subject:(nuclear hormone receptors)

UCLA

1. Monsalve, Gabriela Carolina. Unifying Mechanisms of Developmental Timing: Genetic and Molecular Analysis of the Molting Cycle Timer of Caenorhabditis elegans.

Degree: Biological Chemistry, 2013, UCLA

URL: http://www.escholarship.org/uc/item/56j1x8dd

► Chronobiologists focus on understanding at least two ways of regulating the time of life: biological clocks that anticipate environmental conditions, and temporal switches that regulate… (more)

▼ Chronobiologists focus on understanding at least two ways of regulating the time of life: biological clocks that anticipate environmental conditions, and temporal switches that regulate sequential events. Of the former, the best-characterized biological clocks regulate circadian rhythms in metazoans. These self sustaining oscillators involve transcriptional-translational feedback loops that affect the physiology of the organism. In contrast, progression through development requires the proper temporal coordination of factors that control sequential events. However, the timing mechanisms that coordinate both cyclical and successive events in development are not generally well understood.The molting cycle of C. elegans is an example of both a periodic and sequential developmental program. Molting of the exoskeleton involves the coordinated synthesis, secretion, and assembly of a new skeleton, as well as degradation of the old one. Quiescent behaviors also accompany the molting cycle. Worms molt four times, approximately once every eight hours when cultivated at room temperature. The molts are coordinated with successive transitions in the temporal fates of epidermal stem cells, which are programmed by genes in the heterochronic regulatory network. Every molt is a critical developmental transition and mis-coordination of the either the sequential or reiterative events can lead to larval arrest and death. This thesis describes how the C. elegans heterochronic gene lin-42a, homologous to the mammalian circadian clock protein PERIOD, is required for cyclical and sequential progression of development. The oscillatory expression of lin-42a in the epidermis peaks during the molts. Inactivation of lin-42a results in arrhythmic molts and continuously abnormal epidermal stem cell dynamics. In contrast, forced expression of lin-42a leads to anachronistic larval molts and lethargy in adults. These results suggest that rising and falling levels of LIN-42A allow the start and completion, respectively, of larval molts. Ancillary factors of the molting timer likely include the conserved nuclear hormone receptors NHR-23/RORα and NHR-25/SF1, and the family of let-7 microRNAs. Thus, interconnected positive and negative regulatory interactions among LIN-42A, NHR-23 and -25, and let-7 may drive transitions through each molt. I propose that these factors regulate molting cycles in much the same way that PERIOD-based oscillators drive rhythmic behaviors and metabolic processes in mature mammals.The LIN-42-based timer may synchronize the periodic molts with fluctuations in external or internal conditions, in much the same way that circadian clocks synchronize rhythmic biological processes of higher metazoans with recurrent fluctuations in zeitgebers. To identify novel factors that regulate these molting cues, we designed a forward genetic screen to identify novel factors that regulate the timing of the molt. I identified that the LRP-2/Megalin receptor is required forthe cessation of larval molting cycles. The lrp-2 transcripts are…

Subjects/Keywords: Developmental biology; Molecular biology; Genetics; Circadian Rhythms; Developmental timing; MicroRNAs; Molting; Nuclear Hormone Receptors; Period

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APA (6^th Edition):

Monsalve, G. C. (2013). Unifying Mechanisms of Developmental Timing: Genetic and Molecular Analysis of the Molting Cycle Timer of Caenorhabditis elegans. (Thesis). UCLA. Retrieved from http://www.escholarship.org/uc/item/56j1x8dd

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):

Monsalve, Gabriela Carolina. “Unifying Mechanisms of Developmental Timing: Genetic and Molecular Analysis of the Molting Cycle Timer of Caenorhabditis elegans.” 2013. Thesis, UCLA. Accessed January 27, 2021. http://www.escholarship.org/uc/item/56j1x8dd.

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

MLA Handbook (7^th Edition):

Monsalve, Gabriela Carolina. “Unifying Mechanisms of Developmental Timing: Genetic and Molecular Analysis of the Molting Cycle Timer of Caenorhabditis elegans.” 2013. Web. 27 Jan 2021.

Vancouver:

Monsalve GC. Unifying Mechanisms of Developmental Timing: Genetic and Molecular Analysis of the Molting Cycle Timer of Caenorhabditis elegans. [Internet] [Thesis]. UCLA; 2013. [cited 2021 Jan 27]. Available from: http://www.escholarship.org/uc/item/56j1x8dd.

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

Council of Science Editors:

Monsalve GC. Unifying Mechanisms of Developmental Timing: Genetic and Molecular Analysis of the Molting Cycle Timer of Caenorhabditis elegans. [Thesis]. UCLA; 2013. Available from: http://www.escholarship.org/uc/item/56j1x8dd

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

University of Toronto

2. Boetto, Jonathan F. The Role of ERRγ in Longitudinal Bone Growth.

Degree: 2010, University of Toronto

URL: http://hdl.handle.net/1807/30118

►

Estrogen-receptor-related receptor gamma, ERRγ, is highly expressed in cartilage and upregulates the chondrogenic transcription factor, Sox9, in a chondrocytic cell line. To assess the effect… (more)

Subjects/Keywords: Bone Development; Nuclear Hormone Receptors; Endochondral Ossification; Mouse Transgenesis; Achondroplasia; Dwarfism; Growth Plate; Chondrogenesis; Genetics 0369

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APA (6^th Edition):

Boetto, J. F. (2010). The Role of ERRγ in Longitudinal Bone Growth. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/30118

Chicago Manual of Style (16^th Edition):

Boetto, Jonathan F. “The Role of ERRγ in Longitudinal Bone Growth.” 2010. Masters Thesis, University of Toronto. Accessed January 27, 2021. http://hdl.handle.net/1807/30118.

MLA Handbook (7^th Edition):

Boetto, Jonathan F. “The Role of ERRγ in Longitudinal Bone Growth.” 2010. Web. 27 Jan 2021.

Vancouver:

Boetto JF. The Role of ERRγ in Longitudinal Bone Growth. [Internet] [Masters thesis]. University of Toronto; 2010. [cited 2021 Jan 27]. Available from: http://hdl.handle.net/1807/30118.

Council of Science Editors:

Boetto JF. The Role of ERRγ in Longitudinal Bone Growth. [Masters Thesis]. University of Toronto; 2010. Available from: http://hdl.handle.net/1807/30118

Brigham Young University

3. Salehi, Sayed Mohammad. Engineering Cell-free Protein Synthesis Technology for Codon Reassignment, Biotherapeutics Production using Just-add-Water System, and Biosensing Endocrine Disrupting Compounds.

Degree: PhD, 2017, Brigham Young University

URL: https://scholarsarchive.byu.edu/cgi/viewcontent.cgi?article=7711&context=etd

► Cell-free protein synthesis is an emerging technology that has many applications. The open nature of this system makes it a compelling technology that can be… (more)

▼ Cell-free protein synthesis is an emerging technology that has many applications. The open nature of this system makes it a compelling technology that can be manipulated to answer many needs that are unavailable in other systems. This dissertation reports on engineering this technology for: 1) sense codon emancipation for incorporation of multiple unnatural amino acids; 2) expressing a hard-to-express anticancer biotherapeutic and introducing a just-add-water system; 3) a biosensing ligand that interacts with nuclear hormone receptors. Emancipating sense codons toward a minimized genetic code is of significant interest to science and engineering. A promising approach to sense codon emancipation is the targeted in vitro removal of native tRNA. Here we introduce a new in-vitro or "cell-free" approach to emancipate sense codons via efficient and affordable degradation of endogenous tRNA using RNase-coated superparamagnetic beads. The presented method removes greater than 99% of tRNA in cell lysates, while preserving cell-free protein synthesis activity. The resulting tRNA-depleted lysate is compatible with in vitro-transcribed synthetic tRNA for the production of peptides and proteins. Biotherapeutics have many promising applications, such as anti-cancer treatments, immune suppression, and vaccines. However, due to their biological nature, some biotherapeutics can be challenging to rapidly express and screen for activity through traditional recombinant methods. In this work, we demonstrate the use of cell-free systems for the expression and direct screening of the difficult-to-express cytotoxic protein onconase. Using cell-free systems, onconase can be rapidly expressed in soluble, active form. Furthermore, the open nature of the reaction environment allows for direct and immediate downstream characterization without the need of purification. Also, we report the ability of a "just-add-water" lyophilized cell-fee system to produce onconase. Here we introduce a Rapid Adaptable Portable In-vitro Detection biosensor platform (RAPID) for detecting ligands that interact with nuclear hormone receptors (NHRs). The biosensor is based on an engineered, allosterically-activated fusion protein, which contains the ligand binding domain from a target NHR. The presented RAPID biosensor platform is significantly faster and less labor intensive than commonly available technologies, making it a promising tool for detecting environmental EDC contamination and screening potential NHR-targeted pharmaceuticals.

Subjects/Keywords: Sayed Mohammad Amin Salehi; cell-free protein synthesis; codon emancipation; cancer biotherapeutics; endocrine disrupting compounds; nuclear hormone receptors; biosensor; Chemical Engineering

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APA (6^th Edition):

Salehi, S. M. (2017). Engineering Cell-free Protein Synthesis Technology for Codon Reassignment, Biotherapeutics Production using Just-add-Water System, and Biosensing Endocrine Disrupting Compounds. (Doctoral Dissertation). Brigham Young University. Retrieved from https://scholarsarchive.byu.edu/cgi/viewcontent.cgi?article=7711&context=etd

Chicago Manual of Style (16^th Edition):

Salehi, Sayed Mohammad. “Engineering Cell-free Protein Synthesis Technology for Codon Reassignment, Biotherapeutics Production using Just-add-Water System, and Biosensing Endocrine Disrupting Compounds.” 2017. Doctoral Dissertation, Brigham Young University. Accessed January 27, 2021. https://scholarsarchive.byu.edu/cgi/viewcontent.cgi?article=7711&context=etd.

MLA Handbook (7^th Edition):

Salehi, Sayed Mohammad. “Engineering Cell-free Protein Synthesis Technology for Codon Reassignment, Biotherapeutics Production using Just-add-Water System, and Biosensing Endocrine Disrupting Compounds.” 2017. Web. 27 Jan 2021.

Vancouver:

Salehi SM. Engineering Cell-free Protein Synthesis Technology for Codon Reassignment, Biotherapeutics Production using Just-add-Water System, and Biosensing Endocrine Disrupting Compounds. [Internet] [Doctoral dissertation]. Brigham Young University; 2017. [cited 2021 Jan 27]. Available from: https://scholarsarchive.byu.edu/cgi/viewcontent.cgi?article=7711&context=etd.

Council of Science Editors:

Salehi SM. Engineering Cell-free Protein Synthesis Technology for Codon Reassignment, Biotherapeutics Production using Just-add-Water System, and Biosensing Endocrine Disrupting Compounds. [Doctoral Dissertation]. Brigham Young University; 2017. Available from: https://scholarsarchive.byu.edu/cgi/viewcontent.cgi?article=7711&context=etd

4. Brüggenwirth, Hennie. Genetic and Functional Analysis of Androgen Receptor Gene Mutations.

Degree: Department of Molecular Genetics, 1998, Erasmus University Medical Center

URL: http://hdl.handle.net/1765/17005

► textabstractNuclear hormone receptors (NHRs) are intermediary factors through which extracellular signals regulate expression of genes that are involved in homeostasis, development, and differentiation (Beato et… (more)

Subjects/Keywords: androgeen receptor gen; gene mutations; nuclear hormone receptors

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

APA (6^th Edition):

Brüggenwirth, H. (1998). Genetic and Functional Analysis of Androgen Receptor Gene Mutations. (Doctoral Dissertation). Erasmus University Medical Center. Retrieved from http://hdl.handle.net/1765/17005

Chicago Manual of Style (16^th Edition):

Brüggenwirth, Hennie. “Genetic and Functional Analysis of Androgen Receptor Gene Mutations.” 1998. Doctoral Dissertation, Erasmus University Medical Center. Accessed January 27, 2021. http://hdl.handle.net/1765/17005.

MLA Handbook (7^th Edition):

Brüggenwirth, Hennie. “Genetic and Functional Analysis of Androgen Receptor Gene Mutations.” 1998. Web. 27 Jan 2021.

Vancouver:

Brüggenwirth H. Genetic and Functional Analysis of Androgen Receptor Gene Mutations. [Internet] [Doctoral dissertation]. Erasmus University Medical Center; 1998. [cited 2021 Jan 27]. Available from: http://hdl.handle.net/1765/17005.

Council of Science Editors:

Brüggenwirth H. Genetic and Functional Analysis of Androgen Receptor Gene Mutations. [Doctoral Dissertation]. Erasmus University Medical Center; 1998. Available from: http://hdl.handle.net/1765/17005

5. Heskett, Michael B. Epigenetic Regulation of Nuclear Hormone Receptor DAX-1.

Degree: MSin Biology, Biology, 2014, University of San Francisco

URL: https://repository.usfca.edu/thes/116

► DAX-1 (NR0B1) is an orphan nuclear receptor that plays a key role in the development and maintenance of steroidogenic tissue in mammals. Dax-1 is… (more)

Subjects/Keywords: nuclear receptors; DAX-1; NR0B1; endocrinology; hormone receptors; cancer; Biochemistry, Biophysics, and Structural Biology; Biology; Cell and Developmental Biology; Genetics and Genomics

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

APA (6^th Edition):

Heskett, M. B. (2014). Epigenetic Regulation of Nuclear Hormone Receptor DAX-1. (Thesis). University of San Francisco. Retrieved from https://repository.usfca.edu/thes/116

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):

Heskett, Michael B. “Epigenetic Regulation of Nuclear Hormone Receptor DAX-1.” 2014. Thesis, University of San Francisco. Accessed January 27, 2021. https://repository.usfca.edu/thes/116.

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

MLA Handbook (7^th Edition):

Heskett, Michael B. “Epigenetic Regulation of Nuclear Hormone Receptor DAX-1.” 2014. Web. 27 Jan 2021.

Vancouver:

Heskett MB. Epigenetic Regulation of Nuclear Hormone Receptor DAX-1. [Internet] [Thesis]. University of San Francisco; 2014. [cited 2021 Jan 27]. Available from: https://repository.usfca.edu/thes/116.

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

Council of Science Editors:

Heskett MB. Epigenetic Regulation of Nuclear Hormone Receptor DAX-1. [Thesis]. University of San Francisco; 2014. Available from: https://repository.usfca.edu/thes/116

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

Universitat de Barcelona

6. De Mol, Eva. Structure, dynamics and interactions of the N-terminal domain of the androgen receptor.

Degree: 2014, Universitat de Barcelona

URL: http://hdl.handle.net/10803/147275

► El cáncer de próstata (PCa) es el segundo tipo de cáncer más común en hombres después del cáncer de pulmón. Alrededor de 1.1 millones de… (more)

▼ El cáncer de próstata (PCa) es el segundo tipo de cáncer más común en hombres después del cáncer de pulmón. Alrededor de 1.1 millones de hombres en todo el mundo se les diagnosticó PCa durante el año 2012. El cáncer de próstata depende esencialmente de la estimulación de los andrógenos para el crecimiento y la supervivencia celular. El receptor androgénico (AR) es un receptor de hormonas nuclear que es activado por las hormonas andrógenas y la proteína mediante la cual los efectos fisiológicos de los andrógenos se producen. El AR es necesario para el desarrollo normal de la próstata, su crecimiento y fisiología pero también tiene un papel muy importante en la progresión del cáncer de próstata. Por ello, es un regulador esencial para el crecimiento, diseminación y supervivencia de células cancerígenas en tumores de cáncer de próstata resistente a la castración (CRPC), y por tanto, representa una potencial diana terapéutica. Desde el punto de vista estructural y functional, el AR está compuesto por cuatro dominios: el dominio N-terminal (NTD) que se piensa que es intrínsicamente desordenado, el dominio de unión a DNA (DBD) que contiene dos dedos de zinc, la región bisagra y el dominio de unión de ligando (LBD) que une tanto testosterona como dihidro-testosterona (DHT). El NTD de AR juega un papel crucial en la actividad constitutiva del AR en tumores de pacientes con resistencia a la castración, el cancer de prostata más avanzado. Actualmente no existe un tratamiento efectivo para CRPC. La transactivación del NTD es independiente de los andrógenos y por tanto evita las estrategias actuales de tratamiento dirigidos al eje de señalización de andrógenos. Por esta razón, se ha realizado la caracterización de las propiedades conformacionales del NTD intrínsecamente desordenado del AR y en particular del AF1, la región más potente para la activación del AR que contiene los regiones Tau-1 y Tau-5. Debido a la naturaleza intrínsecamente desordenada de estos regiones, se ha realizado la caracterización por resonancia magnética nuclear (NMR) midiendo los parámetros de NMR que permiten la asignación del esqueleto proteico de AF1 que permiten describir sus características dinámicas y de estructura secundaria. Hemos encontrado que, in vitro, AF1* (AR 142-448) posee una tendencia reducida pero notable a asociarse a sí misma formando un estado dimérico. Además, las regiones de AF1* con una tendencia mayor de estructura secundaria y menor flexibilidad también están involucradas en la dimerización de AF1* y coinciden con las regiones que fueron previamente identificadas como funcionales (regiones centrales de Tau-1 y Tau-5). En esa tesis también se ha investigado el papel del NTD del AR en la activación transcripcional a nivel molecular. Se ha estudiado su interacción con RAP74, una subunidad del factor de transcripción general IIF (TFIIF). La interacción del motivo 433WHTLF437 de AR, localizado en la región Tau-5, permite la transactivación por unión con RAP74 en células CRPC. Este novedoso mecanismo podría explicar la… Advisors/Committee Members: Universitat de Barcelona. Facultat de Farmàcia, [email protected] (authoremail), false (authoremailshow), Salvatella i Giralt, Xavier (director), Salvatella i Giralt, Xavier (tutor), true (authorsendemail).

Subjects/Keywords: Ressonància magnètica nuclear; Resonancia magnètica nuclear (Física); Nuclear magnetic resonance; Oncologia; Oncología; Oncology; Ciències de la salut; Ciencias biomédicas; Medical sciences; Càncer de pròstata; Cáncer de próstata; Prostate cancer; Receptors d'hormones; Receptores de hormonas; Hormone receptors; Ciències de la Salut; 577

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

APA (6^th Edition):

De Mol, E. (2014). Structure, dynamics and interactions of the N-terminal domain of the androgen receptor. (Thesis). Universitat de Barcelona. Retrieved from http://hdl.handle.net/10803/147275

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):

De Mol, Eva. “Structure, dynamics and interactions of the N-terminal domain of the androgen receptor.” 2014. Thesis, Universitat de Barcelona. Accessed January 27, 2021. http://hdl.handle.net/10803/147275.

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

MLA Handbook (7^th Edition):

De Mol, Eva. “Structure, dynamics and interactions of the N-terminal domain of the androgen receptor.” 2014. Web. 27 Jan 2021.

Vancouver:

De Mol E. Structure, dynamics and interactions of the N-terminal domain of the androgen receptor. [Internet] [Thesis]. Universitat de Barcelona; 2014. [cited 2021 Jan 27]. Available from: http://hdl.handle.net/10803/147275.

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

Council of Science Editors:

De Mol E. Structure, dynamics and interactions of the N-terminal domain of the androgen receptor. [Thesis]. Universitat de Barcelona; 2014. Available from: http://hdl.handle.net/10803/147275

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

7. Πέττα, Ιωάννα. Μελέτη των εναλλακτικών ισομορφών του COUP-TF και οι ιδιότητες πρόσδεσής των στο DNA.

Degree: 2010, University of Patras

URL: http://nemertes.lis.upatras.gr/jspui/handle/10889/4766

►

Οι μεταγραφικοί παράγοντες COUP-TF (Chicken Ovalbumin Upstream Promoter Transcription Factor) ανήκουν στην υπεροικογένεια των υποδοχέων στεροειδών/ θυρεοειδών ορμονών και θεωρούνται “ορφανοί”, αφού μέχρι στιγμής δεν… (more)

▼

Οι μεταγραφικοί παράγοντες COUP-TF (Chicken Ovalbumin Upstream Promoter Transcription Factor) ανήκουν στην υπεροικογένεια των υποδοχέων στεροειδών/ θυρεοειδών ορμονών και θεωρούνται “ορφανοί”, αφού μέχρι στιγμής δεν έχει βρεθεί το υπεύθυνο πρόσδεμα για την ενεργοποίηση τους. Πειραματικές διαδικασίες στο εργαστήριο μας έχουν δείξει ότι στο πρωτογενές μετάγραφο των COUP-TFs συμβαίνει εναλλακτικό μάτισμα που έχει ως αποτέλεσμα την παραγωγή δύο mRNAs που κωδικοποιούν δύο πρωτεΐνες οι οποίες διαφέρουν ως προς το μέγεθος λόγω της εισαγωγής 21 επίπρόσθετων αμινοξέων στην καρβοξυτελική περιοχή (Carboxy Terminal Extension) της περιοχής πρόσδεσης στο DNA (DBD). Πειράματα EMSA με τη χρήση in vitro μεταφρασμένων πρωτεϊνών, αποκάλυψαν ότι η μεγάλη πρωτεΐνη δεν μπορεί να προσδεθεί σε κανένα COUP-TF στοιχείο απόκρισης. Επίσης παρατηρήθηκε ότι παρουσία της μεγάλης πρωτεΐνης, η ικανότητα της μικρής πρωτεΐνης να προσδένεται στο DNA μειώνεται με ανταγωνιστικό τρόπο, οδηγώντας στο συμπέρασμα ότι το ετεροδιμερές πρωτεϊνικό σύμπλοκο δεν μπορεί να προσδεθεί στο DNA. Σκοπός μας είναι να ερευνήσουμε το ρόλο της ένθεσης των 21 αμινοξέων στην μεγάλη πρωτεΐνη, ως προς την ικανότητα πρόσδεσης της στο DNA. Στον αχινό Paracentrotus lividus, η αμινοξική ένθεση στην καρβοξυτελική περιοχή (CTE) της μεγάλης πρωτεΐνης περιέχει δύο προλίνες. Η υπόθεση μας είναι ότι αυτές οι δύο προλίνες παίζουν σημαντικό ρόλο στην στερεοδιαμόρφωση της πρωτεΐνης, επηρεάζοντας την ικανότητα πρόσδεσης στο DNA. Για να ελέγξουμε την υπόθεση αυτή, προκαλέσαμε σημειακές μεταλλάξεις, μεταλλάσσοντας συγχρόνως τις δύο προλίνες σε αλανίνες αλλά κάθε μία προλίνη σε αλανίνη μεμονωμένα, καθώς επίσης μελετήσαμε και μια σειρά εσωτερικών αμινοξικών ελλειμάτων μέσα στην ένθεση των 21 αμινοξέων στην καρβοξυτελική περιοχή. Το σύνολο των μεταλλάξεων έδειξε ότι οι μεταλλαγμένες μεγάλες πρωτεΐνες δεν προσδένονται στο DNA καθώς επίσης ότι οι μεταλλαγμένες μεγάλες πρωτεΐνες ετεροδιμερίζονται πιο αποτελεσματικά με την μικρή ισομορφή πιθανότατα λόγω επαγόμενης αλλαγής της στερεοδιαμόρφωσης της μεταλλαγμένης πρωτεΐνης. Επίσης μελετήσαμε την εξάπλωση του εναλλακτικού ματίσματός στα Δευτεροστόμια, χρησιμοποιώντας ειδικούς εκφυλισμένους εκκινητές σε πειράματα PCR. Εναλλακτικό μάτισμα των μεταγράφων COUP-TF παρατηρήθηκε επίσης στους οργανισμούς Sphaerechinus granularis (Εχινόδερμο) και Saccoglossus kowalevskii (Ημιχορδωτό).

COUP-TFs (Chicken Ovalbumin Upstream Promoter- Transcription Factors) belong to the superfamily of steroid/thyroid hormone receptors and they are consider orphans since the proper ligand that activates them is not yet found. Experimental procedures in our laboratory have shown that in Echinoderms the alternative splicing of the COUP-TF primary transcript results in two mRNAs which encode two protein variants that differ by a 21 amino acid insertion in the Carboxy Terminal Extension (CTE) of the DNA Binding Domain (DBD). EMSA experiments with the use of in vitro translated proteins revealed that the large protein variant is incapable of binding…

Advisors/Committee Members: Φλυτζάνης, Κωνσταντίνος, Petta, Ioanna, Μίντζας, Αναστάσιος, Κίλιας, Γεώργιος, Φλυτζάνης, Κωνσταντίνος.

Subjects/Keywords: Εναλλακτικό μάτισμα; Πυρηνικοί υποδοχείς ορμονών; DNA πρόσδεση; Καρβοξυτελική επέκταση; Σημειακές μεταλλάξεις; 572.884 5; Alternative splicing; Nuclear hormone receptors; COUP-TF; DNA binding; Carboxy terminal extension (CTE); Site directed mutagenesis

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

APA (6^th Edition):

Πέττα, �. (2010). Μελέτη των εναλλακτικών ισομορφών του COUP-TF και οι ιδιότητες πρόσδεσής των στο DNA. (Masters Thesis). University of Patras. Retrieved from http://nemertes.lis.upatras.gr/jspui/handle/10889/4766

Chicago Manual of Style (16^th Edition):

Πέττα, Ιωάννα. “Μελέτη των εναλλακτικών ισομορφών του COUP-TF και οι ιδιότητες πρόσδεσής των στο DNA.” 2010. Masters Thesis, University of Patras. Accessed January 27, 2021. http://nemertes.lis.upatras.gr/jspui/handle/10889/4766.

MLA Handbook (7^th Edition):

Πέττα, Ιωάννα. “Μελέτη των εναλλακτικών ισομορφών του COUP-TF και οι ιδιότητες πρόσδεσής των στο DNA.” 2010. Web. 27 Jan 2021.

Vancouver:

Πέττα �. Μελέτη των εναλλακτικών ισομορφών του COUP-TF και οι ιδιότητες πρόσδεσής των στο DNA. [Internet] [Masters thesis]. University of Patras; 2010. [cited 2021 Jan 27]. Available from: http://nemertes.lis.upatras.gr/jspui/handle/10889/4766.

Council of Science Editors:

Πέττα �. Μελέτη των εναλλακτικών ισομορφών του COUP-TF και οι ιδιότητες πρόσδεσής των στο DNA. [Masters Thesis]. University of Patras; 2010. Available from: http://nemertes.lis.upatras.gr/jspui/handle/10889/4766

University of Florida

8. Ignatovich, Igor V. Parvovirus B19 Modulates Nuclear Hormone Receptor Signaling Implications in Skin Cancer.

Degree: PhD, Medical Sciences - Immunology and Microbiology (IDP), 2013, University of Florida

URL: https://ufdc.ufl.edu/UFE0045771

► Parvovirus B19 (B19V) is a human pathogen that causes various blood and vascular-related diseases. Erythroid progenitor cells (EPCs) have been shown to be the only… (more)

▼ Parvovirus B19 (B19V) is a human pathogen that causes various blood and vascular-related diseases. Erythroid progenitor cells (EPCs) have been shown to be the only permissive cells for B19V replication. However B19V has been shown to persist in multiple organs and tissues, including skin, thyroid, brain, liver, testes and others. The mechanism of viral pathogenesis and persistence in these tissues is unclear. The association of B19V infection with certain diseases outside of the erythroid system is poorly understood. Here, part of the B19V-host interaction is unveiled by showing the interconnection between B19V and the nuclear hormone receptor (NR) signaling pathways in both erythroid and non-erythroid cells. In particular, B19V infection of CD36+ EPCs coincided with the downregulation of thyroid hormone receptor a (THRa), retinoid X receptor a (RXRa) and estrogen receptor a (ERa). It was demonstrated that B19V NS1 is sufficient for the downregulationof THRa and RXRa but not ERa. The research scope was expanded by looking at the downstream genes in the NR-signaling pathway that are involved in cancer progression, cell cycle regulation, and cardio-vascular diseases. B19V infection of CD36+ EPCs lead to downregulation of peroxisome proliferator-activated receptor gamma (PPARG), bone morphogeneic protein 2 (BMP2) and upregulation of Cyclin D1 and D2, and mothers against decapentaplegic homolog 9 (SMAD9). For the first time, the persistence, expression and pathogenesis of B19V in the skin cancer environment was investigated. It was shown that B19V has a preference for particular types of skin cancer, such as squamous cell carcinoma (SCC). In addition, it was demonstrated that B19V expression in skin cancer tissues coincides with downregulation of THRa and RXRa expression suggesting that B19V leads to changes in cancer signaling pathways in vivo. Altogether these studies contribute to the overall understanding of the basic B19V biology as well as B19V persistence, both within and outside of the erythroid compartment, especially in skin. ( en ) Advisors/Committee Members: Hobbs, Jacqueline A (committee chair), Muzyczka, Nicholas (committee member), Condit, Richard C (committee member), Srivastava, Arun (committee member), Siemann, Dietmar W (committee member).

Subjects/Keywords: Antibodies; Cells; DNA; Genotypes; Infections; Parvovirus; Receptors; Skin; Skin cancers; Virology; b19 – basal – cancer – erythroid – erythrovirus – hormone – melanoma – nuclear – parvovirus – receptor – retinoid – skin – squamous – thyroid

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

APA (6^th Edition):

Ignatovich, I. V. (2013). Parvovirus B19 Modulates Nuclear Hormone Receptor Signaling Implications in Skin Cancer. (Doctoral Dissertation). University of Florida. Retrieved from https://ufdc.ufl.edu/UFE0045771

Chicago Manual of Style (16^th Edition):

Ignatovich, Igor V. “Parvovirus B19 Modulates Nuclear Hormone Receptor Signaling Implications in Skin Cancer.” 2013. Doctoral Dissertation, University of Florida. Accessed January 27, 2021. https://ufdc.ufl.edu/UFE0045771.

MLA Handbook (7^th Edition):

Ignatovich, Igor V. “Parvovirus B19 Modulates Nuclear Hormone Receptor Signaling Implications in Skin Cancer.” 2013. Web. 27 Jan 2021.

Vancouver:

Ignatovich IV. Parvovirus B19 Modulates Nuclear Hormone Receptor Signaling Implications in Skin Cancer. [Internet] [Doctoral dissertation]. University of Florida; 2013. [cited 2021 Jan 27]. Available from: https://ufdc.ufl.edu/UFE0045771.

Council of Science Editors:

Ignatovich IV. Parvovirus B19 Modulates Nuclear Hormone Receptor Signaling Implications in Skin Cancer. [Doctoral Dissertation]. University of Florida; 2013. Available from: https://ufdc.ufl.edu/UFE0045771

9. Sahin, N. Preconditioning and Dynamic Stimuli.

Degree: 2017, NARCIS

URL: https://research.vu.nl/en/publications/75dee96a-7d14-427b-a057-68113d4f9e8a ; urn:nbn:nl:ui:31-1871/55306 ; 75dee96a-7d14-427b-a057-68113d4f9e8a ; 1871/55306 ; urn:isbn:9789462336414 ; urn:nbn:nl:ui:31-1871/55306 ; https://research.vu.nl/en/publications/75dee96a-7d14-427b-a057-68113d4f9e8a

Subjects/Keywords: Preconditioning; systems biology; apoptosis; mitoptosis; nuclear hormone receptors; dynamic modeling; cortisol

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

APA (6^th Edition):

Sahin, N. (2017). Preconditioning and Dynamic Stimuli. (Doctoral Dissertation). NARCIS. Retrieved from https://research.vu.nl/en/publications/75dee96a-7d14-427b-a057-68113d4f9e8a ; urn:nbn:nl:ui:31-1871/55306 ; 75dee96a-7d14-427b-a057-68113d4f9e8a ; 1871/55306 ; urn:isbn:9789462336414 ; urn:nbn:nl:ui:31-1871/55306 ; https://research.vu.nl/en/publications/75dee96a-7d14-427b-a057-68113d4f9e8a

Chicago Manual of Style (16^th Edition):

Sahin, N. “Preconditioning and Dynamic Stimuli.” 2017. Doctoral Dissertation, NARCIS. Accessed January 27, 2021. https://research.vu.nl/en/publications/75dee96a-7d14-427b-a057-68113d4f9e8a ; urn:nbn:nl:ui:31-1871/55306 ; 75dee96a-7d14-427b-a057-68113d4f9e8a ; 1871/55306 ; urn:isbn:9789462336414 ; urn:nbn:nl:ui:31-1871/55306 ; https://research.vu.nl/en/publications/75dee96a-7d14-427b-a057-68113d4f9e8a.

MLA Handbook (7^th Edition):

Sahin, N. “Preconditioning and Dynamic Stimuli.” 2017. Web. 27 Jan 2021.

Vancouver:

Sahin N. Preconditioning and Dynamic Stimuli. [Internet] [Doctoral dissertation]. NARCIS; 2017. [cited 2021 Jan 27]. Available from: https://research.vu.nl/en/publications/75dee96a-7d14-427b-a057-68113d4f9e8a ; urn:nbn:nl:ui:31-1871/55306 ; 75dee96a-7d14-427b-a057-68113d4f9e8a ; 1871/55306 ; urn:isbn:9789462336414 ; urn:nbn:nl:ui:31-1871/55306 ; https://research.vu.nl/en/publications/75dee96a-7d14-427b-a057-68113d4f9e8a.

Council of Science Editors:

Sahin N. Preconditioning and Dynamic Stimuli. [Doctoral Dissertation]. NARCIS; 2017. Available from: https://research.vu.nl/en/publications/75dee96a-7d14-427b-a057-68113d4f9e8a ; urn:nbn:nl:ui:31-1871/55306 ; 75dee96a-7d14-427b-a057-68113d4f9e8a ; 1871/55306 ; urn:isbn:9789462336414 ; urn:nbn:nl:ui:31-1871/55306 ; https://research.vu.nl/en/publications/75dee96a-7d14-427b-a057-68113d4f9e8a

University of Illinois – Urbana-Champaign

10. Zheng, Yupeng. Site-specific phosphorylation of histone H1 associated with cell cycle progression and transcription.

Degree: PhD, 4094, 2010, University of Illinois – Urbana-Champaign

URL: http://hdl.handle.net/2142/16522

► Histone H1 phosphorylation is thought to affect chromatin condensation and function, but few details are known about the impact of H1 variant-specific phosphorylation in higher… (more)

▼ Histone H1 phosphorylation is thought to affect chromatin condensation and function, but few details are known about the impact of H1 variant-specific phosphorylation in higher eukaryotes. Using novel proteomic approaches, we directly demonstrate that specific sites in the two dominant H1 variants of HeLa S3 cells are phosphorylated either exclusively during mitosis or during both interphase and mitosis. Interphase H1 phosphorylation in HeLa S3 cells is abundant and remarkably hierarchical, contrary to evidence that sites are used fortuitously during the cell cycle. Analyses with antisera to individual H1.2 and H1.4 interphase phosphorylations reveal that they are distributed throughout nuclei but appear to be particularly enriched in nucleoli. Chromatin immunoprecipitation analyses reveal that interphase phosphorylated H1.4 is enriched at active rDNA promoters and is rapidly induced at steroid hormone response elements by hormone treatment. Our results imply that site-specific interphase H1 phosphorylation facilitates transcription by RNA polymerases I and II, and has an unanticipated function in ribosome biogenesis and the control of cell growth. In contrast to histone modifications enriched at gene regulatory regions, site-specific interphase H1 phosphorylation is enriched within the body and the regulatory elements of transcribed genes. Our data suggest CDK8 and CDK9, kinases with known association with the transcriptional machinery, as candidates that could account for this distribution of interphase H1 phosphorylation. Comparative analyses of H1 variant expression and phosphorylation in different human cell lines reveal that H1.3 is significantly less phosphorylated during interphase relative to other H1 variants in the cell lines tested. Analyses of the phosphorylation of site-specific H1 mutants ectopically expressed in human cells identified features of H1.3 that lead to its underphosphorylation. Together these results suggest that differences in interphase phosphorylation may contribute to the functional diversity of H1 variants. Advisors/Committee Members: Mizzen, Craig A. (advisor), Belmont, Andrew S. (Committee Chair), Mizzen, Craig A. (committee member), Bellini, Michel (committee member), Jones, Peter L. (committee member), Shapiro, David J. (committee member).

Subjects/Keywords: histone H1; phosphorylation; chromatin; transcription; nucleoli; ribosomal RNA; nuclear hormone receptors

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

APA (6^th Edition):

Zheng, Y. (2010). Site-specific phosphorylation of histone H1 associated with cell cycle progression and transcription. (Doctoral Dissertation). University of Illinois – Urbana-Champaign. Retrieved from http://hdl.handle.net/2142/16522

Chicago Manual of Style (16^th Edition):

Zheng, Yupeng. “Site-specific phosphorylation of histone H1 associated with cell cycle progression and transcription.” 2010. Doctoral Dissertation, University of Illinois – Urbana-Champaign. Accessed January 27, 2021. http://hdl.handle.net/2142/16522.

MLA Handbook (7^th Edition):

Zheng, Yupeng. “Site-specific phosphorylation of histone H1 associated with cell cycle progression and transcription.” 2010. Web. 27 Jan 2021.

Vancouver:

Zheng Y. Site-specific phosphorylation of histone H1 associated with cell cycle progression and transcription. [Internet] [Doctoral dissertation]. University of Illinois – Urbana-Champaign; 2010. [cited 2021 Jan 27]. Available from: http://hdl.handle.net/2142/16522.

Council of Science Editors:

Zheng Y. Site-specific phosphorylation of histone H1 associated with cell cycle progression and transcription. [Doctoral Dissertation]. University of Illinois – Urbana-Champaign; 2010. Available from: http://hdl.handle.net/2142/16522

11. Xia, Gang. Structural studies of the ligand binding domain of the human retinoid X receptor bound to retinoids and the coactivator peptide GRIP-1.

Degree: PhD, 2010, University of Alabama – Birmingham

URL: http://contentdm.mhsl.uab.edu/u?/etd,850

►

Retinoid X receptors (RXRs) are ligand–dependent transcription factors which belong to the nuclear receptor (NR) superfamily. When a ligand binds to RXRs, it activates the… (more)

▼

Retinoid X receptors (RXRs) are ligand–dependent transcription factors which belong to the nuclear receptor (NR) superfamily. When a ligand binds to RXRs, it activates the protein allosterically for the recruitment of coactivator proteins and enhancement of gene transcription. RXRs form either homodimers or heterodimers with numerous other NRs. Thus, RXRs are involved in many signaling pathways in vivo. 9cRA, Targretin and UAB retinoids are RXR agonists and found to be effective agents to prevent and treat cancers. The structures of retinoid-bound RXRs will be helpful in designing new retinoids. This dissertation focuses on structural studies of the human retinoid X receptor alpha-ligand binding domain (hRXRα-LBD) bound to retinoids and the coactivator peptide GRIP-1. First, the structure of hRXRα-LBD bound to 9cRA and GRIP-1 was determined by X-ray crystallography and compared to the previously reported structure of hRXRα-LBD:9cRA without GRIP-1. It was found GRIP-1 binding caused structural changes on H11 and H12 of the holo-hRXRα-LBD. Second, the crystal structures of hRXRα-LBD bound to either 9cUAB30 or Targretin in the presence of GRIP-1 were solved. Both structures were similar to the structure of the hRXRα-LBD:9cRA:GRIP-1 complex. ITC measurements of the GRIP-1 binding to hRXRα-LBD with 9cRA, Targretin and 9cUAB30 were very similar except for the heat capacity change. In the next two chapters, crystal structures of hRXRα-LBD bound to class I or to class II UAB retinoids and GRIP-1 were reported. Protein structures of these complexes were similar to each other and to the structures containing 9cRA and Targretin. The ligand binding pockets of the hRXRα-LBD containing these UAB retinoids were analyzed. Small structural changes were found between GRIP-1 and the hRXRα-LBD containing the class II UAB retinoids. In summary, this dissertation reports the effects of these structurally unrelated retinoids on the conformation of hRXRα-LBD and on the nature of the coactivator peptide binding site on the surface of hRXRα-LBD. These studies strengthen our understanding of how different retinoids influence the hRXRα-LBD structure, and it may provide helpful insight into designing new RXR-selective retinoids.

1 online resource (xvi, 186 p.) : ill. (some col.)

Chemistry

College of Arts and Sciences

hRXRα-LBD 9cRA 9cUAB30 Targretin UAB retinoids GRIP-1

UNRESTRICTED

Advisors/Committee Members: Muccio, Donald D., Brouillette, Wayne J. <br>, Graves, David E. <br>, Grubbs, Clinton J. <br>, Sha, Bingdong.

Subjects/Keywords: Retinoids <; br>; Tretinoin – Receptors – Structure <; br>; Receptor-ligand complexes <; br>; Nuclear receptors (Biochemistry) – Structure <; br>; Hormone receptors – Structure <; br>; Peptides <; br>; Antineoplastic agents – Synthesis

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

APA (6^th Edition):

Xia, G. (2010). Structural studies of the ligand binding domain of the human retinoid X receptor bound to retinoids and the coactivator peptide GRIP-1. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,850

Chicago Manual of Style (16^th Edition):

Xia, Gang. “Structural studies of the ligand binding domain of the human retinoid X receptor bound to retinoids and the coactivator peptide GRIP-1.” 2010. Doctoral Dissertation, University of Alabama – Birmingham. Accessed January 27, 2021. http://contentdm.mhsl.uab.edu/u?/etd,850.

MLA Handbook (7^th Edition):

Xia, Gang. “Structural studies of the ligand binding domain of the human retinoid X receptor bound to retinoids and the coactivator peptide GRIP-1.” 2010. Web. 27 Jan 2021.

Vancouver:

Xia G. Structural studies of the ligand binding domain of the human retinoid X receptor bound to retinoids and the coactivator peptide GRIP-1. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2010. [cited 2021 Jan 27]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,850.

Council of Science Editors:

Xia G. Structural studies of the ligand binding domain of the human retinoid X receptor bound to retinoids and the coactivator peptide GRIP-1. [Doctoral Dissertation]. University of Alabama – Birmingham; 2010. Available from: http://contentdm.mhsl.uab.edu/u?/etd,850

Universidade de Brasília

12. Juana Bottega Woitechumas. Mecanismos moleculares envolvidos na dominância negativa na síndrome de resistência ao hormônio tireoideano : I. genes regulados negativamente pelo receptor de hormônio tireoideano; II. genes regulados pelos receptores ativos por proliferadores de peroxissoma.

Degree: 2010, Universidade de Brasília

URL: http://bdtd.bce.unb.br/tedesimplificado/tde_busca/arquivo.php?codArquivo=6930

►

A Síndrome de Resistência ao Hormônio Tireoideano (SRHT) é uma patologia caracterizada pela resposta reduzida dos tecidos-alvo ao hormônio tireoideano (HT). Ocorre comumente devido a… (more)

▼

A Síndrome de Resistência ao Hormônio Tireoideano (SRHT) é uma patologia caracterizada pela resposta reduzida dos tecidos-alvo ao hormônio tireoideano (HT). Ocorre comumente devido a mutações em um alelo do gene do receptor do hormônio tireoideano β (TRβ) que codifica para um TR mutante, o qual inibe a função do TRβ wt, fenômeno conhecido como dominância negativa. Em genes regulados positivamente pelo T3, o mecanismo molecular de dominância negativa tem sido bastante estudado. Porém, o mecanismo com que esta ocorre em genes cuja transcrição é reprimida por T3 precisa ser melhor elucidado. Estudos indicam que o PPAR é capaz de se dimerizar com o TR e inibir seletivamente a atividade transcricional exercida pelos TRs por competição com o RXR na ligação ao DNA e que o TR também é capaz de inibir a atividade transcricional exercida pelo PPAR. O mecanismo dessa inibição não está bem esclarecido. O primeiro objetivo do presente estudo foi investigar o mecanismo molecular do efeito dominante negativo exercido pelo mutante TRβ-F451X, em genes regulados negativamente pelo T3 e a importância da dimerização nesse fenômeno. Essa mutação é encontrada em pacientes com SRHT que apresentam severo retardo mental, distúrbio no desenvolvimento da fala e hiperatividade. Nossos resultados mostraram que o mutante F451X exerce dominância negativa sobre TRβ nativo em promotor de TRH e AP-1. Observamos que o TRβ1 wt e os mutantes F451X e G345R, outro mutante da síndrome, se heterodimerizam com o RXR em TRH e essa dimerização parece ser importante para que o efeito de dominância negativa em TRH seja observado. Essa heterodimerização não foi observada em AP-1, porém ocorre dominância negativa, sugerindo que outro mecanismo diferente da heterodimerização esteja envolvido no fenômeno. O segundo objetivo foi investigar a presença de dominância negativa do TRβ1 wt e TRβ1 F451X em genes regulados pelo receptor ativado por proliferadores de peroxissoma (PPAR). Observamos que o TRβ1 wt na proporção 1:5 e o mutante F451X na proporção 1:1 apresentaram inibição da ação do PPARγ e que a dimerização e a interação com correpressores parece ser importante para a ocorrência da dominância negativa sobre PPAR em DR1.

The Syndrome of Resistance to Thyroid Hormone (RTH) is a disease characterized by reduced response of target tissues to thyroid hormone (TH). Commonly occurs due to mutations in one allele of the thyroid hormone receptor β (TRβ), which encodes a TR mutant, which inhibits the function of TRβ wt, a phenomenon known as a dominant negative. In positively regulated genes by T3, the molecular mechanism of negative dominance has been well studied. However, the mechanism through which this occurs in genes whose transcription is repressed by T3 needs to be better elucidated. Studies indicate that PPAR is able to dimerize with TR and selectively inhibit the transcriptional activity exerted by TRs by competing with RXR on DNA binding and that the TR is also able to inhibit the…

Advisors/Committee Members: Ana Carolina Acevedo Poppe, Rutnéia de Paula Pessanha, Marie Togashi, Francisco de Assis Neves.

Subjects/Keywords: Thyroid hormone; Thyroid hormone receptor; Hormônios tireoideano; Receptores nucleares; Dominância negativa; Receptor de hormônio; CIENCIAS DA SAUDE; Syndrome of resistance; Nuclear receptors; Dominant negative; Peroxisome proliferators; Síndrome de resistência; Proliferadores de peroxissoma

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

APA (6^th Edition):

Woitechumas, J. B. (2010). Mecanismos moleculares envolvidos na dominância negativa na síndrome de resistência ao hormônio tireoideano : I. genes regulados negativamente pelo receptor de hormônio tireoideano; II. genes regulados pelos receptores ativos por proliferadores de peroxissoma. (Thesis). Universidade de Brasília. Retrieved from http://bdtd.bce.unb.br/tedesimplificado/tde_busca/arquivo.php?codArquivo=6930

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):

Woitechumas, Juana Bottega. “Mecanismos moleculares envolvidos na dominância negativa na síndrome de resistência ao hormônio tireoideano : I. genes regulados negativamente pelo receptor de hormônio tireoideano; II. genes regulados pelos receptores ativos por proliferadores de peroxissoma.” 2010. Thesis, Universidade de Brasília. Accessed January 27, 2021. http://bdtd.bce.unb.br/tedesimplificado/tde_busca/arquivo.php?codArquivo=6930.

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

MLA Handbook (7^th Edition):

Woitechumas, Juana Bottega. “Mecanismos moleculares envolvidos na dominância negativa na síndrome de resistência ao hormônio tireoideano : I. genes regulados negativamente pelo receptor de hormônio tireoideano; II. genes regulados pelos receptores ativos por proliferadores de peroxissoma.” 2010. Web. 27 Jan 2021.

Vancouver:

Woitechumas JB. Mecanismos moleculares envolvidos na dominância negativa na síndrome de resistência ao hormônio tireoideano : I. genes regulados negativamente pelo receptor de hormônio tireoideano; II. genes regulados pelos receptores ativos por proliferadores de peroxissoma. [Internet] [Thesis]. Universidade de Brasília; 2010. [cited 2021 Jan 27]. Available from: http://bdtd.bce.unb.br/tedesimplificado/tde_busca/arquivo.php?codArquivo=6930.

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

Council of Science Editors:

Woitechumas JB. Mecanismos moleculares envolvidos na dominância negativa na síndrome de resistência ao hormônio tireoideano : I. genes regulados negativamente pelo receptor de hormônio tireoideano; II. genes regulados pelos receptores ativos por proliferadores de peroxissoma. [Thesis]. Universidade de Brasília; 2010. Available from: http://bdtd.bce.unb.br/tedesimplificado/tde_busca/arquivo.php?codArquivo=6930

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

Stellenbosch University

13. Sadie, Hanel. Interaction of SF-1 and Nur77 proteins from a gonadotrope cell line with the promoter of the GnRH receptor gene : implications for gene regulation.

Degree: MSc, Biochemistry, 2001, Stellenbosch University

URL: http://hdl.handle.net/10019.1/52307

►

ENGLISH ABSTRACT: The regulation of gonadotropin releasing hormone (GnRH) receptor numbers in the pituitary is a crucial control point in reproduction. Pituitary sensitivity to GnRH… (more)

▼

ENGLISH ABSTRACT: The regulation of gonadotropin releasing hormone (GnRH) receptor numbers in the pituitary is a crucial control point in reproduction. Pituitary sensitivity to GnRH can be directly correlated with GnRH receptor levels, which can be regulated at transcriptional and post-transcriptional level. The proximal promoter of the mouse GnRH receptor gene contains two cis elements bearing the consensus sequence for a Steroidogenic Factor-l (SF -1) binding site. The distal site has previously been shown to be involved in basal and tissue-specific transcriptional regulation, whereas the function of the proximal site was not established. SF-I, a member of the nuclear receptor superfamily of transcription factors, is involved in the transcriptional regulation of a large number of genes involved in steroidogenesis and reproduction. The consensus SF-I binding site can serve as a binding site for several members of the nuclear receptor superfamily. The aim of this study was to investigate the binding of SF-I protein from the aT3-1 gonadotrope cell line to the two putative SF-I binding sites in the mouse GnRH receptor promoter in vitro, in order to provide supporting evidence for their functional roles in GnRH receptor gene regulation. It was shown by Western blotting that SF-I and Nur77, another nuclear receptor transcription factor, are both expressed in aT3-1 cells, in a manner that is influenced by cell culture conditions. Gel mobility shift assays using specific antibodies showed that both SF-I and Nur77 protein in aT3-1 nuclear extracts bind to both sites in a mutually exclusive fashion. As shown by competition assays using mutated versions of the two sites, Nur77 protein had different base pair requirements than that of SF-I protein for binding to the sites. Additionally, SF-I mRNA was shown by Northern blotting to be increased in aT3-1 cells in response to stimulation of the Protein Kinase A (PKA) pathway by forskolin. These results highlight unexpected degeneracy in so-called "consensus" nuclear receptor binding sites. Furthermore, since Nur77 protein is involved in the stress response of the hypothalamic-pituitary-adrenal (HPA) axis, the unexpected presence of Nur77 protein in a gonadotrope cell line has potentially important implications for cross-talk between the HPA and hypothalamic-pituitary-gonadal (HPG) axes.

AFRIKAANSE OPSOMMING: Daar bestaan 'n direkte verband tussen pituïtêre sensitiwiteit vir gonadotropien-vrystellingshormoon (GnRH) en GnRH-reseptorvlakke Die regulering van GnRH-reseptorvlakke op transkripsionele en post-transkripsionele vlak in die pituïtêre klier is belangrik by die beheer van voortplantingsfunksies. Die proksimale promotor van die GnRH-reseptorgeen in die muis bevat twee cis elemente met die konsensus volgorde vir 'n Steroidogenic Factor-l (SF-I) bindingsetel. Die distale element is betrokke by basale en weefsel-spesifieke transkripsionele regulering, maar die funksie van die proksimale element is nog nie vasgestel nie. SF-1 is 'n lid van die…

Advisors/Committee Members: Hapgood, J. P., Stellenbosch University. Faculty of Science. Dept. of Biochemistry..

Subjects/Keywords: Gonadotropin; Luteinizing hormone releasing hormone; Nuclear receptors (Biochemistry); Genetic regulation; Biosynthesis; Protein binding; Dissertations – Biochemistry

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

APA (6^th Edition):

Sadie, H. (2001). Interaction of SF-1 and Nur77 proteins from a gonadotrope cell line with the promoter of the GnRH receptor gene : implications for gene regulation. (Masters Thesis). Stellenbosch University. Retrieved from http://hdl.handle.net/10019.1/52307

Chicago Manual of Style (16^th Edition):

Sadie, Hanel. “Interaction of SF-1 and Nur77 proteins from a gonadotrope cell line with the promoter of the GnRH receptor gene : implications for gene regulation.” 2001. Masters Thesis, Stellenbosch University. Accessed January 27, 2021. http://hdl.handle.net/10019.1/52307.

MLA Handbook (7^th Edition):

Sadie, Hanel. “Interaction of SF-1 and Nur77 proteins from a gonadotrope cell line with the promoter of the GnRH receptor gene : implications for gene regulation.” 2001. Web. 27 Jan 2021.

Vancouver:

Sadie H. Interaction of SF-1 and Nur77 proteins from a gonadotrope cell line with the promoter of the GnRH receptor gene : implications for gene regulation. [Internet] [Masters thesis]. Stellenbosch University; 2001. [cited 2021 Jan 27]. Available from: http://hdl.handle.net/10019.1/52307.

Council of Science Editors:

Sadie H. Interaction of SF-1 and Nur77 proteins from a gonadotrope cell line with the promoter of the GnRH receptor gene : implications for gene regulation. [Masters Thesis]. Stellenbosch University; 2001. Available from: http://hdl.handle.net/10019.1/52307

14. Sahin, N. Preconditioning and Dynamic Stimuli .

Degree: 2017, Vrije Universiteit Amsterdam

URL: http://hdl.handle.net/1871/55306

Subjects/Keywords: Preconditioning; systems biology; apoptosis; mitoptosis; nuclear hormone receptors; dynamic modeling; cortisol

…M, Gnerre C, and Meyer UA. 2004. The evolution of drug-activated nuclear receptors: one… …ancestral gene diverged into two xenosensor genes in mammals. Nuclear Receptors 2(1):7… …nuclear receptors: roles for CAR, PXR, LXR, and FXR. Archives of Biochemistry and Biophysics 433… …2009. Nuclear receptors: the controlling force in drug metabolism of the liver? Xenobiotica… …Twenty-four hour plasma cortisol and adrenocorticotropic hormone in Gulf War Veterans…

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APA (6^th Edition):

Sahin, N. (2017). Preconditioning and Dynamic Stimuli . (Doctoral Dissertation). Vrije Universiteit Amsterdam. Retrieved from http://hdl.handle.net/1871/55306

Chicago Manual of Style (16^th Edition):

Sahin, N. “Preconditioning and Dynamic Stimuli .” 2017. Doctoral Dissertation, Vrije Universiteit Amsterdam. Accessed January 27, 2021. http://hdl.handle.net/1871/55306.

MLA Handbook (7^th Edition):

Sahin, N. “Preconditioning and Dynamic Stimuli .” 2017. Web. 27 Jan 2021.

Vancouver:

Sahin N. Preconditioning and Dynamic Stimuli . [Internet] [Doctoral dissertation]. Vrije Universiteit Amsterdam; 2017. [cited 2021 Jan 27]. Available from: http://hdl.handle.net/1871/55306.

Council of Science Editors:

Sahin N. Preconditioning and Dynamic Stimuli . [Doctoral Dissertation]. Vrije Universiteit Amsterdam; 2017. Available from: http://hdl.handle.net/1871/55306

University of Cambridge

15. Cacciottolo, Tessa. The role of Steroid Receptor Coactivator-1 in human metabolic disease.

Degree: PhD, 2019, University of Cambridge

URL: https://www.repository.cam.ac.uk/handle/1810/297848https://www.repository.cam.ac.uk/bitstream/1810/297848/3/215af9a5-96a1-4327-857f-a62457cd9781_confirmations.txt

Subjects/Keywords: Steroid Receptor Coactivator-1; SRC-1; obesity; metabolism; adipose tissue fibrosis; liver fibrosis; coactivators; nuclear hormone receptors

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APA (6^th Edition):

Cacciottolo, T. (2019). The role of Steroid Receptor Coactivator-1 in human metabolic disease. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/297848https://www.repository.cam.ac.uk/bitstream/1810/297848/3/215af9a5-96a1-4327-857f-a62457cd9781_confirmations.txt

Chicago Manual of Style (16^th Edition):

Cacciottolo, Tessa. “The role of Steroid Receptor Coactivator-1 in human metabolic disease.” 2019. Doctoral Dissertation, University of Cambridge. Accessed January 27, 2021. https://www.repository.cam.ac.uk/handle/1810/297848https://www.repository.cam.ac.uk/bitstream/1810/297848/3/215af9a5-96a1-4327-857f-a62457cd9781_confirmations.txt.

MLA Handbook (7^th Edition):

Cacciottolo, Tessa. “The role of Steroid Receptor Coactivator-1 in human metabolic disease.” 2019. Web. 27 Jan 2021.

Vancouver:

Cacciottolo T. The role of Steroid Receptor Coactivator-1 in human metabolic disease. [Internet] [Doctoral dissertation]. University of Cambridge; 2019. [cited 2021 Jan 27]. Available from: https://www.repository.cam.ac.uk/handle/1810/297848https://www.repository.cam.ac.uk/bitstream/1810/297848/3/215af9a5-96a1-4327-857f-a62457cd9781_confirmations.txt.

Council of Science Editors:

Cacciottolo T. The role of Steroid Receptor Coactivator-1 in human metabolic disease. [Doctoral Dissertation]. University of Cambridge; 2019. Available from: https://www.repository.cam.ac.uk/handle/1810/297848https://www.repository.cam.ac.uk/bitstream/1810/297848/3/215af9a5-96a1-4327-857f-a62457cd9781_confirmations.txt

16. Godart, Matthias. Interactions fonctionnelles entre voies signalétiques intrinsèques et voie des hormones thyroïdiennes dans les cellules souches et progéniteurs de l'épithélium intestinal : Functional interactions between intrinsic pathways and thyroid hormone-dependent signalling in intestinal epithelium stem and progenitor cells.

Degree: Docteur es, Biologie cellulaire et moléculaire, 2019, Lyon

URL: http://www.theses.fr/2019LYSE1138

►

Les hormones thyroïdiennes (HTs) contrôlent plusieurs aspects du développement et de l’homéostasie intestinale. Elles agissent via des récepteurs nucléaires (TRs), facteurs de transcription modulés par… (more)

▼

Les hormones thyroïdiennes (HTs) contrôlent plusieurs aspects du développement et de l’homéostasie intestinale. Elles agissent via des récepteurs nucléaires (TRs), facteurs de transcription modulés par la T3. Le paradigme est la métamorphose des amphibiens où elles sont responsables du remodelage du tube digestif et de l’émergence des cellules souches (Ishizuya-Oka et al, 2009). Des études précédentes ont montré que les HTs jouent un rôle fondamental en régulant la balance entre prolifération et différenciation des précurseurs épithéliaux murins. Du point de vue moléculaire, le récepteur nucléaire TRα1 contrôle plusieurs gènes du cycle cellulaire/prolifération ainsi que les voies de signalisation Wnt et Notch (rev. in Sirakov et al, 2104; Skah et al, 2017). En accord avec ces fonctions, l’expression ciblée de TRα1 dans l’épithélium intestinal (souris vil-TRα1) est suffisante pour induire des cryptes aberrantes, hyper-prolifératives et confère une sensibilité accrue au programme de tumorigénèse intestinale dépendant de la mutation dans le gène Apc (vil-TRα1/Apc+/1638N mice) (Kress et al, 2010). Le but de mon travail a été d’étudier le contrôle des cellules souches intestinales, dépendant des HTs/TRs. En effet, j’ai utilisé des souris Lgr5-EGFP-ires-CreERT2 permettant de traquer, trier et cibler les cellules souches (Barker et al, 2007) que j’ai croisées avec le modèle murin inductible au tamoxifène TRα1-LOF (Loss-of-function) (Quignodon et al, 2007). J’ai étudié les effets de l’altération de la voie HTs/TRα1 in vivo et dans des organoïdes intestinaux (ex vivo). Nos résultats indiquent que les HTs et la modulation de l’expression ou de l’activité de TRα1 affectent rapidement et fortement les cellules souches intestinales. Ce travail ouvre de nouvelles perspectives dans l’étude des signaux dépendants des HTs/ TRα1 dans la physiopathologie des cellules souches intestinales

Thyroid hormones (THs) control several aspects of gut development and homeostasis. They act through the thyroid hormone nuclear receptors (TRs) that are T3-modulated transcription factors. The paradigm is the amphibian metamorphosis, where they are responsible for gut remodeling and emergence of the stem cells (Ishizuya-Oka et al, 2009). In previous studies we showed that THs play a fundamental role in regulating the balance between cell proliferation and cell differentiation of the murine intestinal epithelial precursors. From a molecular point of view the nuclear receptor TRα1 controls several proliferation/cell-cycle genes as well as the Wnt and Notch pathways (rev. in Sirakov et al, 2104; Skah et al, 2017). In accordance with these functions, targeted expression of TRα1 in the intestinal epithelium (vil-TRα1 mice) is sufficient to induce aberrant and hyper-proliferative crypts and confers increased susceptibility to Apc-mutation dependent intestinal tumorigenic program (vil-TRα1/Apc+/1638N mice) (Kress et al, 2010). The aim of my work was to study TH- and TRα1-dependent control of intestinal stem cells. Indeed, I used the Lgr5-EGFP-ires-CreERT2…

Advisors/Committee Members: Plateroti, Michelina (thesis director).

Subjects/Keywords: Intestin; Épithélium; Cellules souches; Culture 3D d'organoïdes; Hormones thyroïdiennes; Récepteurs nucléaires des hormones thyroïdiennes; Prolifération; Différenciation; Intestine; Epithelium; Stem cells; Organoid 3D culture; Thyroid hormones; Thyroid hormone nuclear receptors; Proliferation; Differentiation; 570

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APA (6^th Edition):

Godart, M. (2019). Interactions fonctionnelles entre voies signalétiques intrinsèques et voie des hormones thyroïdiennes dans les cellules souches et progéniteurs de l'épithélium intestinal : Functional interactions between intrinsic pathways and thyroid hormone-dependent signalling in intestinal epithelium stem and progenitor cells. (Doctoral Dissertation). Lyon. Retrieved from http://www.theses.fr/2019LYSE1138

Chicago Manual of Style (16^th Edition):

Godart, Matthias. “Interactions fonctionnelles entre voies signalétiques intrinsèques et voie des hormones thyroïdiennes dans les cellules souches et progéniteurs de l'épithélium intestinal : Functional interactions between intrinsic pathways and thyroid hormone-dependent signalling in intestinal epithelium stem and progenitor cells.” 2019. Doctoral Dissertation, Lyon. Accessed January 27, 2021. http://www.theses.fr/2019LYSE1138.

MLA Handbook (7^th Edition):

Godart, Matthias. “Interactions fonctionnelles entre voies signalétiques intrinsèques et voie des hormones thyroïdiennes dans les cellules souches et progéniteurs de l'épithélium intestinal : Functional interactions between intrinsic pathways and thyroid hormone-dependent signalling in intestinal epithelium stem and progenitor cells.” 2019. Web. 27 Jan 2021.

Vancouver:

Godart M. Interactions fonctionnelles entre voies signalétiques intrinsèques et voie des hormones thyroïdiennes dans les cellules souches et progéniteurs de l'épithélium intestinal : Functional interactions between intrinsic pathways and thyroid hormone-dependent signalling in intestinal epithelium stem and progenitor cells. [Internet] [Doctoral dissertation]. Lyon; 2019. [cited 2021 Jan 27]. Available from: http://www.theses.fr/2019LYSE1138.

Council of Science Editors:

Godart M. Interactions fonctionnelles entre voies signalétiques intrinsèques et voie des hormones thyroïdiennes dans les cellules souches et progéniteurs de l'épithélium intestinal : Functional interactions between intrinsic pathways and thyroid hormone-dependent signalling in intestinal epithelium stem and progenitor cells. [Doctoral Dissertation]. Lyon; 2019. Available from: http://www.theses.fr/2019LYSE1138

University of Cincinnati

17. Hess-Wilson, Janet Katherine. Influence of the Nuclear Hormone Receptor Axis in the Progression and Treatment of Hormone Dependent Cancers.

Degree: PhD, Medicine : Cell and Molecular Biology, 2007, University of Cincinnati

URL: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1168452681

► Due to its pivotal role in prostatic growth and survival, the androgen receptor (AR) is the primary target of disseminated prostate cancer (CaP), as achieved… (more)

▼ Due to its pivotal role in prostatic growth and survival, the androgen receptor (AR) is the primary target of disseminated prostate cancer (CaP), as achieved via androgen deprivation therapy (ADT). Unfortunately, ADT is circumvented by restoration of AR activity, resulting in ADT resistant tumors for which there is no alternate treatment option. Through multiple mechanisms, reactivation of the AR specifically underlies the progression to therapy resistant tumors. The environmentally prevalent endocrine disrupting compound (EDC), bisphenol A (BPA) is able to activate specific somatically mutated ARs commonly found in CaP, resulting in androgen-independent proliferation of CaP cells. To directly assess the effect of BPA on ADT, we used an in vivo xenograft model of CaP that expresses a BPA-sensitive mutant AR, and mimics standard human cytotoxic response to ADT, followed by subsequent tumor re-growth. When tumor-bearing animals were exposed to environmentally relevant levels of BPA during ADT, the tumors failed therapy more rapidly (compared to placebo controls), with AR re-activation and concomitant increased tumor cell proliferation. These data suggest that environmentally relevant exposure to EDCs may reduce the efficacy of mainline ADT for CaP. We next determined that the environmentally persistent pesticide, DDE, was able to activate select AR mutants, and in in vitro models of CaP, DDE induces cellular proliferation in the absence of androgen, demonstrating that this observed response was not unique to BPA. Strikingly, the mechanism of DDE impact on CaP cells was distinct from BPA, in that at low doses this agent also activated the MAPK pathway, and requires this activation for mitogenesis. Given the context specific impact of AR activation by EDCs, and the deleterious effect of exposure to BPA on ADT in vivo, we next addressed the impact of AR action on taxane-based therapy. These cytotoxic agents have recently been shown to improve survival outcome for patients with advanced CaP, and are potentially new second line therapies, however the impact of AR action on this cytotoxic modality had yet to be assessed. Contrary to the stigma of AR as a survival factor, we found that AR activation by both endogenous and exogenous agonists (i.e. DHT and BPA), synergized with taxanes to decrease cell survival, through p53-mediated, caspase dependent apoptosis. This synergistic action was attributed directly to the AR-dependent mitogenic capacity of these agents. Importantly, these data further support the conclusion that the environmental impact on AR action and CaP therapeutic outcome is context specific. We further evaluated the complexity of EDC affects by assessing the impact of these agents under clinically relevant conditions in another hormone-dependent tissue, breast cancer. BPA and the phytoestrogen, coumestrol (COU), were able to activate the estrogen receptor (ER-alpha), but this activation was restricted to estrogen-depleted conditions, and could be blocked by the standard ER antagonist, tamoxifen. Additionally,… Advisors/Committee Members: Knudsen, Dr. Karen (Advisor).

Subjects/Keywords: nuclear hormone receptors; endocrine disrupting compounds; androgen receptor; bishphenol A; taxanes; DDE; prostate cancer; breast cancer

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APA (6^th Edition):

Hess-Wilson, J. K. (2007). Influence of the Nuclear Hormone Receptor Axis in the Progression and Treatment of Hormone Dependent Cancers. (Doctoral Dissertation). University of Cincinnati. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=ucin1168452681

Chicago Manual of Style (16^th Edition):

Hess-Wilson, Janet Katherine. “Influence of the Nuclear Hormone Receptor Axis in the Progression and Treatment of Hormone Dependent Cancers.” 2007. Doctoral Dissertation, University of Cincinnati. Accessed January 27, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1168452681.

MLA Handbook (7^th Edition):

Hess-Wilson, Janet Katherine. “Influence of the Nuclear Hormone Receptor Axis in the Progression and Treatment of Hormone Dependent Cancers.” 2007. Web. 27 Jan 2021.

Vancouver:

Hess-Wilson JK. Influence of the Nuclear Hormone Receptor Axis in the Progression and Treatment of Hormone Dependent Cancers. [Internet] [Doctoral dissertation]. University of Cincinnati; 2007. [cited 2021 Jan 27]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1168452681.

Council of Science Editors:

Hess-Wilson JK. Influence of the Nuclear Hormone Receptor Axis in the Progression and Treatment of Hormone Dependent Cancers. [Doctoral Dissertation]. University of Cincinnati; 2007. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1168452681

18. Wu, Xiaoyang. Regulation of Nuclear Hormone Receptors by Corepressors and Coactivators: a Dissertation.

Degree: Biochemistry and Molecular Pharmacology, Department of Biochemistry and Molecular Pharmacology, 2001, U of Massachusetts : Med

URL: https://escholarship.umassmed.edu/gsbs_diss/106

► Nuclear hormone receptors (NHR) constitute a superfamily of ligand inducible transcriptional activators that enable an organism to regulate development and homeostasis through switching on… (more)

▼ Nuclear hormone receptors (NHR) constitute a superfamily of ligand inducible transcriptional activators that enable an organism to regulate development and homeostasis through switching on or off target genes in response to stimuli reflecting changes in environment as well as endocrine. NHRs include classical steroid hormone receptors (GR, AR, ER and MR) and retinoid, thyroid hormone receptors. One long-term goal of our lab is to understand the molecular mechanisms through which the transcriptional activity of NHRs is regulated. Extensive studies in the past few years have revealed that in addition to the dependence on ligand availability, the transcriptional activity of NHRs is also regulated by two types of proteins: co activators and corepressors. In the absence of ligand, many NHRs, including TR and RAR can actively repress target gene transcription with the help of corepressors, proteins that physically interact with both NHRs and histone deacetylases (HDACs). Functional interactions between NHRs and corepressors therefore lead to tightly compact and transcriptionally non-permissive chromatin structures after the removal of obstructive acetyl groups from histone tails by HDACs. On the other hand, ligand binding stabilizes NHRs in a conformation that favors interaction with proteins other than corepressors; many of these proteins are able to potentiate the transcriptional activity of NHRs through various mechanisms, such as histone acetylation, chromatin remodeling and recruitment of basal transcription machinery and are collectively termed coactivators. Two highly related corepressors, SMRT (silencing mediator of retinoid and thyroid hormone receptors) and N-CoR (nuclear receptor corepressor), have been cloned. This research in corepressor SMRT started by a systematic study of its subcellular localization. We found that SMRT predominantly forms a specific nuclear punctuate structure that does not appear to overlap with any other well-known subnuclear domains/speckles. Although our searching for specific sequence signals that may determine the specific speckle localization of SMRT did not yield conclusive results, we discovered the colocalization of unliganded RAR and certain HDACs, including HDAC1, 3,4 and 5, in the SMRT nuclear speckles. Moreover, SMRT is likely to be the organizer of such speckles since it appears to be able to recruit other proteins into these speckles. The presence of HDAC1 in the SMRT speckles suggests a direct association between these two proteins, which has not been detected by previous biochemical analyses. Interestingly, HDAC1 point mutants that are completely defective in deacetylase activity failed to locate to SMRT nuclear speckles, while another partially active mutant maintained the colocalization. These discoveries may indicate SMRT nuclear speckles as novel nuclear domains involved in transcriptional repression. More physiologically relevant support for this hypothesis arises from study of HDAC4 and 5. HDAC4… Advisors/Committee Members: J. Don Chen.

Subjects/Keywords: Transcription Factors; Receptors; Cytoplasmic and Nuclear; Repressor Proteins; Histone Deacetylases; Myogenic Regulatory Factors; Receptors; Estrogen; Amino Acids, Peptides, and Proteins; Chemical Actions and Uses; Genetic Phenomena; Hormones, Hormone Substitutes, and Hormone Antagonists

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

APA (6^th Edition):

Wu, X. (2001). Regulation of Nuclear Hormone Receptors by Corepressors and Coactivators: a Dissertation. (Doctoral Dissertation). U of Massachusetts : Med. Retrieved from https://escholarship.umassmed.edu/gsbs_diss/106

Chicago Manual of Style (16^th Edition):

Wu, Xiaoyang. “Regulation of Nuclear Hormone Receptors by Corepressors and Coactivators: a Dissertation.” 2001. Doctoral Dissertation, U of Massachusetts : Med. Accessed January 27, 2021. https://escholarship.umassmed.edu/gsbs_diss/106.

MLA Handbook (7^th Edition):

Wu, Xiaoyang. “Regulation of Nuclear Hormone Receptors by Corepressors and Coactivators: a Dissertation.” 2001. Web. 27 Jan 2021.

Vancouver:

Wu X. Regulation of Nuclear Hormone Receptors by Corepressors and Coactivators: a Dissertation. [Internet] [Doctoral dissertation]. U of Massachusetts : Med; 2001. [cited 2021 Jan 27]. Available from: https://escholarship.umassmed.edu/gsbs_diss/106.

Council of Science Editors:

Wu X. Regulation of Nuclear Hormone Receptors by Corepressors and Coactivators: a Dissertation. [Doctoral Dissertation]. U of Massachusetts : Med; 2001. Available from: https://escholarship.umassmed.edu/gsbs_diss/106

19. Leo, Christopher. Differential Mechanisms of Nuclear Receptor Regulation by the Coactivator RAC3: A Dissertation.

Degree: Biochemistry and Molecular Pharmacology, Biochemistry and Molecular Pharmacology, 2000, U of Massachusetts : Med

URL: https://escholarship.umassmed.edu/gsbs_diss/110

► The steroid/thyroid hormone receptor superfamily is a large class of ligand-dependent transcription factors that plays a critical role in regulating the expression of genes… (more)

▼ The steroid/thyroid hormone receptor superfamily is a large class of ligand-dependent transcription factors that plays a critical role in regulating the expression of genes involved in a broad range of physiological functions, including development, homeostasis, and reproduction. In the absence of cognate hormone, several receptors are able to repress transcription below the basal level via the recruitment of the nuclear receptor corepressors SMRT and NCoR. Upon hormone binding by the receptor, the corepressor complex is dissociated and a coactivator complex is subsequently recruited. This thesis details the mechanisms by which receptor-associated coactivator 3 (RAC3) interacts with nuclear receptors, particularly the vitamin D, estrogen, and retinoid receptors, and modulates their transcriptional activity. It was discovered that these receptors interact with different α-helical LXXLL motifs of RAC3 in vitro. Mutation of specific motifs differentially impairs the ability of RAC3 to enhance transcription by the receptors in vivo. In addition, the intrinsic transcriptional activation function of RAC3 was also characterized. Here, a single LXXLL motif, NR box v, was found to be essential to activation by serving as a binding surface for the general transcriptional integrator CBP/p300. Finally, the cofactor binding pocket of retinoid receptors was characterized. It was demonstrated that, to a large extent, the coactivator pocket of RARα overlaps with the corepressor pocket, with the exception of helix 12, which is required for coactivator, but not corepressor binding. Recruitment of RAC3 or SMRT also correlates directly with the ability of RARα to activate or repress transcription, respectively. Intriguingly, it was discovered that the AF-2 domain of RXRα inhibited cofactor binding to RXRα heterodimers, for deletion of this domain dramatically enhanced RAC3 and SMRT binding. In addition, it was demonstrated that the RXRα cofactor binding pocket contributed minimally to recruitment of cofactors. Conversely, the AF-2 domain of the partnering monomer and its cofactor pocket were required for these interactions. These findings suggest that the partner of RXRα is the primary docking point for cofactors at RXRα heterodimeric complexes. Taken together, this work contributes significantly to the field of nuclear receptor function in detailing the mechanisms by which the coactivator RAC3 is recruited to nuclear receptors and regulates their transcriptional activity. Advisors/Committee Members: J. Don Chen.

Subjects/Keywords: Receptors; Cytoplasmic and Nuclear; RAC3 protein; Gene Expression Regulation; Amino Acids, Peptides, and Proteins; Chemical Actions and Uses; Genetic Phenomena; Hormones, Hormone Substitutes, and Hormone Antagonists; Polycyclic Compounds

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

APA (6^th Edition):

Leo, C. (2000). Differential Mechanisms of Nuclear Receptor Regulation by the Coactivator RAC3: A Dissertation. (Doctoral Dissertation). U of Massachusetts : Med. Retrieved from https://escholarship.umassmed.edu/gsbs_diss/110

Chicago Manual of Style (16^th Edition):

Leo, Christopher. “Differential Mechanisms of Nuclear Receptor Regulation by the Coactivator RAC3: A Dissertation.” 2000. Doctoral Dissertation, U of Massachusetts : Med. Accessed January 27, 2021. https://escholarship.umassmed.edu/gsbs_diss/110.

MLA Handbook (7^th Edition):

Leo, Christopher. “Differential Mechanisms of Nuclear Receptor Regulation by the Coactivator RAC3: A Dissertation.” 2000. Web. 27 Jan 2021.

Vancouver:

Leo C. Differential Mechanisms of Nuclear Receptor Regulation by the Coactivator RAC3: A Dissertation. [Internet] [Doctoral dissertation]. U of Massachusetts : Med; 2000. [cited 2021 Jan 27]. Available from: https://escholarship.umassmed.edu/gsbs_diss/110.

Council of Science Editors:

Leo C. Differential Mechanisms of Nuclear Receptor Regulation by the Coactivator RAC3: A Dissertation. [Doctoral Dissertation]. U of Massachusetts : Med; 2000. Available from: https://escholarship.umassmed.edu/gsbs_diss/110

McMaster University

20. Delvecchio, Christopher J. LXR Regulation And Function In Human Airway Smooth Muscle.

Degree: PhD, 2009, McMaster University

URL: http://hdl.handle.net/11375/17287

►

The liver X receptors (LXRs) are members of the nuclear hormone receptor (NHR) superfamily of transcription factors and are activated by oxysterols. As such,… (more)

▼

The liver X receptors (LXRs) are members of the nuclear hormone receptor (NHR) superfamily of transcription factors and are activated by oxysterols. As such, LXRs act as "cholesterol sensors" and play an integral role in cholesterol homeostasis by modulating the expression of genes involved in lipid transport and metabolism as well as inflammation. This thesis begins by describing the modulation of LXR transactivation by PKC. Specifically, transactivation by LXRα is decreased upon activation of PKC signalling pathways as assessed by LXR reporter gene analysis and endogenous target gene expression. These findings reveal a mode of regulation of LXRα that may be relevant to disease conditions where aberrant PKC signalling is observed. The second and third part of the thesis turns the attention to the role of LXR in human airway smooth muscle (hASM), a crucial effector cell in asthma progression. For the first time, research described here indicates that primary human ASM cells express functional LXRs. Moreover, LXR target genes ABCA 1 and ABCG I were highly induced upon the addition of LXR agonists leading to enhanced cholesterol efflux to apoAI and HDL, a process dependant entirely on ABCA I. Furthermore, activation of LXR inhibited the expression of multiple cytokines in response to inflammatory mediators and inhibited the proliferation and migration of hASM cells, two important processes that contribute to the airway remodelling observed in the asthmatic lung. This body of work suggests that modulation of LXR offers prospects for new therapeutic approaches in the treatment of asthma. Furthermore, it establishes a critical role for ABCA 1 in lipid transport in ASM cells and suggests that dysregulation of cholesterol homeostasis in these cells may be important. These findings have broad implications in the association of hypercholesterolemia and AHR and places LXR at the forefront of novel therapeutic avenues to treat inflammatory lung disease.

Thesis

Doctor of Philosophy (PhD)

Advisors/Committee Members: Capone, John P., Biochemistry and Biomedical Sciences.

Subjects/Keywords: liver X receptors; nuclear hormone receptor; NHR; oxysterols; cholesterol homeostasis; lipid transport; metabolism; inflammation; PKC; hASM; crucial effector cell; asthma progression; ABCA1; ABCG1; cytokines

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

APA (6^th Edition):

Delvecchio, C. J. (2009). LXR Regulation And Function In Human Airway Smooth Muscle. (Doctoral Dissertation). McMaster University. Retrieved from http://hdl.handle.net/11375/17287

Chicago Manual of Style (16^th Edition):

Delvecchio, Christopher J. “LXR Regulation And Function In Human Airway Smooth Muscle.” 2009. Doctoral Dissertation, McMaster University. Accessed January 27, 2021. http://hdl.handle.net/11375/17287.

MLA Handbook (7^th Edition):

Delvecchio, Christopher J. “LXR Regulation And Function In Human Airway Smooth Muscle.” 2009. Web. 27 Jan 2021.

Vancouver:

Delvecchio CJ. LXR Regulation And Function In Human Airway Smooth Muscle. [Internet] [Doctoral dissertation]. McMaster University; 2009. [cited 2021 Jan 27]. Available from: http://hdl.handle.net/11375/17287.

Council of Science Editors:

Delvecchio CJ. LXR Regulation And Function In Human Airway Smooth Muscle. [Doctoral Dissertation]. McMaster University; 2009. Available from: http://hdl.handle.net/11375/17287

21. Braliou, Georgia. Transcriptional regulation by v-ErbA, the oncogenic counterpart of thyroid hormone receptor (TR).

Degree: 2001, Institutes outside Greece; Ιδρύματα Εξωτερικού

URL: http://hdl.handle.net/10442/hedi/39407

► Thyroid hormone (T3) exhibits a vast array of profound effects on homeostasis, development, amphibian metamorphosis, differentiation and neoplasia. The action of T3 is mediated via… (more)

▼ Thyroid hormone (T3) exhibits a vast array of profound effects on homeostasis, development, amphibian metamorphosis, differentiation and neoplasia. The action of T3 is mediated via its binding to the cognate thyroid hormone receptor (TR) which in turn binds to specific DNA sequences called thyroid responsive elements (TREs). TR in the presence of T3 activates transcription while unliganded TR leads to repression utilizing a multitude of mechanisms to regulate transcription. The v-ErbA oncoprotein is a mutated viral variant of TRα encoded by the Avian Erythroblastosis virus (AEV). The co-operation of v-erbA with v-erbB, the second oncogene of AEV with tyrosine kinase activity, leads to fatal erythroleukemia as a result of enhanced proliferation and arrest of differentiation. Due to mutations, v-ErbA cannot bind T3 hormone and thus it cannot activate transcription like TR its cellular counterpart. The hypothesis that v-ErbA behaves as a constitutive unliganded TR is attractive but not consistent with a number of experimental observations. The aim of the studies in the present thesis is to unravel the molecular mechanisms that constitute the oncogenic activity of v-erbA.Using DNase I hypersensitive site mapping we identified two candidate regions (designated HS1 and HS2) to convey transcriptional regulation of the erythroid gene carbonic anhydrase II (CA II) by v-erbA. HS1 is located 7 kb upstream while HS2 is located 8 kb downstream the transcription start site within the second intron. Immunoprecipitation of v-ErbA/DNA complexes and in vitro and in vivo footprinting experiments demonstrated that the intronic HS2 region has a binding site for v-ErbA (VRE). Interestingly, the in vivo occupancy of the VRE by v-ErbA coincides with CA II repression while this binding is alleviated when cells are triggered to differentiation and CA II is up regulated. Using mutagenesis analysis and transfection experiments we demonstrated that the HS2 region activates transcription independent of the position and the orientation relative to promoters, and that the enhancer activity of HS2 is governed by erythroid-specific factors that bind to GATA sequences located adjacently to VRE. Thus, v-ErbA appears to neutralize the positive activity of erythroid specific GATA-factors and HS2 behaves as a potent erythroid specific enhancer that is repressed by v-ErbA. We also showed that the chromatin architecture of HS2 can be modulated by liganded TR in erythroid progenitor cells and that v-ErbA occludes liganded TR from binding to VRE resulting in ablation of the T3-induced activation. This feature of v-ErbA correlates very well with its observed oncogenic activity. Using immunoprecipitation assays we showed that v-ErbA can interact with the endogenous transcriptional co-repressor NCoR. However, NCoR is not crucial for the v-ErbA mediated repression, while other co-repressor might be more potent in v-ErbA complexes. In summary, our studies have provided new insight into the mechanism of the v-ErbA-mediated transcriptional repression, that is by…

Subjects/Keywords: Μεταγραφική ρύθμιση; Υποδοχέας θυρεοειδούς ορμόνης; Πυρηνικός υποδοχέας; Ογκογονίδια; Καρβονική ανυδράση; Συνκαταστολείς πυρηνικών υποδοχέων; Συνενεργοποιητές πυρηνικών υποδοχέων; Αιματοποίηση; Λευχαιμία; Μεταγραφικός ενισχυτής; Ερυθροειδικότητα; Στοιχεία απόκρισης στη θυρεοειδή ορμόνη; Transcriptional regulation; Thyroid hormone receptors; Nuclear receptors; v-erbA; Oncogene; Carbonic anhydrase; Nuclear receptor corepressor; Nuclear receptor coactivator; Hematopoiesis; Leukemia; Transcriptional enhancer; Erythroid specific; Thyroid response elements (TRE)

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

APA (6^th Edition):

Braliou, G. (2001). Transcriptional regulation by v-ErbA, the oncogenic counterpart of thyroid hormone receptor (TR). (Thesis). Institutes outside Greece; Ιδρύματα Εξωτερικού. Retrieved from http://hdl.handle.net/10442/hedi/39407

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):

Braliou, Georgia. “Transcriptional regulation by v-ErbA, the oncogenic counterpart of thyroid hormone receptor (TR).” 2001. Thesis, Institutes outside Greece; Ιδρύματα Εξωτερικού. Accessed January 27, 2021. http://hdl.handle.net/10442/hedi/39407.

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

MLA Handbook (7^th Edition):

Braliou, Georgia. “Transcriptional regulation by v-ErbA, the oncogenic counterpart of thyroid hormone receptor (TR).” 2001. Web. 27 Jan 2021.

Vancouver:

Braliou G. Transcriptional regulation by v-ErbA, the oncogenic counterpart of thyroid hormone receptor (TR). [Internet] [Thesis]. Institutes outside Greece; Ιδρύματα Εξωτερικού; 2001. [cited 2021 Jan 27]. Available from: http://hdl.handle.net/10442/hedi/39407.

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

Council of Science Editors:

Braliou G. Transcriptional regulation by v-ErbA, the oncogenic counterpart of thyroid hormone receptor (TR). [Thesis]. Institutes outside Greece; Ιδρύματα Εξωτερικού; 2001. Available from: http://hdl.handle.net/10442/hedi/39407

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

22. Νικολαΐδου - Νεοκοσμίδου, Βαρβάρα. Μονοπάτια σηματοδότησης που ρυθμίζουν την έκφραση των γονιδίων των απολιποπρωτεϊνών του ανθρώπου.

Degree: 2007, University of Crete (UOC); Πανεπιστήμιο Κρήτης

URL: http://hdl.handle.net/10442/hedi/15795

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The focus of the present work is the elucidation of the role of signal transduction pathways involving pro-inflammatory cytokines and hormone nuclear receptors in the… (more)

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The focus of the present work is the elucidation of the role of signal transduction pathways involving pro-inflammatory cytokines and hormone nuclear receptors in the transcriptional regulation of the genes coding for apolipoproteins in human hepatocytes. Apolipoproteins, along with plasma enzymes, lipid transfer proteins and the lipoprotein receptors participate in the biogenesis and catabolism of lipoproteins. In principle, changes in the regulation of synthesis of any apolipoprotein or another protein of the lipoprotein system may affect the concentration or the function of a specific group of lipoproteins, and may in some instances contribute to the pathogenesis of hyperilipidemia or even atherosclerosis.

Η παρούσα διδακτορική διατριβή στοχεύει στην διαλεύκανση του ρόλου των σηματοδοτικών μονοπατιών προ-φλεγμονωδών κυτταροκινών και πυρηνικών υποδοχέων ορμονών στην ρύθμιση της έκφρασης των γονιδίων των απολιποπρωτεϊνών του ανθρώπου σε ηπατικά κύτταρα. Οι απολιποπρωτεΐνες, μαζί με ένζυμα του πλάσματος, τις πρωτεΐνες μεταφοράς λιπιδίων και τους υποδοχείς των λιποπρωτεϊνών συμμετέχουν στην βιογένεση και τον καταβολισμό των λιποπρωτεϊνών. Θεωρητικά, αλλαγές στη ρύθμιση της έκφρασης οποιασδήποτε απολιποπρωτεΐνης ή άλλης πρωτεΐνης του συστήματος των λιποπρωτεϊνών, μπορεί να επηρεάσει τη συγκέντρωση ή τη λειτουργία συγκεκριμένων ομάδων λιποπρωτεϊνών και σε μερικές περιπτώσεις να συνεισφέρει στη παθογένεση υπερλιπιδαιμίας ή ακόμα και στην ανάπτυξη αθηροσκλήρυνσης.

Subjects/Keywords: Απολιποπρωτεΐνες; Πυρηνικοί υποδοχείς ορμονών; Απόκριση; Μεταγραφικοί συν-παράγοντες; Ρύθμιση γονιδιακής έκφρασης; Απολιποπρωτείνη CIII; Ηπατικός πυρηνικός παράγοντας 4α; Παράγοντας νέκρωσης όγκων; Apolipoproteins; Hormone nuclear receptors; Acute phase response (APR); Transcriptional co-factors; Regulation of transcription; Apolipoprotein CIII; Hepatic nuclear factor 4A (HNF-4a); Tumor necrosis factor (TNF)

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):

Νικολαΐδου - Νεοκοσμίδου, . �. (2007). Μονοπάτια σηματοδότησης που ρυθμίζουν την έκφραση των γονιδίων των απολιποπρωτεϊνών του ανθρώπου. (Thesis). University of Crete (UOC); Πανεπιστήμιο Κρήτης. Retrieved from http://hdl.handle.net/10442/hedi/15795

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):

Νικολαΐδου - Νεοκοσμίδου, Βαρβάρα. “Μονοπάτια σηματοδότησης που ρυθμίζουν την έκφραση των γονιδίων των απολιποπρωτεϊνών του ανθρώπου.” 2007. Thesis, University of Crete (UOC); Πανεπιστήμιο Κρήτης. Accessed January 27, 2021. http://hdl.handle.net/10442/hedi/15795.

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

MLA Handbook (7^th Edition):

Νικολαΐδου - Νεοκοσμίδου, Βαρβάρα. “Μονοπάτια σηματοδότησης που ρυθμίζουν την έκφραση των γονιδίων των απολιποπρωτεϊνών του ανθρώπου.” 2007. Web. 27 Jan 2021.

Vancouver:

Νικολαΐδου - Νεοκοσμίδου �. Μονοπάτια σηματοδότησης που ρυθμίζουν την έκφραση των γονιδίων των απολιποπρωτεϊνών του ανθρώπου. [Internet] [Thesis]. University of Crete (UOC); Πανεπιστήμιο Κρήτης; 2007. [cited 2021 Jan 27]. Available from: http://hdl.handle.net/10442/hedi/15795.

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

Council of Science Editors:

Νικολαΐδου - Νεοκοσμίδου �. Μονοπάτια σηματοδότησης που ρυθμίζουν την έκφραση των γονιδίων των απολιποπρωτεϊνών του ανθρώπου. [Thesis]. University of Crete (UOC); Πανεπιστήμιο Κρήτης; 2007. Available from: http://hdl.handle.net/10442/hedi/15795

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

Open Access Theses and Dissertations