ana. Das Tumorsuppressorprotein p14ARF reguliert die Checkpoint Kontrolle des Zellzyklus und induziert Zelltod.

Degree: 2010, Freie Universität Berlin

URL: http://dx.doi.org/10.17169/refubium-11756

► Das INK4a Gen kodiert für das Suppressorprotein p14ARF, welches in fast der Hälfte aller Tumore mutiert ist. Es wurde gezeigt, dass p14ARF eine wichtige Rolle… (more)

▼ Das INK4a Gen kodiert für das Suppressorprotein p14ARF, welches in fast der Hälfte aller Tumore mutiert ist. Es wurde gezeigt, dass p14ARF eine wichtige Rolle in der Regulation des Zellzyklusarrestes und der Apoptose spielt. Das Ziel dieser Arbeit war es, die Regulation des p14ARF-induzierten Zelltodes zu untersuchen. Aus diesem Grund wurde eine MCF-7 p53 wildtyp Brustkrebs Zelllinie verwendet, welche keine Effektor Caspase-3 exprimiert, sowie MCF-7 Zellen die stabil mit Caspase-3 retransfiziert wurden. Die Expression von p14ARF induzierte einen G1 Arrest, sowohl in Caspase-3 defizienten als auch in Caspase-3 exprimierenden MCF-7 Transfektanten, jedoch konnte kein Zelltod detektiert werden. Eine zusätzliche Behandlung mit dem Kinase Inhibitor Koffein führte zu einem Verlust der Zellviabilität in den Caspase-3 profizienten als auch defizienten MCF-7 Zellen. Die MCF-7 Zellen starben dabei aus der G2 Phase des Zellzykluses heraus, unabhängig von der Caspase-3 Expression. In Caspase-3 exprimierenden MCF-7 Zellen, induzierte p14ARF, nach Sensibilisierung mit Koffein, Apoptose. Die Vermittlung erfolgte über den mitochondrialen Apoptosesignalweg, detektiert durch den Zusammenbruch des mitochondrialen Membranpotentials, der Cytochrom c Freisetzung und der Caspaseaktivierung. Im Gegensatz dazu, starben Caspase-3 defiziente MCF-7 Zellen durch einen nicht apoptotischen Mechanismus, welcher als Autophagie charakterisiert werden konnte. Die durch Koffein ausgelöste Hemmung der Zellantwort auf DNA-Schäden verminderte die Expression des CDK Inhibitors p21, was zu einer Zelltodinduktion durch p14ARF führte. Der Verlust von p21 führte zu einer Caspase-3 anhängigen p14ARF-induzierten Apoptose bzw. zu Autophagy in Abwesenheit einer effizienten Caspaseaktivierung durch den Verlust von Caspase-3. Diese Daten zeigen, dass die Beeinflussung des Zellzyklus entscheidend für die p14ARF-induzierte Apoptose ist, welche von der Expression von Caspase-3 abhängig ist. Der Verlust der Caspase-3 führt zu einem Zelltod der durch Autophagie vermittelt wird. Des Weiteren wurde der Einfluss des anti-apoptotischen Proteins Bcl-2 auf die p14ARF-induzierte Apoptose in Kombination mit Koffein in SW480 Zellen untersucht, die stabil Bcl-2 entweder am Endoplasmatischen Retikulum oder an den Mitochondrien exprimieren. Die Ergebnisse zeigten eindeutig, dass die Überexpression von Bcl-2, die p14ARF- induzierte Apoptose komplett hemmt, jedoch nur, wenn Bcl-2 an den Mitochondrien lokalisiert war. Dies legt den Schluss nahe, dass nach Sensibilisierung mit Koffein, p14ARF vorzugsweise über die Mitochondrien Apoptose induziert. Ein weiteres wichtiges Ziel dieser Arbeit war es, neue brauchbare Therapien für bestrahlungsresistente MCF-7 Zellen zu entwickeln. Hier zeigte sich, dass eine Sensitivierung der Zellen für strahlungsinduzierten apoptotischen Zelltod und eine begünstigte Zellzyklusprogression durch p14ARF von Caspase-3 abhängig ist. Advisors/Committee Members: [email protected] (contact), w (gender), Prof. Dr. Peter T. Daniel (firstReferee), Prof. Dr. Carsten Niemitz (furtherReferee).

Subjects/Keywords: p14ARF; apoptosis; mitochondria; cytochrome c; autophagy; LC3; p21CDKN1; 500 Naturwissenschaften und Mathematik::570 Biowissenschaften; Biologie

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Milojkovic, A. (2010). Das Tumorsuppressorprotein p14ARF reguliert die Checkpoint Kontrolle des Zellzyklus und induziert Zelltod. (Thesis). Freie Universität Berlin. Retrieved from http://dx.doi.org/10.17169/refubium-11756

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Milojkovic, Ana. “Das Tumorsuppressorprotein p14ARF reguliert die Checkpoint Kontrolle des Zellzyklus und induziert Zelltod.” 2010. Thesis, Freie Universität Berlin. Accessed April 12, 2021. http://dx.doi.org/10.17169/refubium-11756.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Milojkovic, Ana. “Das Tumorsuppressorprotein p14ARF reguliert die Checkpoint Kontrolle des Zellzyklus und induziert Zelltod.” 2010. Web. 12 Apr 2021.

Vancouver:

Milojkovic A. Das Tumorsuppressorprotein p14ARF reguliert die Checkpoint Kontrolle des Zellzyklus und induziert Zelltod. [Internet] [Thesis]. Freie Universität Berlin; 2010. [cited 2021 Apr 12]. Available from: http://dx.doi.org/10.17169/refubium-11756.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Milojkovic A. Das Tumorsuppressorprotein p14ARF reguliert die Checkpoint Kontrolle des Zellzyklus und induziert Zelltod. [Thesis]. Freie Universität Berlin; 2010. Available from: http://dx.doi.org/10.17169/refubium-11756

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Iowa State University

21. Ritchie, Jennifer Ann. Brucella abortus intracellular survival and intercellular trafficking.

Degree: 2011, Iowa State University

URL: https://lib.dr.iastate.edu/etd/10162

► Brucella spp. are host specific facultative intracellular pathogens. Brucella abortus is responsible for causing abortions in cattle and is also able to cause disease in… (more)

Subjects/Keywords: Autophagy; Brucella abortus; Brucellosis; LC3; LRG-47; Rab7; Veterinary Preventive Medicine, Epidemiology, and Public Health

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Ritchie, J. A. (2011). Brucella abortus intracellular survival and intercellular trafficking. (Thesis). Iowa State University. Retrieved from https://lib.dr.iastate.edu/etd/10162

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Ritchie, Jennifer Ann. “Brucella abortus intracellular survival and intercellular trafficking.” 2011. Thesis, Iowa State University. Accessed April 12, 2021. https://lib.dr.iastate.edu/etd/10162.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Ritchie, Jennifer Ann. “Brucella abortus intracellular survival and intercellular trafficking.” 2011. Web. 12 Apr 2021.

Vancouver:

Ritchie JA. Brucella abortus intracellular survival and intercellular trafficking. [Internet] [Thesis]. Iowa State University; 2011. [cited 2021 Apr 12]. Available from: https://lib.dr.iastate.edu/etd/10162.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Ritchie JA. Brucella abortus intracellular survival and intercellular trafficking. [Thesis]. Iowa State University; 2011. Available from: https://lib.dr.iastate.edu/etd/10162

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Western Ontario

22. Shyam, Vidhyasree. Investigating the Role of Tp53INP1 and Tp53INP2 in Neuronal Autophagy and Mitophagy.

Degree: 2019, University of Western Ontario

URL: https://ir.lib.uwo.ca/etd/6013

► Autophagy is highly conserved cellular process that functions in ensuring the turnover of proteins and organelles in a number of different cell types. Mitophagy is… (more)

Subjects/Keywords: Tp53INP1; Tp53INP2; Autophagy; Mitophagy; Hypoxia; Mitochondrial stress; LC3; Molecular and Cellular Neuroscience

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APA (6^th Edition):

Shyam, V. (2019). Investigating the Role of Tp53INP1 and Tp53INP2 in Neuronal Autophagy and Mitophagy. (Thesis). University of Western Ontario. Retrieved from https://ir.lib.uwo.ca/etd/6013

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Shyam, Vidhyasree. “Investigating the Role of Tp53INP1 and Tp53INP2 in Neuronal Autophagy and Mitophagy.” 2019. Thesis, University of Western Ontario. Accessed April 12, 2021. https://ir.lib.uwo.ca/etd/6013.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Shyam, Vidhyasree. “Investigating the Role of Tp53INP1 and Tp53INP2 in Neuronal Autophagy and Mitophagy.” 2019. Web. 12 Apr 2021.

Vancouver:

Shyam V. Investigating the Role of Tp53INP1 and Tp53INP2 in Neuronal Autophagy and Mitophagy. [Internet] [Thesis]. University of Western Ontario; 2019. [cited 2021 Apr 12]. Available from: https://ir.lib.uwo.ca/etd/6013.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Shyam V. Investigating the Role of Tp53INP1 and Tp53INP2 in Neuronal Autophagy and Mitophagy. [Thesis]. University of Western Ontario; 2019. Available from: https://ir.lib.uwo.ca/etd/6013

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Victoria

23. Spowart, Jaeline E. Defining the roles of autophagy in ovarian carcinoma.

Degree: Dept. of Biochemistry and Microbiology, 2012, University of Victoria

URL: http://hdl.handle.net/1828/4061

► Ovarian cancer is a significant concern for women’s health as it is the most lethal of all gynaecological malignancies. One of the reasons for the… (more)

▼ Ovarian cancer is a significant concern for women’s health as it is the most lethal of all gynaecological malignancies. One of the reasons for the high mortality of this disease is that traditionally used chemotherapeutic treatments tend to have poor initial or sustained efficacy against ovarian tumours. Resistance to such treatments may in part be mediated by autophagy, a cell survival process in which unnecessary or damaged components of the cytoplasm are engulfed within a double-membraned vesicle known as an autophagosome and ultimately degraded upon fusion of the autophagosome with a lysosome. Autophagy has been shown to be employed by cells to aid in their survival under stresses such as nutrient deprivation, hypoxia, chemotherapy treatment, and growth factor withdrawal. As these stresses are commonly encountered by ovarian cancer cells, it is possible that autophagy promotes ovarian cancer cell survival. This thesis aims to investigate which stimuli induce autophagy in ovarian cancer cells and whether or not this induction can promote cell survival. In addition, there is a particular focus on the comparison of autophagy utilization between subtypes of ovarian cancer, as the subtypes are in fact considered different diseases and may vary in their usage of autophagy. The first chapter of this thesis provides relevant background information on autophagy as well as ovarian cancer and its subtypes. In the second chapter, I describe studies in which tumours from a large cohort of patients with ovarian cancer are assessed for LC3A, a marker of autophagy, in addition to markers of other cellular processes including hypoxia. Here I found that LC3A was significantly associated with poor patient survival in patients with the clear cell subtype of ovarian cancer, but not other subtypes. I also found that LC3A expression was associated with markers of hypoxia in the clear cell patient tumours and that clear cell carcinoma cell lines preferentially induced autophagy in response to hypoxia in vitro as compared to cell lines of the high-grade serous subtype. These results indicate that clear cell ovarian tumours are uniquely dependent upon autophagy in response to hypoxia. In the third chapter, I investigated the autophagic response to treatment with the standard ovarian cancer chemotherapy drugs carboplatin and paclitaxel in a syngeneic mouse model of ovarian cancer. I found that these drugs did indeed induce autophagy and that the cancer cells utilized autophagy to promote resistance to these chemotherapeutics. In addition, when the tumour cells were grown in syngeneic mice, treatment with the autophagy inhibitor hydroxychloroquine resulted in a significant suppression of tumour growth. Together, my findings indicate that further investigation into the use of autophagy inhibitors in ovarian cancer patients is warranted and that different specific rational drug combinations for each subtype will likely yield optimal results. Advisors/Committee Members: Lum, Julian J. (supervisor), Pearson, Terry W. (supervisor).

Subjects/Keywords: Autophagy; Ovarian Cancer; Hypoxia; Chemotherapy; LC3; Ovarian Clear Cell Carcinoma; Immunohistochemistry; Prognosis; Cancer

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Spowart, J. E. (2012). Defining the roles of autophagy in ovarian carcinoma. (Masters Thesis). University of Victoria. Retrieved from http://hdl.handle.net/1828/4061

Chicago Manual of Style (16^th Edition):

Spowart, Jaeline E. “Defining the roles of autophagy in ovarian carcinoma.” 2012. Masters Thesis, University of Victoria. Accessed April 12, 2021. http://hdl.handle.net/1828/4061.

MLA Handbook (7^th Edition):

Spowart, Jaeline E. “Defining the roles of autophagy in ovarian carcinoma.” 2012. Web. 12 Apr 2021.

Vancouver:

Spowart JE. Defining the roles of autophagy in ovarian carcinoma. [Internet] [Masters thesis]. University of Victoria; 2012. [cited 2021 Apr 12]. Available from: http://hdl.handle.net/1828/4061.

Council of Science Editors:

Spowart JE. Defining the roles of autophagy in ovarian carcinoma. [Masters Thesis]. University of Victoria; 2012. Available from: http://hdl.handle.net/1828/4061

University of New Mexico

24. Cole, Nathan H. Coordination Between Autophagy and the Heat Shock Response: Evidence From Exercise in Animals and Humans.

Degree: Health, Exercise, and Sports Sciences, 2015, University of New Mexico

URL: http://hdl.handle.net/1928/30325

► Proteins play a critical role in nearly every biological activity. In consequence, organismal health and homeostasis often hinges on the ability of intracellular regulatory… (more)

Subjects/Keywords: Autophagy; Heat Shock Response; Exercise; Hsp70; LC3; Humans; Animals; Health and Physical Education

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Cole, N. H. (2015). Coordination Between Autophagy and the Heat Shock Response: Evidence From Exercise in Animals and Humans. (Masters Thesis). University of New Mexico. Retrieved from http://hdl.handle.net/1928/30325

Chicago Manual of Style (16^th Edition):

Cole, Nathan H. “Coordination Between Autophagy and the Heat Shock Response: Evidence From Exercise in Animals and Humans.” 2015. Masters Thesis, University of New Mexico. Accessed April 12, 2021. http://hdl.handle.net/1928/30325.

MLA Handbook (7^th Edition):

Cole, Nathan H. “Coordination Between Autophagy and the Heat Shock Response: Evidence From Exercise in Animals and Humans.” 2015. Web. 12 Apr 2021.

Vancouver:

Cole NH. Coordination Between Autophagy and the Heat Shock Response: Evidence From Exercise in Animals and Humans. [Internet] [Masters thesis]. University of New Mexico; 2015. [cited 2021 Apr 12]. Available from: http://hdl.handle.net/1928/30325.

Council of Science Editors:

Cole NH. Coordination Between Autophagy and the Heat Shock Response: Evidence From Exercise in Animals and Humans. [Masters Thesis]. University of New Mexico; 2015. Available from: http://hdl.handle.net/1928/30325

Universiteit Utrecht

25. V'kovski, P. The unconventional roles of autophagy-related proteins in infections and immunity.

Degree: 2013, Universiteit Utrecht

URL: http://dspace.library.uu.nl:8080/handle/1874/287100

► Autophagy is a well-known, evolutionary conserved catabolic pathway leading to the degradation of large cytoplasmic elements by the lysosome. Autophagy-related gene (Atg) protein complexes catalyze… (more)

▼ Autophagy is a well-known, evolutionary conserved catabolic pathway leading to the degradation of large cytoplasmic elements by the lysosome. Autophagy-related gene (Atg) protein complexes catalyze the formation of double-membrane vesicles called autophagosomes. Bulk cytosol, protein aggregates and damaged organelles but also cytoplasmic microbes such as bacteria, viruses and parasites are sequestered into double-membrane autophagosomes and delivered to the lysosome where they are degraded. Hence, autophagy is essentially induced upon stress situations while also providing protection against intracellular pathogens, adding to the cellular innate immune arsenal. In turn, several pathogens have evolved strategies to evade the autophagy pathway or even manipulate it to sustain their intracellular life cycle. In addition to their traditional role in autophagosome formation, recent finding have attributed novel functions, which are distinct from the classical autophagy pathway, to autophagy-related protein complexes. Autophagy-independent roles of Atg proteins include the maintenance of cellular homeostasis and resistance against invading pathogens. As such, autophagy proteins have been shown to assist and enhance the degradation of dead cells, bacteria and parasites upon their macroendocytic engulfment. It was also demonstrated that a subset of Atg proteins has a direct antiviral function by inhibiting Murine norovirus’ replication complex. Moreover, bone resorption by osteoclasts, innate immune regulation upon double-stranded DNA-triggered signaling and the ER-associated degradation pathway regulation all have in common the requirement of some of the Atg proteins in an autophagosome formation-independent manner. On the other hand, microorganisms, such as coronaviruses, Chlamydia or Brucella, have evolved ways to manipulate and benefit from autophagy-independent functions of autophagy-related proteins in order to ensure the completion of their intracellular life cycle. These novel mechanisms that involve autophagy-related proteins independently from their role during canonical autophagosome formation add to the functional repertoire of Atg proteins and extend the cellular processes in which autophagy proteins are implicated. Advisors/Committee Members: Bestebroer, J..

Subjects/Keywords: Autophagy; Autophagy-related (Atg) proteins; unconventional autophagy; LC3-associated phagocytosis; Murine norovirus; Toxoplasma gondii; osteoclasts; STING; Coronavirus; Chlamydia; Brucella

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

V'kovski, P. (2013). The unconventional roles of autophagy-related proteins in infections and immunity. (Masters Thesis). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/287100

Chicago Manual of Style (16^th Edition):

V'kovski, P. “The unconventional roles of autophagy-related proteins in infections and immunity.” 2013. Masters Thesis, Universiteit Utrecht. Accessed April 12, 2021. http://dspace.library.uu.nl:8080/handle/1874/287100.

MLA Handbook (7^th Edition):

V'kovski, P. “The unconventional roles of autophagy-related proteins in infections and immunity.” 2013. Web. 12 Apr 2021.

Vancouver:

V'kovski P. The unconventional roles of autophagy-related proteins in infections and immunity. [Internet] [Masters thesis]. Universiteit Utrecht; 2013. [cited 2021 Apr 12]. Available from: http://dspace.library.uu.nl:8080/handle/1874/287100.

Council of Science Editors:

V'kovski P. The unconventional roles of autophagy-related proteins in infections and immunity. [Masters Thesis]. Universiteit Utrecht; 2013. Available from: http://dspace.library.uu.nl:8080/handle/1874/287100

26. Blasi Beriain, Ignacio. Porphyromonas gingivalis LPS stimulates autophagy using a TLR mediated pathway.

Degree: Departament d'Odontologia, 2017, Universitat Internacional de Catalunya

URL: http://hdl.handle.net/10803/461098

► Resum: Porphyromonas gingivalis often subverts host cell autophagic processes for its own survival. Our previous studies document the association of the cargo sorting protein, melanoregulin… (more)

Subjects/Keywords: GFP-LC3; Human gingival epithelia; Periodontal pathogens; Porphyromonas gingivalis LPS1690; Saos-2 cells; Toll-like receptor agonist; Odontologia; 616.3

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Blasi Beriain, I. (2017). Porphyromonas gingivalis LPS stimulates autophagy using a TLR mediated pathway. (Thesis). Universitat Internacional de Catalunya. Retrieved from http://hdl.handle.net/10803/461098

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Blasi Beriain, Ignacio. “Porphyromonas gingivalis LPS stimulates autophagy using a TLR mediated pathway.” 2017. Thesis, Universitat Internacional de Catalunya. Accessed April 12, 2021. http://hdl.handle.net/10803/461098.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Blasi Beriain, Ignacio. “Porphyromonas gingivalis LPS stimulates autophagy using a TLR mediated pathway.” 2017. Web. 12 Apr 2021.

Vancouver:

Blasi Beriain I. Porphyromonas gingivalis LPS stimulates autophagy using a TLR mediated pathway. [Internet] [Thesis]. Universitat Internacional de Catalunya; 2017. [cited 2021 Apr 12]. Available from: http://hdl.handle.net/10803/461098.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Blasi Beriain I. Porphyromonas gingivalis LPS stimulates autophagy using a TLR mediated pathway. [Thesis]. Universitat Internacional de Catalunya; 2017. Available from: http://hdl.handle.net/10803/461098

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of New Mexico

27. Escobar, Kurt A. Autophagy is stimulated by acute high intensity interval exercise in human skeletal muscle and electrical pulse stimulation in C2C12 myotubes in vitro.

Degree: Health, Exercise, and Sports Sciences, 2018, University of New Mexico

URL: https://digitalrepository.unm.edu/educ_hess_etds/99

► Purpose: 1) To compare the effects of an acute bout of HIIT exercise (treadmill running) on autophagy to MICT exercise in human skeletal muscle… (more)

▼ Purpose: 1) To compare the effects of an acute bout of HIIT exercise (treadmill running) on autophagy to MICT exercise in human skeletal muscle 3 hours post exercise, and 2) to test an in vitro model of muscle contraction-induced autophagy using electrical pulse stimulation in C2C12 myotubes. Methods: Study 1: Ten recreationally active males and females completed a bout of high intensity interval training (HIIT) exercise and moderate intensity continuous exercise (MICT) exercise in a fasted state. Muscle biopsies from the vastus lateralis were taken pre and 3 hours post-exercise. Muscle tissue was analyzed for protein expression of markers of autophagy (LC3I, LC3II) and autophagy signaling (p38MAPK). Study 2: C2C12 myoblasts were differentiated into myotubes and underwent 8 hours of low-frequency electrical pulse stimulation (EPS) and starvation (St) and EPS+St conditions with and without bafilomycin A1 (Baf) or non-treatment control conditions (Con). Cells were harvested immediately following EPS and analyzed for protein expression of markers of autophagy (LC3I, LC3II, and p62). Results: Study 1: No differences were detected for LC3I, LC3II, and p38MAPK at the 3h time point vs. pre-exercise in both HIIT and MICT conditions. The LC3II:LC3I ratio increased 3-h post exercise in the HIIT (162.4, SE: 45.9%), which was significantly higher than the 3h timepoint in the MICT (48.8, SE: 9.4%; p<0.05) Study 2: LC3II (324.4, SE: 29.8%) LC3II:I (258.2, SE: 323.3%), and p62 (437.8, SE: 9.7%) were significantly higher in EPS+Baf conditions compared to control (100%, SE: 9.3, 8.8, 22.6%, respectively) and EPS alone (127.7, SE: 24.3%; 95.5, SE: 13.2%, 251.2, SE: 33.2%) . p62 protein expression was also higher in EPS compared to Con and in St+Baf (320.9, SE: 65.9%) compared Con and St (91, SE: 20.3%). There were no differences between EPS and St alone vs. combined EPS+St conditions in LC3I, LC3II, LC3II:I or p62. Conclusions: HIIT stimulates autophagy in a distinct fashion compared to MICT. Additionally, EPS may serve as an in vitro model for muscle contraction-induced autophagy in C2C12 myotubes in fed and fasted conditions. s. Advisors/Committee Members: Fabiano Amorim, Christine Mermier (co-chair), Carlos Hiroshi Nitta, Trisha VanDusseldorp.

Subjects/Keywords: training; proteostasis; LC3; cell culture; muscle contraction; Cellular and Molecular Physiology; Exercise Physiology; Health and Physical Education; Life Sciences; Physiology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Escobar, K. A. (2018). Autophagy is stimulated by acute high intensity interval exercise in human skeletal muscle and electrical pulse stimulation in C2C12 myotubes in vitro. (Doctoral Dissertation). University of New Mexico. Retrieved from https://digitalrepository.unm.edu/educ_hess_etds/99

Chicago Manual of Style (16^th Edition):

Escobar, Kurt A. “Autophagy is stimulated by acute high intensity interval exercise in human skeletal muscle and electrical pulse stimulation in C2C12 myotubes in vitro.” 2018. Doctoral Dissertation, University of New Mexico. Accessed April 12, 2021. https://digitalrepository.unm.edu/educ_hess_etds/99.

MLA Handbook (7^th Edition):

Escobar, Kurt A. “Autophagy is stimulated by acute high intensity interval exercise in human skeletal muscle and electrical pulse stimulation in C2C12 myotubes in vitro.” 2018. Web. 12 Apr 2021.

Vancouver:

Escobar KA. Autophagy is stimulated by acute high intensity interval exercise in human skeletal muscle and electrical pulse stimulation in C2C12 myotubes in vitro. [Internet] [Doctoral dissertation]. University of New Mexico; 2018. [cited 2021 Apr 12]. Available from: https://digitalrepository.unm.edu/educ_hess_etds/99.

Council of Science Editors:

Escobar KA. Autophagy is stimulated by acute high intensity interval exercise in human skeletal muscle and electrical pulse stimulation in C2C12 myotubes in vitro. [Doctoral Dissertation]. University of New Mexico; 2018. Available from: https://digitalrepository.unm.edu/educ_hess_etds/99

University of Guelph

28. Liu, Juan-Ting. Autophagy and resistance to VHSV IVb in RTgill-W1 and Flavobacterium psychrophilum in rainbow trout (Oncorhynchus mykiss).

Degree: PhD, Department of Pathobiology, 2019, University of Guelph

URL: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/17608

► Autophagy is a highly conserved process in eukaryotic cells that sequesters intracellular components in the autophagosome for degradation by lysosomal enzymes. Western blot (WB) and… (more)

▼ Autophagy is a highly conserved process in eukaryotic cells that sequesters intracellular components in the autophagosome for degradation by lysosomal enzymes. Western blot (WB) and immunofluorescence assay for LC3II were applied to detect autophagy modulation in the RTgill-W1 cell line. Two percent fetal bovine serum (FBS), 1M deoxynivalenol (DON) and 50M chloroquine (CQ) significantly (p < 0.05) activated, inhibited and blocked autophagy, respectively, after 3 d. Rapamycin and 3-methyladenine (3-MA) inconsistently activated or inhibited autophagy, respectively, after 3 d. Quantitative PCR (qPCR) for autophagy-related (Atg) genes showed that pattern of expression of lc3 and gabarap best reflected the LC3II signal using WB, while atg7, atg12 and atg4 had similar results. A potential feedback loop resulting in broad up-regulation of Atg genes, most notably becn1, lc3, gabarap and atg9, was seen after treatment with 3-MA and CQ. Autophagy activity in RTgill-W1 was significantly (p < 0.05) decreased for 2 d after infection with viral hemorrhagic septicemia virus (VHSV) IVb. Using qPCR and WB, the VHSV gene copy number and viral N-protein were suppressed by autophagy inhibiting (DON; p < 0.001 and 3-MA; p < 0.05) and blocking (CQ; p < 0.05) chemicals. In an in vivo trial, rainbow trout were experimentally infected with Flavobacterium psychrophilum. Fish fed 5ppm DON (p < 0.001) or pair-fed (p < 0.05) for 12 d before and then during infection had significantly decreased mortality after infection, while the effect of 250ppm CQ was marginally significant (p = 0.052). After 15 d treatment, the LC3II signal was significantly increased in the liver (p < 0.01) and decreased (p < 0.01) in the muscle of fasted fish. The LC3II signal was also significantly increased in the liver of DON-treated fish (p < 0.05) but there were no significant differences between treatments in the spleen. Pair-fed and fasted fish had significantly (p < 0.05) increased expression of gabarap, atg7 and atg12 in muscle after 15 d while 250ppm CQ significantly (p < 0.05) up-regulated hepatic becn1 and atg4. Autophagy modulation alone cannot explain the resistance of rainbow trout to experimental infection with F. psychrophilum. Advisors/Committee Members: Lumsden, John (advisor).

Subjects/Keywords: autophagy; LC3; RTgill-W1; VHSV IVb; rainbow trout; Flavobacterium psychrophilum; atg gene; deoxynivalenol (DON); chloroquine (CQ)

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APA (6^th Edition):

Liu, J. (2019). Autophagy and resistance to VHSV IVb in RTgill-W1 and Flavobacterium psychrophilum in rainbow trout (Oncorhynchus mykiss). (Doctoral Dissertation). University of Guelph. Retrieved from https://atrium.lib.uoguelph.ca/xmlui/handle/10214/17608

Chicago Manual of Style (16^th Edition):

Liu, Juan-Ting. “Autophagy and resistance to VHSV IVb in RTgill-W1 and Flavobacterium psychrophilum in rainbow trout (Oncorhynchus mykiss).” 2019. Doctoral Dissertation, University of Guelph. Accessed April 12, 2021. https://atrium.lib.uoguelph.ca/xmlui/handle/10214/17608.

MLA Handbook (7^th Edition):

Liu, Juan-Ting. “Autophagy and resistance to VHSV IVb in RTgill-W1 and Flavobacterium psychrophilum in rainbow trout (Oncorhynchus mykiss).” 2019. Web. 12 Apr 2021.

Vancouver:

Liu J. Autophagy and resistance to VHSV IVb in RTgill-W1 and Flavobacterium psychrophilum in rainbow trout (Oncorhynchus mykiss). [Internet] [Doctoral dissertation]. University of Guelph; 2019. [cited 2021 Apr 12]. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/17608.

Council of Science Editors:

Liu J. Autophagy and resistance to VHSV IVb in RTgill-W1 and Flavobacterium psychrophilum in rainbow trout (Oncorhynchus mykiss). [Doctoral Dissertation]. University of Guelph; 2019. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/17608

29. Fanidi, Anouar. Le métabolisme monocarboné et les cancers liés au tabac : One-carbon metabolism ans smoking related cancers.

Degree: Docteur es, Épidémiologie et santé publique, 2016, Lyon

URL: http://www.theses.fr/2016LYSE1002

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Les vitamines B et les facteurs liés au métabolisme monocarboné (C1) aident à maintenir la synthèse de l'ADN, régulent l'expression des gènes, et peuvent affecter… (more)

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Les vitamines B et les facteurs liés au métabolisme monocarboné (C1) aident à maintenir la synthèse de l'ADN, régulent l'expression des gènes, et peuvent affecter le risque de cancer. L'objectif général de cette thèse est d'étudier l'importance des biomarqueurs du C1 dans l'étiologie de trois cancers distincts qui diffèrent dans leur force d'association avec le tabagisme. Les articles inclus dans cette thèse ont été conduits au sein de deux études prospectives : l'étude prospective européenne sur la nutrition et le cancer (EPIC) et le consortium de cohortes du cancer du poumon (LC3). Dans l'article 1, nous avons étudié la relation entre les biomarqueurs du C1 et l'incidence ainsi que le pronostic du cancer de la sphère oto-rhino-laryngée (ORL) et de l'oesophage au sein de l'étude EPIC. Nous avons observé que les sujets ayant des concentrations élevées d'homocystéine avaient un risque accru de développer un cancer de la sphère ORL. Dans l'article 2, nous avons examiné la relation entre les biomarqueurs du C1 et l'incidence ainsi que le pronostic du carcinome à cellules rénales (CCR) au sein de l'étude EPIC. Nous avons constaté que les participants ayant des concentrations de vitamine B6 élevées avaient une diminution du risque de CCR avec un effet dose-réponse ainsi qu'une amélioration de la survie post-diagnostic. Dans l'article 3, nous avons étudié si les biomarqueurs du C1 sont associés au risque de cancer du poumon au sein de l'étude LC3. Dans l'ensemble, nous avons mis en exergue une faible association inverse, sans tendance claire, entre les concentrations de vitamine B6 et de folate et le risque du cancer du poumon. La principale conclusion de nos études est que les concentrations élevées de vitamine B6 sont associées à un risque plus faible de développer un CCR, et également à un meilleur pronostic chez les patients atteints de cette pathologie. Davantage d'études sont nécessaires afin d'évaluer si la vitamine B6 exerce une influence causale sur l'étiologie et la mortalité du CCR, ou si d'autres facteurs métaboliques sont impliqués

B-vitamins and factors related to one-carbon metabolism (OCM) pathway help to maintain DNA synthesis and regulate gene expression and may affect cancer risk. The overarching aim of this thesis is to investigate the importance of OCM biomarkers in the etiology of three distinct cancer sites that differed in their strength of association with smoking. Papers included in this thesis were conducted within two prospective studies, the European Prospective Investigation into nutrition and Cancer (EPIC) study and the Lung Cancer Cohort Consortium (LC3). In paper 1, we investigated if OCM biomarkers are associated with incidence and survival of cancer of the head and neck and esophagus in the EPIC study. We observed that subjects with higher concentrations of homocysteine had increased risk of developing head and neck cancer. In paper 2, we investigated if OCM biomarkers are associated with incidence and survival of renal cell carcinoma (RCC) in the EPIC study. We observed that study…

Advisors/Committee Members: Brennan, Paul (thesis director), Johansson, Mattias (thesis director).

Subjects/Keywords: Métabolisme monocarboné; Cancer du poumon; Cancer de la tête et du cou; Carcinome à cellules rénales; EPIC; LC3; Étude prospective; One-carbon metabolism; Lung cancer; Head and neck cancer; Renal cell carcinoma; EPIC; LC3; Prospective study; 614

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Fanidi, A. (2016). Le métabolisme monocarboné et les cancers liés au tabac : One-carbon metabolism ans smoking related cancers. (Doctoral Dissertation). Lyon. Retrieved from http://www.theses.fr/2016LYSE1002

Chicago Manual of Style (16^th Edition):

Fanidi, Anouar. “Le métabolisme monocarboné et les cancers liés au tabac : One-carbon metabolism ans smoking related cancers.” 2016. Doctoral Dissertation, Lyon. Accessed April 12, 2021. http://www.theses.fr/2016LYSE1002.

MLA Handbook (7^th Edition):

Fanidi, Anouar. “Le métabolisme monocarboné et les cancers liés au tabac : One-carbon metabolism ans smoking related cancers.” 2016. Web. 12 Apr 2021.

Vancouver:

Fanidi A. Le métabolisme monocarboné et les cancers liés au tabac : One-carbon metabolism ans smoking related cancers. [Internet] [Doctoral dissertation]. Lyon; 2016. [cited 2021 Apr 12]. Available from: http://www.theses.fr/2016LYSE1002.

Council of Science Editors:

Fanidi A. Le métabolisme monocarboné et les cancers liés au tabac : One-carbon metabolism ans smoking related cancers. [Doctoral Dissertation]. Lyon; 2016. Available from: http://www.theses.fr/2016LYSE1002

Université Paris-Sud – Paris XI

30. Laurent, Anne-Coline. Rôles et mécanismes d’action de la protéine Epac dans l’hypertrophie cardiaque : Functions and signaling of Epac protein in cardiac hypertrophy.

Degree: Docteur es, Biologie Cellulaire et Moléculaire, Science de la Santé, 2013, Université Paris-Sud – Paris XI

URL: http://www.theses.fr/2013PA11T044

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Les catécholamines induisent la synthèse d’AMPc par une stimulation des récepteurs β-adrénergiques et contrôlent ainsi la fonction cardiaque en activant une pléiade de voies de… (more)

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Les catécholamines induisent la synthèse d’AMPc par une stimulation des récepteurs β-adrénergiques et contrôlent ainsi la fonction cardiaque en activant une pléiade de voies de signalisation intracellulaires. Les protéines Epac sont des facteurs d’échange pour les petites protéines G et sont directement activés par l’AMPc. Devant l’importance de la voie β-adrénergique dans la physiopathologie cardiaque et dans le but de mieux comprendre la régulation des processus cellulaires dépendants de l’AMPc dans le cœur, il apparaît essentiel de caractériser le rôle des facteurs d’échange Epac dans le myocarde. Dans une première partie, cette étude démontre que les effets de Epac sur l’hypertrophie des cardiomyocytes ventriculaires de rats nouveaux nés requièrent les GTPases H-Ras et Rap2B. Epac active la voie PLC/IP3/Ca2+ qui est nécessaire pour l’activation de H-Ras. Au niveau transcriptionnel, Epac induit l’export nucléaire de HDAC4 permettant l’activation d’un programme génique d’hypertrophie. Dans une deuxième partie, cette étude révèle l’implication de Epac1 dans l’hypertrophie des cardiomyocytes in vivo, chez la souris. La délétion de Epac1 protège du remodelage cardiaque induit par l’activation prolongée des récepteurs β-adrénergiques et améliore la fonction cardiaque. La surexpression de Epac1 spécifiquement dans le myocarde entraîne une hypertrophie des cardiomyocytes. Par ailleurs, la voie β-AR/Epac1 induit l’accumulation de protéines ubiquitinylées et provoque l’activation du processus d’autophagie in vitro et in vivo. L’autophagie protège des effets délétères de la voie β-adrénergique/Epac en participant à l’élimination des agrégats protéiques et en contrant les effets hypertrophiques de Epac1. Ces résultats ouvrent de nouvelles perspectives pour le traitement de l’hypertrophie et de l’insuffisance cardiaque.

Catecholamines regulate cardiac function by stimulating β-adrenergic receptors (β-AR), leading to cAMP production and activation of a multiplicity of signaling pathways. Epac proteins are exchange factors for small G proteins which are directly activated by cAMP. Given the importance of the β-adrenergic pathway in cardiac physiopathology, it becomes essential to characterize functions of Epac protein in myocardium. In a first part, this study shows that H-Ras and Rap2B GTPases are involved in Epac-induced neonatal rat cardiac myocytes hypertrophy. Epac induces activation of the PLC/IP3/Ca2+ pathway which is necessary for H-Ras activation. At the transcriptional level, Epac causes HDAC4 nuclear export leading to activation of a hypertrophic gene program. In a second part, this study reveals implication of Epac1 in cardiac hypertrophy in vivo. Deletion of Epac1 in mice protects from cardiac remodeling induced by chronic isoproterenol infusion and enhances cardiac function. Cardiac specific overexpression of Epac1 in mice induces cardiac myocytes hypertrophy. Interestingly, β-AR/Epac1 pathway triggers ubiquitinated proteins accumulation and activation of autophagy both in vitro and in vivo. By eliminating…

Advisors/Committee Members: Lezoualc'h, Frank (thesis director).

Subjects/Keywords: Hypertrophie et insuffisance cardiaque; Autophagie; Récepteur β-adrénergique; AMP cyclique; Epac; Petites protéines G; HDAC; Protéines ubiquitinylées; Bécline 1; P62; LC3; Cardiac hypertrophy and failure; Autophagy; Β-adrenergic receptor; Cyclic AMP; Epac; Small GTPases; HDAC; Ubiquitinated proteins; Beclin 1; P62; LC3

Record Details Similar Records Cite « Share

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Laurent, A. (2013). Rôles et mécanismes d’action de la protéine Epac dans l’hypertrophie cardiaque : Functions and signaling of Epac protein in cardiac hypertrophy. (Doctoral Dissertation). Université Paris-Sud – Paris XI. Retrieved from http://www.theses.fr/2013PA11T044

Chicago Manual of Style (16^th Edition):

Laurent, Anne-Coline. “Rôles et mécanismes d’action de la protéine Epac dans l’hypertrophie cardiaque : Functions and signaling of Epac protein in cardiac hypertrophy.” 2013. Doctoral Dissertation, Université Paris-Sud – Paris XI. Accessed April 12, 2021. http://www.theses.fr/2013PA11T044.

MLA Handbook (7^th Edition):

Laurent, Anne-Coline. “Rôles et mécanismes d’action de la protéine Epac dans l’hypertrophie cardiaque : Functions and signaling of Epac protein in cardiac hypertrophy.” 2013. Web. 12 Apr 2021.

Vancouver:

Laurent A. Rôles et mécanismes d’action de la protéine Epac dans l’hypertrophie cardiaque : Functions and signaling of Epac protein in cardiac hypertrophy. [Internet] [Doctoral dissertation]. Université Paris-Sud – Paris XI; 2013. [cited 2021 Apr 12]. Available from: http://www.theses.fr/2013PA11T044.

Council of Science Editors:

Laurent A. Rôles et mécanismes d’action de la protéine Epac dans l’hypertrophie cardiaque : Functions and signaling of Epac protein in cardiac hypertrophy. [Doctoral Dissertation]. Université Paris-Sud – Paris XI; 2013. Available from: http://www.theses.fr/2013PA11T044

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