subject:(glucocorticoid receptor)

Univerzitet u Beogradu

1. Antić, Jadranka A., 1967-. Značaj polimorfizama u genima za glukokortikoidni i adrenokortikotropni receptor u nastanku adrenalnih incidentaloma.

Degree: Biološki fakultet, 2016, Univerzitet u Beogradu

URL: https://fedorabg.bg.ac.rs/fedora/get/o:10662/bdef:Content/get

►

Biologija - Genetika tumora / Biology - Genetics of tumors

UVOD: Glukokortikoidni hormoni (GC) ostvaruju svoje efekte vezivanjem za glukokortikoidni receptor (GR). Adrenokortikotropni hormon (ACTH)… (more)

▼

Biologija - Genetika tumora / Biology - Genetics of tumors

UVOD: Glukokortikoidni hormoni (GC) ostvaruju svoje efekte vezivanjem za glukokortikoidni receptor (GR). Adrenokortikotropni hormon (ACTH) reguliše sintezu GC vezivanjem za ACTH receptor (ACTHR). Prisustvo polimorfizama u genu za GR (BclI, N363S, ER22/23EK and A3669G) i promotoru ACTHR može uticati na efekte glukokortikoida i predispoziciju za nastanak unilateralnih adrenalnih incidentaloma. CILJ RADA: Utvrđivanje mogućeg uticaja funkcionalnih polimorfizama u genima za GR i ACTHR na predispoziciju za nastanak adrenalnih incidentaloma i osetljivost na GC i ispitivanje ekspresije GR u tumorskom, peritumorskom i zdravom adrenokortikalnom tkivu. METODE: U ispitivanje je bilo uključeno 112 pacijenata i 100 zdravih dobrovoljaca, koji su podvrgnuti metaboličkom, genetičkom, biohemijskom i antropometrijskom testiranju. DNK je dobijena iz leukocita periferne krvi. Prisustvo polimorfizama je detektovano metodama PCR, RFLP i sekvenciranja DNK. Uzorci tkiva su analizirani imunohistohemijskom metodom. REZULTATI: Prisustvo dužeg C alela BclI (p<0.001) polimorfizma i kraćeg G alela A3669G (p<0.001) polimorfizma GR gena su bili nezavisni prediktori adrenalnih incidentaloma. Pacijenti sa prisutnim C alelom BclI su imali veće tumore (p=0.002), a oni sa G alelom A3669G više vrednosti postdeksametazonskog kortizola (p=0.025). Istovremeno prisustvo oba alela je koreliralo sa manjim obimom struka (p=0.002), a višim baznim i postdeksametazonskog kortizolom (p=0.024). Smanjena ekspresija GRα i GRβ izoformi zapažena je u tumorskom, a GRα u peritumorskom tkivu. Lokalizacija GRβ je bila dominantno nukleusna. ZAKLJUČAK: Prisustvo C alela BclI i G alela A3669G polimorfizmama gena za GR se nalaze u vezi sa nastankom unilateralnih adrenalnim incidentalomima, a njihovo zajedničko prisustvo dovodi do smanjene osetljivosti na GC. Stečena intraadenomatozna glukokortikoidna rezistencija može da dovede do disregulacije produkcije kortizola i rasta tumora u isto vreme, dok prirodna osetljivost na glukokortikoide najverovatnije modifikuje ove efekte.

Advisors/Committee Members: Damjanović, Svetozar, 1953-.

Subjects/Keywords: glucocorticoid hormones; glucocorticoid receptor; adrenocorticotrop receptor; adrenal incidentalomas; polymorphisms; glucocorticoid resistance

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Antić, Jadranka A., 1. (2016). Značaj polimorfizama u genima za glukokortikoidni i adrenokortikotropni receptor u nastanku adrenalnih incidentaloma. (Thesis). Univerzitet u Beogradu. Retrieved from https://fedorabg.bg.ac.rs/fedora/get/o:10662/bdef:Content/get

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):

Antić, Jadranka A., 1967-. “Značaj polimorfizama u genima za glukokortikoidni i adrenokortikotropni receptor u nastanku adrenalnih incidentaloma.” 2016. Thesis, Univerzitet u Beogradu. Accessed January 18, 2021. https://fedorabg.bg.ac.rs/fedora/get/o:10662/bdef:Content/get.

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

MLA Handbook (7^th Edition):

Antić, Jadranka A., 1967-. “Značaj polimorfizama u genima za glukokortikoidni i adrenokortikotropni receptor u nastanku adrenalnih incidentaloma.” 2016. Web. 18 Jan 2021.

Vancouver:

Antić, Jadranka A. 1. Značaj polimorfizama u genima za glukokortikoidni i adrenokortikotropni receptor u nastanku adrenalnih incidentaloma. [Internet] [Thesis]. Univerzitet u Beogradu; 2016. [cited 2021 Jan 18]. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:10662/bdef:Content/get.

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

Council of Science Editors:

Antić, Jadranka A. 1. Značaj polimorfizama u genima za glukokortikoidni i adrenokortikotropni receptor u nastanku adrenalnih incidentaloma. [Thesis]. Univerzitet u Beogradu; 2016. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:10662/bdef:Content/get

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

University of Edinburgh

2. Richardson, Rachel Victoria. The role of the glucocorticoid receptor in cardiac growth and remodeling.

Degree: PhD, 2014, University of Edinburgh

URL: http://hdl.handle.net/1842/17930

► The glucocorticoid receptor (GR) is expressed throughout the cardiovascular system and glucocorticoids (GC) are known to influence cardiovascular processes ranging from angiogenesis and vascular tone… (more)

▼ The glucocorticoid receptor (GR) is expressed throughout the cardiovascular system and glucocorticoids (GC) are known to influence cardiovascular processes ranging from angiogenesis and vascular tone to cardiomyocyte hypertrophy and inflammation. Genetic variation in the human GR gene that associates with relative glucocorticoid resistance is also linked to hypertension and increased risk of cardiovascular disease. Mice with global GR haploinsufficiency (GR+/-) are similarly glucocorticoid resistant, with increased hypothalamic-pituitary-adrenal (HPA) axis activity and elevated blood pressure in adulthood. Previous work from the laboratory has demonstrated that the GR is essential for normal growth and maturation of the foetal heart in late gestation and in vitro studies show that GC can alter cardiomyocyte function and induce cardiomyocyte hypertrophy. I hypothesised that reduced GR density during development would have consequences for cardiovascular function and disease risk in adulthood and that cardiovascular GR signalling is important for postnatal growth of the heart, as well as physiological and pathological cardiac remodeling in adulthood. I tested this hypothesis in GR+/- mice with global alteration in GR density as well as in SMGRKO mice, with deletion of GR in cardiomyocytes and vascular smooth muscle. To investigate the association between GC resistance and cardiovascular disease risk, I have characterised the cardiac phenotype of GR+/- mice, basally and following physiological and pathological cardiac remodeling induced by a swim training programme and Angiotensin II treatment, respectively. Survival to weaning was reduced by 35% in GR+/- mice compared with wild-type (WT) littermates. Ultrasound analysis revealed impairment of systolic cardiac function in utero (E17.5) and at postnatal day (P) 2. However, by P7 cardiac function had normalised in surviving GR+/- mice and remained equivalent to WT littermates in adulthood. Heart weight and morphology were normal in GR+/- mice in adulthood but cardiomyocyte cross sectional area was reduced, in combination with an increase in nuclei per unit area implying an increased number of cardiomyocytes. This could arise from a delay in the developmental transition from hyperplasic to hypertrophic growth of cardiomyocytes and suggests that GR+/- mice may have a reduced ability to respond to the increased cardiac workload at birth and during the early postnatal period. Further cardiac challenge may be posed by the elevated blood pressure, compensatory increase in HPA axis activity and aldosterone levels previously reported in GR+/- mice. Adaptation to pathological cardiac challenge was assessed in adult GR+/- mice and WT littermates in response to AngII treatment, which has a direct hypertrophic effect on cardiomyocytes and, at higher doses, elevates blood pressure. GR+/- and WT mice showed an equivalent, dose-dependent increase in cardiomyocyte hypertrophy and cardiac fibrosis in response to AngII, as well as similar alterations in expression of Ca2+ handling genes.…

Subjects/Keywords: 616.1; glucocorticoid receptor; cardiac modeling

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Richardson, R. V. (2014). The role of the glucocorticoid receptor in cardiac growth and remodeling. (Doctoral Dissertation). University of Edinburgh. Retrieved from http://hdl.handle.net/1842/17930

Chicago Manual of Style (16^th Edition):

Richardson, Rachel Victoria. “The role of the glucocorticoid receptor in cardiac growth and remodeling.” 2014. Doctoral Dissertation, University of Edinburgh. Accessed January 18, 2021. http://hdl.handle.net/1842/17930.

MLA Handbook (7^th Edition):

Richardson, Rachel Victoria. “The role of the glucocorticoid receptor in cardiac growth and remodeling.” 2014. Web. 18 Jan 2021.

Vancouver:

Richardson RV. The role of the glucocorticoid receptor in cardiac growth and remodeling. [Internet] [Doctoral dissertation]. University of Edinburgh; 2014. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1842/17930.

Council of Science Editors:

Richardson RV. The role of the glucocorticoid receptor in cardiac growth and remodeling. [Doctoral Dissertation]. University of Edinburgh; 2014. Available from: http://hdl.handle.net/1842/17930

University of Minnesota

3. Perez Kerkvliet, Carlos. Post-translationally Modified Glucocorticoid Receptors and Protein Tyrosine Kinase 6 Modulate Triple Negative Breast Cancer Phenotypes.

Degree: PhD, Microbiology, Immunology and Cancer Biology, 2020, University of Minnesota

URL: http://hdl.handle.net/11299/216350

► Triple negative breast cancer (TNBC) is the most metastatic and deadly breast cancer subtype, accounting for 20-30% of all breast cancer cases. There is a… (more)

▼ Triple negative breast cancer (TNBC) is the most metastatic and deadly breast cancer subtype, accounting for 20-30% of all breast cancer cases. There is a critical need to identify molecular targets that could be exploited as new biomarkers of TNBC prognosis and for improving therapies. Although TNBC lacks estrogen and progesterone receptors, 15-40% of TNBC patients express the glucocorticoid receptor (GR). Women with TNBC that express high levels of GR have poor outcomes. We hypothesize that GR is a key mediator of advanced cancer phenotypes in TNBC. Altered signaling pathways typify breast cancer and serve as direct inputs to steroid hormone receptor “sensors.” We previously reported that phospho-Ser134-GR (pS134-GR) species are elevated in TNBC and cooperate with hypoxia-inducible factors, providing a novel avenue for activation of GR in response to local or cellular stress. Specifically, we propose that GR acts as a “sensor” for stress signaling pathways commonly activated by soluble factors that are abundant within the tumor microenvironment (TME) of TNBC. Herein, we show that in the absence of GR ligands, GR is transcriptionally activated via p38-dependent phosphorylation of Ser134 as a mechanism of homeostatic stress-sensing and regulated upon exposure of TNBC cells to TME-derived agents. The ligand-independent pS134-GR transcriptome encompasses Transforming Growth Factor β1 (TGFβ1) and Mitogen Activated Protein Kinase (MAPK) signaling gene sets associated with TNBC cell survival and migration/invasion. Accordingly, pS134-GR was essential for TNBC cell anchorage-independent growth in soft-agar, migration, invasion, and tumorsphere formation, an in vitro readout of cancer stemness properties. Both pS134-GR and expression of the MAPK-scaffolding molecule 14-3-3ζ were essential for a functionally intact p38 MAPK signaling pathway downstream of MAP3K5/ASK1, indicative of a feed-forward signaling loop wherein self-perpetuated GR phosphorylation enables cancer cell autonomy. A 24-gene pS134-GR-dependent signature induced by TGFβ1 predicts shortened overall survival in breast cancer patients. Additionally, GR is known to induce the expression of PTK6, a soluble protein tyrosine kinase important in mediating signaling in response to cellular stress. PTK6 is overexpressed in 86% of breast cancer patients, regardless of subtypes. Although GR is known to modulate PTK6 expression in TNBC, PTK6-driven signaling events in the context of TNBC are largely undefined. We sought to delineate the functions of downstream of PTK6. To do this, we created kinase-dead (KM) and kinase-intact domain structure mutants of PTK6 via in frame deletions of the N-terminal SH3 or SH2 domains. While the PTK6 kinase domain contributed to soft-agar colony formation, PTK6 kinase activity was entirely dispensable for cell migration. Specifically, TNBC models expressing a PTK6 variant lacking the SH2 domain (SH2-del PTK6) were unresponsive to growth factor-stimulated cell motility relative to SH3-del, KM or wild-type PTK6 controls. Reverse phase…

Subjects/Keywords: Breast Cancer; Glucocorticoid Receptor; phosphorylation

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Perez Kerkvliet, C. (2020). Post-translationally Modified Glucocorticoid Receptors and Protein Tyrosine Kinase 6 Modulate Triple Negative Breast Cancer Phenotypes. (Doctoral Dissertation). University of Minnesota. Retrieved from http://hdl.handle.net/11299/216350

Chicago Manual of Style (16^th Edition):

Perez Kerkvliet, Carlos. “Post-translationally Modified Glucocorticoid Receptors and Protein Tyrosine Kinase 6 Modulate Triple Negative Breast Cancer Phenotypes.” 2020. Doctoral Dissertation, University of Minnesota. Accessed January 18, 2021. http://hdl.handle.net/11299/216350.

MLA Handbook (7^th Edition):

Perez Kerkvliet, Carlos. “Post-translationally Modified Glucocorticoid Receptors and Protein Tyrosine Kinase 6 Modulate Triple Negative Breast Cancer Phenotypes.” 2020. Web. 18 Jan 2021.

Vancouver:

Perez Kerkvliet C. Post-translationally Modified Glucocorticoid Receptors and Protein Tyrosine Kinase 6 Modulate Triple Negative Breast Cancer Phenotypes. [Internet] [Doctoral dissertation]. University of Minnesota; 2020. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/11299/216350.

Council of Science Editors:

Perez Kerkvliet C. Post-translationally Modified Glucocorticoid Receptors and Protein Tyrosine Kinase 6 Modulate Triple Negative Breast Cancer Phenotypes. [Doctoral Dissertation]. University of Minnesota; 2020. Available from: http://hdl.handle.net/11299/216350

University of Manchester

4. Trebble, Peter. Glucocorticoid receptor function : new insights from genetic and chemical biology approaches.

Degree: PhD, 2013, University of Manchester

URL: https://www.research.manchester.ac.uk/portal/en/theses/glucocorticoid-receptor-function-new-insights-from-genetic-and-chemical-biology-approaches(b55c612b-eda1-4908-a0df-ec916f03ade2).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.588151

► Glucocorticoids (Gc) are vital for development, maintenance of glucose homeostasis and the resolution of inflammation. As potent modulators of the immune response Gc are routinely… (more)

▼ Glucocorticoids (Gc) are vital for development, maintenance of glucose homeostasis and the resolution of inflammation. As potent modulators of the immune response Gc are routinely prescribed in the management of a variety of inflammatory diseases including asthma and rheumatoid arthritis. However clinical use of Gc is limited by variation in patient sensitivity to Gc treatment and development of a wide range of side effects. In this thesis I present two studies that have advanced our understanding of Gc action in vivo. The first defines and characterises the cause of familial glucocorticoid resistance, and the second describes the action of two potent non-steroidal Gc in a cell line model. Familial Gc Resistance: Cases of primary generalised Gc resistance are very rare and typically present as mineralocorticoid and androgen excess leading to hypertension, hypokalemia and hirsutism. Gc resistance is attributed to loss of function mutations within the glucocorticoid receptor (GR). Here I identify a family with a novel mutation in GR exon 6 that gives rise to a very mild phenotype. Analysis of transformed patient peripheral blood lymphocytes revealed a 50% reduction in full length GR but no expression of a mutant form. As this did not rule out expression in vivo, the mutant receptor (Δ612GR) was characterised in a cell line. Investigation using reporter genes revealed that Δ612GR lacked any activity, but had dominant negative action when co expressed with full length GR. In response to Gc Δ612GR was not phosphorylated or targeted for degradation. Fluorophore tagged Δ612GR was unable to translocate to the nucleus in response to Gc, but delayed the translocation of full length GR when co-expressed. Together this indicates that Δ612GR is unable to bind ligand but has dominant negative action upon full length GR most likely due to heterodimerisation. Therefore I describe a novel GR mutation that results in Gc resistance but presents with a mild very phenotype. Novel Non-steroidal Gc: Non-steroidal Gc can be used as tools to determine how ligand structure directs GR function. Here I describe two highly potent non steroidal Gc ligands, GSK47867A and GSK47869A which alter the kinetics of receptor activity. Treatment with either ligand induces slow GR nuclear translocation, promotes GR nuclear retention and prolongs transcriptional activity following ligand withdrawal. Crystal structure analysis revealed that GSK47867A and GSK47869A specifically alter the surface charge of the GR at a site important for Hsp90 binding. GR bound to GSK47867A and GSK47869A shows prolonged activity in the presence of Hsp90 inhibitor geldanamycin. Therefore this work identifies a new chemical series that could prolong GR activity due to altered pharmacodynamics rather than altered pharmacokinetics.In summary this work uses a combination of genetic and chemical biology approaches to broaden our understanding of GR function. Characterisation of naturally occurring GR mutations gives insight into the complex function of the GR, and non-steroidal Gc act…

Subjects/Keywords: 616.07; Glucocorticoid receptor; Non steroidal glucocorticoid; Crystal structure; Familial glucocorticoid resistance

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Trebble, P. (2013). Glucocorticoid receptor function : new insights from genetic and chemical biology approaches. (Doctoral Dissertation). University of Manchester. Retrieved from https://www.research.manchester.ac.uk/portal/en/theses/glucocorticoid-receptor-function-new-insights-from-genetic-and-chemical-biology-approaches(b55c612b-eda1-4908-a0df-ec916f03ade2).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.588151

Chicago Manual of Style (16^th Edition):

Trebble, Peter. “Glucocorticoid receptor function : new insights from genetic and chemical biology approaches.” 2013. Doctoral Dissertation, University of Manchester. Accessed January 18, 2021. https://www.research.manchester.ac.uk/portal/en/theses/glucocorticoid-receptor-function-new-insights-from-genetic-and-chemical-biology-approaches(b55c612b-eda1-4908-a0df-ec916f03ade2).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.588151.

MLA Handbook (7^th Edition):

Trebble, Peter. “Glucocorticoid receptor function : new insights from genetic and chemical biology approaches.” 2013. Web. 18 Jan 2021.

Vancouver:

Trebble P. Glucocorticoid receptor function : new insights from genetic and chemical biology approaches. [Internet] [Doctoral dissertation]. University of Manchester; 2013. [cited 2021 Jan 18]. Available from: https://www.research.manchester.ac.uk/portal/en/theses/glucocorticoid-receptor-function-new-insights-from-genetic-and-chemical-biology-approaches(b55c612b-eda1-4908-a0df-ec916f03ade2).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.588151.

Council of Science Editors:

Trebble P. Glucocorticoid receptor function : new insights from genetic and chemical biology approaches. [Doctoral Dissertation]. University of Manchester; 2013. Available from: https://www.research.manchester.ac.uk/portal/en/theses/glucocorticoid-receptor-function-new-insights-from-genetic-and-chemical-biology-approaches(b55c612b-eda1-4908-a0df-ec916f03ade2).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.588151

5. Matsusue, Yumiko; Horii-Hayashi, Noriko; Kirita, Tadaaki. Distribution of corticosteroid receptors in mature oligodendrocytes and oligodendrocyte progenitors of the adult mouse brain. : 成体マウス脳の成熟および未成熟オリゴデンドロサイトにおけるコルチコイステロイドレセプタ−の分布.

Degree: 博士（医学）, 2014, Nara Medical University / 奈良県立医科大学

URL: http://hdl.handle.net/10564/2705

►

The expression of glucocorticoid receptors (GRs) was investigated immunohistochemically in two different lineages of oligodendrocytes, using carbonic anhydrase (CA) II and neuron glial antigen (NG)… (more)

Subjects/Keywords: Glucocorticoid receptor; cofactor; corticosteroid (glucocorticoid); mineralocorticoid receptor; oligodendrocyte; oligodendrocyte progenitor

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Matsusue, Yumiko; Horii-Hayashi, Noriko; Kirita, T. (2014). Distribution of corticosteroid receptors in mature oligodendrocytes and oligodendrocyte progenitors of the adult mouse brain. : 成体マウス脳の成熟および未成熟オリゴデンドロサイトにおけるコルチコイステロイドレセプタ−の分布. (Thesis). Nara Medical University / 奈良県立医科大学. Retrieved from http://hdl.handle.net/10564/2705

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):

Matsusue, Yumiko; Horii-Hayashi, Noriko; Kirita, Tadaaki. “Distribution of corticosteroid receptors in mature oligodendrocytes and oligodendrocyte progenitors of the adult mouse brain. : 成体マウス脳の成熟および未成熟オリゴデンドロサイトにおけるコルチコイステロイドレセプタ−の分布.” 2014. Thesis, Nara Medical University / 奈良県立医科大学. Accessed January 18, 2021. http://hdl.handle.net/10564/2705.

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

MLA Handbook (7^th Edition):

Matsusue, Yumiko; Horii-Hayashi, Noriko; Kirita, Tadaaki. “Distribution of corticosteroid receptors in mature oligodendrocytes and oligodendrocyte progenitors of the adult mouse brain. : 成体マウス脳の成熟および未成熟オリゴデンドロサイトにおけるコルチコイステロイドレセプタ−の分布.” 2014. Web. 18 Jan 2021.

Vancouver:

Matsusue, Yumiko; Horii-Hayashi, Noriko; Kirita T. Distribution of corticosteroid receptors in mature oligodendrocytes and oligodendrocyte progenitors of the adult mouse brain. : 成体マウス脳の成熟および未成熟オリゴデンドロサイトにおけるコルチコイステロイドレセプタ−の分布. [Internet] [Thesis]. Nara Medical University / 奈良県立医科大学; 2014. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/10564/2705.

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

Council of Science Editors:

Matsusue, Yumiko; Horii-Hayashi, Noriko; Kirita T. Distribution of corticosteroid receptors in mature oligodendrocytes and oligodendrocyte progenitors of the adult mouse brain. : 成体マウス脳の成熟および未成熟オリゴデンドロサイトにおけるコルチコイステロイドレセプタ−の分布. [Thesis]. Nara Medical University / 奈良県立医科大学; 2014. Available from: http://hdl.handle.net/10564/2705

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

Univerzitet u Beogradu

6. Ognjanović, Sanja I., 1967-. Glukokortikoidna senzitivnost, funkcionalni polimorfizmi gena za gltokortikoidni receptor i ekspresija glukokortikoidnog receptora u tumorskom tkivu kod pacijenata sa slučajno otkrivenim tumorima kore nadbubrežne žlezde.

Degree: Medicinski fakultet, 2016, Univerzitet u Beogradu

URL: https://fedorabg.bg.ac.rs/fedora/get/o:14120/bdef:Content/get

►

Medicina - Interna medicina-endokrinologija / Medicine - Internal medicine - endocrinology

Uvod: Adrenalni incidentalomi su tumori otkriveni različitim vizualizacionim metodama učinjenim bez sumnje na adrenalnu… (more)

▼

Medicina - Interna medicina-endokrinologija / Medicine - Internal medicine - endocrinology

Uvod: Adrenalni incidentalomi su tumori otkriveni različitim vizualizacionim metodama učinjenim bez sumnje na adrenalnu patologiju. Većina ovih tumora su nefunkcijski adrenokortikalni adenomi. Izvestan broj AI se prezentuje subkliničkim hiperkorticizmom (SH), stanjem biohemijskog kortizolskog ekscesa, u odsustvu klasičnih znakova i simptoma hiperkorticizma. Prevalencija SH kod pacijenata sa AI se procenjuje između 5 i 24%. Polimorfizam gena za glukokortikoidni receptor (GR) menja glukokortikoidnu (GC) senzitivnost, što dovodi do promena u metaboličkom profilu. Cilj studije: je bio da se ispita prevalenca subkliničkog hiperkorticizma (SH) i pridruženih bolesti kod pacijenata sa unilateralnim (UAI) i bilateralnim AI (BAI). Ispitivali smo učestalost četiri polimorfizma gena za GR (BclI, ER22/23EK, N363S i 9β) i predispoziciju za nastanak AI. Analizirali smo ekspresiju GR u tumorskom, peritumorskom i normalnom adrenalnom tkivu. Materijal i metode: Ispitivanje je obuhvatilo 152 pacijenta, 105 (69.1%) sa UAI i 47 (30.9%) sa BAI. SH je definisan na osnovu serumskog kortizola >50nmol/L nakon prekonoćnog deksametazon supresivnog testa (DST) sa 1mg ili nakon dvodnevnog niskodoznog DST (LDDST) sa 2mg deksametazona, uz još jedan navedeni parametar (ponoćni serumski kortizol >208nmol/L, 24-h urinarni slobodni kortizol >245nmol/L ili ACTH<10ng/L). Telesni sastav i koštana gustina su mereni dual-energy X-ray absorptiometry metodom na nivou lumbalnog dela kičme, vrata femura i celog skeleta. DNK je dobijena iz leukocita periferne krvi. Prisustvo polimorfizama je detektovano metodama PCR, RFLP i sekvenciranjem DNK. Uzorci tkiva su analizirani Western blot metodom. Rezultati: Pacijenti sa BAI se nisu razlikovali u odnosu na pacijente sa UAI po starosti, BMI, obimu struka, učestalosti dijabetesa, hipertenzije i dislipidemije. Prevalencija SH u celoj grupi iznosila je 20.5% (prekonoćni DST), odnosno 20.0% (LDDST) i bila je značajno veća kod pacijenata sa BAI u odnosu na pacijente sa UAI (31.1% vs 15.2%, p=0.026). Nezavisni prediktor SH je bila veličina adrenalnog adenoma (odds ratio [OR]=1.055, 95% confidence interval [CI] 1.017-1.094, p=0.004), nakon korekcije za godine, obim struka, indeks telesne mase i prisustvo BAI. Kostna gustina na nivou kičme je bila značajno niža kod pacijenata sa BAI u odnosu na UAI (0.96±0.14 vs 0.87±0.15, p=0.002). Nije nađena razlika u kostnoj gustini na nivou vrata femura...

Advisors/Committee Members: Damjanović, Svetozar, 1953-.

Subjects/Keywords: adrenal incidentaloma; osteoporosis; subclinical hypercortisolism, glucocorticoid receptor, polymorphisms, glucocorticoid sensitivity

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Ognjanović, Sanja I., 1. (2016). Glukokortikoidna senzitivnost, funkcionalni polimorfizmi gena za gltokortikoidni receptor i ekspresija glukokortikoidnog receptora u tumorskom tkivu kod pacijenata sa slučajno otkrivenim tumorima kore nadbubrežne žlezde. (Thesis). Univerzitet u Beogradu. Retrieved from https://fedorabg.bg.ac.rs/fedora/get/o:14120/bdef:Content/get

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):

Ognjanović, Sanja I., 1967-. “Glukokortikoidna senzitivnost, funkcionalni polimorfizmi gena za gltokortikoidni receptor i ekspresija glukokortikoidnog receptora u tumorskom tkivu kod pacijenata sa slučajno otkrivenim tumorima kore nadbubrežne žlezde.” 2016. Thesis, Univerzitet u Beogradu. Accessed January 18, 2021. https://fedorabg.bg.ac.rs/fedora/get/o:14120/bdef:Content/get.

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

MLA Handbook (7^th Edition):

Ognjanović, Sanja I., 1967-. “Glukokortikoidna senzitivnost, funkcionalni polimorfizmi gena za gltokortikoidni receptor i ekspresija glukokortikoidnog receptora u tumorskom tkivu kod pacijenata sa slučajno otkrivenim tumorima kore nadbubrežne žlezde.” 2016. Web. 18 Jan 2021.

Vancouver:

Ognjanović, Sanja I. 1. Glukokortikoidna senzitivnost, funkcionalni polimorfizmi gena za gltokortikoidni receptor i ekspresija glukokortikoidnog receptora u tumorskom tkivu kod pacijenata sa slučajno otkrivenim tumorima kore nadbubrežne žlezde. [Internet] [Thesis]. Univerzitet u Beogradu; 2016. [cited 2021 Jan 18]. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:14120/bdef:Content/get.

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

Council of Science Editors:

Ognjanović, Sanja I. 1. Glukokortikoidna senzitivnost, funkcionalni polimorfizmi gena za gltokortikoidni receptor i ekspresija glukokortikoidnog receptora u tumorskom tkivu kod pacijenata sa slučajno otkrivenim tumorima kore nadbubrežne žlezde. [Thesis]. Univerzitet u Beogradu; 2016. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:14120/bdef:Content/get

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

NSYSU

7. Lee, Bi-yao. Investigations of The Effects of Glucocorticoid Receptor SNPs and SUMO-2 Autoantibody in Patients with Systemic Lupus Erythematosus.

Degree: Master, Institute of Biomedical Sciences, 2008, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0730108-135015

► For more than fifty years glucocorticoids (GCs) has been used to treat a wide range of inflammatory diseases, such as allergies, asthma, rheumatoid arthritis, and… (more)

Subjects/Keywords: polymorphism; SUMO-2; glucocorticoid receptor; SLE

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Lee, B. (2008). Investigations of The Effects of Glucocorticoid Receptor SNPs and SUMO-2 Autoantibody in Patients with Systemic Lupus Erythematosus. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0730108-135015

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):

Lee, Bi-yao. “Investigations of The Effects of Glucocorticoid Receptor SNPs and SUMO-2 Autoantibody in Patients with Systemic Lupus Erythematosus.” 2008. Thesis, NSYSU. Accessed January 18, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0730108-135015.

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

MLA Handbook (7^th Edition):

Lee, Bi-yao. “Investigations of The Effects of Glucocorticoid Receptor SNPs and SUMO-2 Autoantibody in Patients with Systemic Lupus Erythematosus.” 2008. Web. 18 Jan 2021.

Vancouver:

Lee B. Investigations of The Effects of Glucocorticoid Receptor SNPs and SUMO-2 Autoantibody in Patients with Systemic Lupus Erythematosus. [Internet] [Thesis]. NSYSU; 2008. [cited 2021 Jan 18]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0730108-135015.

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

Council of Science Editors:

Lee B. Investigations of The Effects of Glucocorticoid Receptor SNPs and SUMO-2 Autoantibody in Patients with Systemic Lupus Erythematosus. [Thesis]. NSYSU; 2008. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0730108-135015

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

Queens University

8. Nesset, Kirsten A. Characterization of Glucocorticoid Receptor Promoter Methylation in Breast Cancer .

Degree: Biochemistry, 2012, Queens University

URL: http://hdl.handle.net/1974/7521

► Epidemiological studies have identified psychological stress as a significant risk factor in breast cancer. The stress response is regulated by the HPA axis in the… (more)

▼ Epidemiological studies have identified psychological stress as a significant risk factor in breast cancer. The stress response is regulated by the HPA axis in the brain and is mediated by glucocorticoid receptor (GR) signalling. It has been found that early life events can affect epigenetic programming of GR, and methylation of the GR promoter has been reported in colorectal tumourigenesis. Decreased GR expression has also been observed in breast cancer. In addition, it has been previously demonstrated that unliganded GR can serve as a direct activator of the BRCA1 promoter in mammary epithelial cells. We propose a model whereby methylation of the GR promoter in the breast significantly lowers GR expression, resulting in insufficient BRCA1 promoter activation and an increased risk of developing cancer. Antibody-based methylated DNA enrichment was followed by qPCR analysis (MeDIP-qPCR) in a novel assay developed to detect locus-specific methylation levels. It was found that 13% of primary breast tumours were hypermethylated at the GR proximal promoter whereas no methylation was detected in normal tissue. RT-PCR and 5’ RACE analysis identified exon 1B as the predominant alternative first exon in the breast. Tumours methylated near exon 1B had decreased GR expression compared to unmethylated samples, suggesting that this region is important for transcriptional regulation of GR. It was also determined that GR and BRCA1 expression was decreased in breast tumour compared to normal tissue. Furthermore, the relative expression of GR and BRCA1 measured by qRT-PCR was correlated in normal tissue but this association was not found in tumour tissue. From this, it appears that lower GR levels with associated decreased BRCA1 expression in tissues may be a predisposing factor for breast cancer. Based on these results we propose a role for GR as a potential tumour suppressor gene in the breast due to its association with BRCA1, also a tumour suppressor gene, as well as its consistently decreased expression in breast tumours and methylation of its proximal promoter in a subset of cancer patients.

Subjects/Keywords: Glucocorticoid Receptor ; Epigenetic ; Breast cancer ; Methylation

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Nesset, K. A. (2012). Characterization of Glucocorticoid Receptor Promoter Methylation in Breast Cancer . (Thesis). Queens University. Retrieved from http://hdl.handle.net/1974/7521

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):

Nesset, Kirsten A. “Characterization of Glucocorticoid Receptor Promoter Methylation in Breast Cancer .” 2012. Thesis, Queens University. Accessed January 18, 2021. http://hdl.handle.net/1974/7521.

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

MLA Handbook (7^th Edition):

Nesset, Kirsten A. “Characterization of Glucocorticoid Receptor Promoter Methylation in Breast Cancer .” 2012. Web. 18 Jan 2021.

Vancouver:

Nesset KA. Characterization of Glucocorticoid Receptor Promoter Methylation in Breast Cancer . [Internet] [Thesis]. Queens University; 2012. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1974/7521.

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

Council of Science Editors:

Nesset KA. Characterization of Glucocorticoid Receptor Promoter Methylation in Breast Cancer . [Thesis]. Queens University; 2012. Available from: http://hdl.handle.net/1974/7521

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

Queens University

9. Ritter, Heather. The Unliganded Glucocorticoid Receptor as a Transcriptional Regulator in Mammary Epithelial Cells .

Degree: Biochemistry, 2012, Queens University

URL: http://hdl.handle.net/1974/7672

► This work presents the first evidence of a ligand-independent role for the glucocorticoid receptor (GR) as a positive regulator of gene expression in mammary cells.… (more)

▼ This work presents the first evidence of a ligand-independent role for the glucocorticoid receptor (GR) as a positive regulator of gene expression in mammary cells. We have demonstrated that unliganded GR interacts directly with the promoter of the tumour suppressor gene BRCA1, and upregulates its expression. The presence of the stress hormone hydrocortisone (HC) abolished this interaction and resulted in repression of BRCA1. Since low levels of BRCA1 have been implicated in the development of sporadic breast cancer, this may represent a novel mechanism through which prolonged stress signaling increases breast cancer risk. We determined that the interaction between unliganded GR and BRCA1 is mediated through the beta subunit of the Ets transcription factor GABP at the RIBS promoter element. GR and GABPβ were shown to interact in both co-immunoprecipitation and mammalian two-hybrid assays, and this interaction involved the N-terminal to central regions of both proteins. To further characterize the role of unliganded GR in breast cells, we used shRNA to generate mouse mammary cell lines with depleted endogenous GR expression. Loss of GR resulted in an impaired capacity of cells to differentiate into acini, but this effect was rescued by the addition of glucocorticoids, implicating both the liganded and unliganded forms of GR as key regulators of differentiation. We performed expression microarray to identify targets of unliganded GR using the GR-depleted cell lines. This analysis revealed 260 genes negatively regulated and 343 genes positively regulated by unliganded GR. Many of the positively regulated genes were involved in pro-apoptotic networks, and appeared to oppose the activity of liganded GR targets. Validation and further analysis of five candidates of positive regulation by unliganded GR indicated that two of these, Hsd11b1 and Ch25h, were regulated by unliganded GR in a manner similar to Brca1. The Hsd11b1 enzyme regulates intracellular glucocorticoid levels by interconverting cortisol and its inactive metabolite, cortisone. Further investigation of Hsd11b1 expression and regulation indicated that Hsd11b1 activity appears to be unidirectional in breast cells, specifically inactivating cortisol. Overall, this work suggests that gene regulation by unliganded GR represents a mechanism for protecting the breast from tumourigenesis during stress.

Subjects/Keywords: Stress ; Unliganded ; Glucocorticoid Receptor ; Breast Cancer

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Ritter, H. (2012). The Unliganded Glucocorticoid Receptor as a Transcriptional Regulator in Mammary Epithelial Cells . (Thesis). Queens University. Retrieved from http://hdl.handle.net/1974/7672

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):

Ritter, Heather. “The Unliganded Glucocorticoid Receptor as a Transcriptional Regulator in Mammary Epithelial Cells .” 2012. Thesis, Queens University. Accessed January 18, 2021. http://hdl.handle.net/1974/7672.

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

MLA Handbook (7^th Edition):

Ritter, Heather. “The Unliganded Glucocorticoid Receptor as a Transcriptional Regulator in Mammary Epithelial Cells .” 2012. Web. 18 Jan 2021.

Vancouver:

Ritter H. The Unliganded Glucocorticoid Receptor as a Transcriptional Regulator in Mammary Epithelial Cells . [Internet] [Thesis]. Queens University; 2012. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1974/7672.

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

Council of Science Editors:

Ritter H. The Unliganded Glucocorticoid Receptor as a Transcriptional Regulator in Mammary Epithelial Cells . [Thesis]. Queens University; 2012. Available from: http://hdl.handle.net/1974/7672

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

University of Manchester

10. Platt, Eleanor. Mechanisms of glucocorticoid-induced apoptosis in small cell lung cancer.

Degree: 2014, University of Manchester

URL: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:217997

►

Small cell lung cancer (SCLC) tumours are very aggressive. Patients often present with metastases at diagnosis and prognosis is very poor. SCLC cell lines have… (more)

▼

Small cell lung cancer (SCLC) tumours are very aggressive. Patients often present with metastases at diagnosis and prognosis is very poor. SCLC cell lines have been shown to be resistant to glucocorticoids due to impaired glucocorticoid receptor (GR) expression (Gaitan et al, 1995; Ray et al, 1996). Restoration of GR expression in these cells triggers apoptosis in vitro (Sommer et al, 2007) and in vivo (Sommer et al, 2010). It is possible that loss of GR expression plays a role in SCLC pathogenesis and therefore GR could be considered as a novel tumour suppressor gene for SCLC.Over-expression of exogenous GR restores glucocorticoid sensitivity in SCLC cells and triggers glucocorticoid-induced apoptosis, both in vitro (Sommer et al, 2007) and in vivo. (Sommer et al, 2010). The mechanisms underlying regulation of GR expression and glucocorticoid-induced apoptosis in these cells are not fully understood. This thesis aims to investigate the regulation of GR in relation to glucocorticoid-induced apoptosis in SCLC cell lines.Quantitative PCR data showed that GR gene expression was not altered by glucocorticoid treatment in SCLC cell line DMS-79 cells. Levels of GR protein were seen to be very low in these cells and were not affected by an increase in cell number / density or treatment with low concentrations of glucocorticoids. A decrease in GR protein levels was observed following treatment of DMS-79 cells with very high concentrations of dexamethasone or hydrocortisone, however GR protein levels returned to that of untreated cells following removal of glucocorticoids. GR protein levels were also found to be very low in vivo, as demonstrated by immunohistochemistry of DMS-79 cell xenografts. This suggests that DMS-79 cells tightly regulate GR protein levels in order to evade glucocorticoid-induced apoptosis.A number of approaches to increase GR protein levels in DMS-79 cells were investigated, with a view to conferring glucocorticoid sensitivity to these cells. DMS-79 cells did not show auto-upregulation of GR from promoter 1A following treatment with glucocorticoids and attempts to stably transfect these cells with a construct containing GR under the control of a tetracycline-inducible promoter were unsuccessful. Further investigation into approaches to increase GR protein levels should be undertaken since understanding the mechanisms underlying glucocorticoid-induced apoptosis may provide insight into novel therapeutic approaches for SCLC patients.

Small cell lung cancer (SCLC) is a very aggressive form of lung cancer. Tumours can quickly spread throughout the patient’s body and treatment of SCLC is very difficult. We use human SCLC cells, derived from patient tumours as a way to investigate how to kill these tumour cells. The glucocorticoid receptor (GR) is a regulator which can help kill tumour cells. We have found that SCLC cells have less GR than non-SCLC cells, allowing these cells to survive and grow. Increasing the amount of GR in SCLC cell lines makes these cells more likely to die. Therefore it is important…

Advisors/Committee Members: TOURNIER, CATHY C, White, Anne, Tournier, Cathy.

Subjects/Keywords: Glucocorticoid receptor; Small cell lung cancer

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Platt, E. (2014). Mechanisms of glucocorticoid-induced apoptosis in small cell lung cancer. (Doctoral Dissertation). University of Manchester. Retrieved from http://www.manchester.ac.uk/escholar/uk-ac-man-scw:217997

Chicago Manual of Style (16^th Edition):

Platt, Eleanor. “Mechanisms of glucocorticoid-induced apoptosis in small cell lung cancer.” 2014. Doctoral Dissertation, University of Manchester. Accessed January 18, 2021. http://www.manchester.ac.uk/escholar/uk-ac-man-scw:217997.

MLA Handbook (7^th Edition):

Platt, Eleanor. “Mechanisms of glucocorticoid-induced apoptosis in small cell lung cancer.” 2014. Web. 18 Jan 2021.

Vancouver:

Platt E. Mechanisms of glucocorticoid-induced apoptosis in small cell lung cancer. [Internet] [Doctoral dissertation]. University of Manchester; 2014. [cited 2021 Jan 18]. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:217997.

Council of Science Editors:

Platt E. Mechanisms of glucocorticoid-induced apoptosis in small cell lung cancer. [Doctoral Dissertation]. University of Manchester; 2014. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:217997

University of Edinburgh

11. Rog-Zielinska, Eva Alicia. Role of glucocorticoid signalling in fetal heart development and maturation.

Degree: PhD, 2013, University of Edinburgh

URL: http://hdl.handle.net/1842/8086

► Glucocorticoids are steroid hormones that affect a variety of physiological and pathological processes both throughout development and in adult life. During mammalian fetal growth, the… (more)

▼ Glucocorticoids are steroid hormones that affect a variety of physiological and pathological processes both throughout development and in adult life. During mammalian fetal growth, the late gestation rise in fetal glucocorticoid levels is essential for the maturation of tissues and organs in preparation for birth. In humans, glucocorticoids are routinely administered to women threatened by a preterm labour to accelerate fetal lung maturation and prevent neonatal respiratory distress and mice lacking glucocorticoid receptor (GR-/- mice) die neonatally as they are unable to inflate their lungs due to severe pulmonary immaturity. Apart from their importance for proper lung maturation, the physiological role of glucocorticoids in the development of other organs and tissues is not well known. However, prenatal exposure to excess glucocorticoids was shown to elicit detrimental “programming” effects, raising the susceptibility to adult diseases such as hypertension, obesity and metabolic disturbances in both humans and animal models. I therefore used global and conditional GR knock out mouse models to investigate the role and importance of adequate glucocorticoid signalling in fetal heart development and maturation. I further confirmed the direct effects of glucocorticoids on the cardiomyocyte structure and function in an in vitro setting. GR-/- fetuses are under-represented in late gestation (>50% of the number of GR+/+ littermates) but are present in the expected mendelian ratio at E14.5. At E17.5, GR-/- fetuses show edema (increased fluid accumulation and body sodium content). Excess extracellular fluid accumulation could be a result of a congenital heart failure. During development, corticosterone levels sharply increase within the fetal hearts at E15.5-E16.5, coincident with nuclear translocation of GR. Consistent with activation of GR only after this time, the phenotypic consequences of GR deficiency can be seen after E16.5 and not before. At E17.5, hearts of GR-/- fetuses are smaller than in GR+/+ but display no structural abnormalities. Cardiac function however is severely impaired, with left ventricular systolic and diastolic performance inferior in GR-/- fetuses compared to their wild-type littermates. Microscopically, at E17.5, the structure of the cardiac muscle and individual cardiomyocytes are affected by the lack of GR. The normal outer muscle layer, with characteristic rod-shaped, aligned cardiomyocytes is not discernable in the GR-/- heart. Within the cardiomyocytes, myofibrils are short, undefined and randomly scattered within the cell. Lack of the maturational progression in the GR-/- hearts at E17.5 is evident in the pattern of gene expression. GR-/- fetuses do not display the normal gestational changes between E14.5 and E17.5 that are seen in control mice, including in genes involved in the maturation of cardiac structure (eg myosin heavy chain-α, MyHC-α), function (atrial natriuretic peptide, ANP), energy metabolism (eg hexokinase-1, PPARγ coactivator-1α, PGC-1α) and calcium handling (ryanodine…

Subjects/Keywords: 612.6; fetal heart; glucocorticoid receptor; maturation

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Rog-Zielinska, E. A. (2013). Role of glucocorticoid signalling in fetal heart development and maturation. (Doctoral Dissertation). University of Edinburgh. Retrieved from http://hdl.handle.net/1842/8086

Chicago Manual of Style (16^th Edition):

Rog-Zielinska, Eva Alicia. “Role of glucocorticoid signalling in fetal heart development and maturation.” 2013. Doctoral Dissertation, University of Edinburgh. Accessed January 18, 2021. http://hdl.handle.net/1842/8086.

MLA Handbook (7^th Edition):

Rog-Zielinska, Eva Alicia. “Role of glucocorticoid signalling in fetal heart development and maturation.” 2013. Web. 18 Jan 2021.

Vancouver:

Rog-Zielinska EA. Role of glucocorticoid signalling in fetal heart development and maturation. [Internet] [Doctoral dissertation]. University of Edinburgh; 2013. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1842/8086.

Council of Science Editors:

Rog-Zielinska EA. Role of glucocorticoid signalling in fetal heart development and maturation. [Doctoral Dissertation]. University of Edinburgh; 2013. Available from: http://hdl.handle.net/1842/8086

University of Manchester

12. Morgan, David. Application of systems biology to dissect glucocorticoid receptor function.

Degree: PhD, 2013, University of Manchester

URL: https://www.research.manchester.ac.uk/portal/en/theses/application-of-systems-biology-to-dissect-glucocorticoid-receptor-function(95b588bd-e84c-4f06-8341-d17cf47f235e).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.607066

► Glucocorticoids (Gc) are essential for life. Clinically, Gcs are potent anti-inflammatory agents, prescribed as first line treatment for a range of inflammatory disorders, including rheumatoid… (more)

▼ Glucocorticoids (Gc) are essential for life. Clinically, Gcs are potent anti-inflammatory agents, prescribed as first line treatment for a range of inflammatory disorders, including rheumatoid arthritis and asthma. In this thesis I present two studies that advance our understanding of the diverse actions of Gcs by using bioinformatics approaches. I have identified the functional network of two glucocorticoid receptor (GR) isoforms and characterised the effects of Gcs on cell function. Study 1 Systems analysis of GR function: Gcs regulate a diverse range of biological processes through a single receptor. How this is achieved is unclear, but it is thought at least in part to be due to the tissue specific expression of GR isoforms. The constitutive splice variant, GRγ is conserved through mammalian evolution, suggesting a gain of function, but currently no clear biological role has been identified. GRγ differs from the most abundant GR isoform, GRα by a single arginine inserted in the DNA binding domain (DBD) of GRγ, and may therefore affect the transcriptome profile and protein interactions of the receptor. Indeed, marked differences between the GRα and GRγ interactomes were revealed by proteomic analysis, identifying a potential association of GRγ with the mitochondria. These differences in the protein interactomes were accompanied by altered intracellular distributions. A clear tangible result of these differences is an observed delay in both the translocation kinetics and transactivation potential of GRγ. Analysis of the GRγ regulated transcriptome revealed a clear distinction in the regulation of a subset of target genes. Gene ontology and gene enrichment analysis identified oxidative phosphorylation protein degradation and cell morphology as potential GRγ specific functions. These findings suggest a distinct biological role is conferred by the additional arginine in the level arm of the DBD.Study 2 Mathematical modelling of GR function: Cell migration is a fundamental biological process. Clinically, Gcs inhibit wound healing, yet the mechanisms by which Gcs regulate migration remain unclear. The impact of Gcs on cellular motility was initially characterised through traditional migration assays. However, as cell populations are heterogeneous, live cell microscopy and mathematical modelling were employed to monitor the response of single cells. Dynamic tracking of migration in individual cells revealed that the movement of A549 cells is modelled by an alpha stable distribution. Gcs changes the parameters of the distribution, without altering the nature of the walk statistics. Gcs reduce the overall displacement of a cell, by causing a significant shift in step length selection, resulting in a reduction of the large steps, and replacement with short steps. Changes in migration following treatment with Gcs were seen within hours, which is much faster than previously reported. To identify a potential mechanism a panel of actin cytoskeleton regulators were screened, but prolonged exposure of Gcs were required to see a…

Subjects/Keywords: 615.7; Glucocorticoid Receptor; Systems Biology; Migration; GRgamma

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Morgan, D. (2013). Application of systems biology to dissect glucocorticoid receptor function. (Doctoral Dissertation). University of Manchester. Retrieved from https://www.research.manchester.ac.uk/portal/en/theses/application-of-systems-biology-to-dissect-glucocorticoid-receptor-function(95b588bd-e84c-4f06-8341-d17cf47f235e).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.607066

Chicago Manual of Style (16^th Edition):

Morgan, David. “Application of systems biology to dissect glucocorticoid receptor function.” 2013. Doctoral Dissertation, University of Manchester. Accessed January 18, 2021. https://www.research.manchester.ac.uk/portal/en/theses/application-of-systems-biology-to-dissect-glucocorticoid-receptor-function(95b588bd-e84c-4f06-8341-d17cf47f235e).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.607066.

MLA Handbook (7^th Edition):

Morgan, David. “Application of systems biology to dissect glucocorticoid receptor function.” 2013. Web. 18 Jan 2021.

Vancouver:

Morgan D. Application of systems biology to dissect glucocorticoid receptor function. [Internet] [Doctoral dissertation]. University of Manchester; 2013. [cited 2021 Jan 18]. Available from: https://www.research.manchester.ac.uk/portal/en/theses/application-of-systems-biology-to-dissect-glucocorticoid-receptor-function(95b588bd-e84c-4f06-8341-d17cf47f235e).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.607066.

Council of Science Editors:

Morgan D. Application of systems biology to dissect glucocorticoid receptor function. [Doctoral Dissertation]. University of Manchester; 2013. Available from: https://www.research.manchester.ac.uk/portal/en/theses/application-of-systems-biology-to-dissect-glucocorticoid-receptor-function(95b588bd-e84c-4f06-8341-d17cf47f235e).html ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.607066

University of Toronto

13. Campbell, Charlie. Disruption of the FK506 Binding Protein 5 and Glucocorticoid Receptor Protein Complex with an Intravenous Therapeutic Peptide Decreases Fear-like Freezing Behavior in an Animal Model of Post-traumatic Stress Disorder.

Degree: 2020, University of Toronto

URL: http://hdl.handle.net/1807/103397

►

Post-traumatic Stress Disorder (PTSD) is a debilitating mental health disorder provoked in response to a wide range of traumatic events where patients experience recurrent physical… (more)

Subjects/Keywords: FKBP51; Glucocorticoid Receptor; Interfering Peptide; PTSD; 0307

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Campbell, C. (2020). Disruption of the FK506 Binding Protein 5 and Glucocorticoid Receptor Protein Complex with an Intravenous Therapeutic Peptide Decreases Fear-like Freezing Behavior in an Animal Model of Post-traumatic Stress Disorder. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/103397

Chicago Manual of Style (16^th Edition):

Campbell, Charlie. “Disruption of the FK506 Binding Protein 5 and Glucocorticoid Receptor Protein Complex with an Intravenous Therapeutic Peptide Decreases Fear-like Freezing Behavior in an Animal Model of Post-traumatic Stress Disorder.” 2020. Masters Thesis, University of Toronto. Accessed January 18, 2021. http://hdl.handle.net/1807/103397.

MLA Handbook (7^th Edition):

Campbell, Charlie. “Disruption of the FK506 Binding Protein 5 and Glucocorticoid Receptor Protein Complex with an Intravenous Therapeutic Peptide Decreases Fear-like Freezing Behavior in an Animal Model of Post-traumatic Stress Disorder.” 2020. Web. 18 Jan 2021.

Vancouver:

Campbell C. Disruption of the FK506 Binding Protein 5 and Glucocorticoid Receptor Protein Complex with an Intravenous Therapeutic Peptide Decreases Fear-like Freezing Behavior in an Animal Model of Post-traumatic Stress Disorder. [Internet] [Masters thesis]. University of Toronto; 2020. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1807/103397.

Council of Science Editors:

Campbell C. Disruption of the FK506 Binding Protein 5 and Glucocorticoid Receptor Protein Complex with an Intravenous Therapeutic Peptide Decreases Fear-like Freezing Behavior in an Animal Model of Post-traumatic Stress Disorder. [Masters Thesis]. University of Toronto; 2020. Available from: http://hdl.handle.net/1807/103397

University of Arizona

14. Kadiyala, Vineela. Class I Lysine Deacetylases Facilitate Glucocorticoid Receptor-Mediated Transcriptional Activation .

Degree: 2013, University of Arizona

URL: http://hdl.handle.net/10150/311669

► Glucocorticoid receptor (GR) is known to associate with KATs and KDACs to regulate transcription. The current model of GR-mediated transcription focuses on agonist-dependent recruitment of… (more)

▼ Glucocorticoid receptor (GR) is known to associate with KATs and KDACs to regulate transcription. The current model of GR-mediated transcription focuses on agonist-dependent recruitment of KATs to acetylate histones and casts KDACs as corepressors in the presence of antagonist. Recent studies have shown KDACs to function as coactivators in the GR-mediated activation of the MMTV promoter and inhibition of KDACs impairs this activation. Nevertheless, the effect of KDAC inhibition on the GR-regulated transcriptome is unknown. Our expression profiling studies in a glucocorticoid (GC) responsive hepatoma-derived cell line, show that the class I-selective KDACi, VPA, has a profound impact on the GR-regulated hepatic transcriptome. VPA treatment alone mimics GC signaling at some GR-target genes and cooperates with GC to activate a small number of genes. However, the predominant effect of VPA, seen in more than 50% of the GR-target genes, is impairment of normal GR-mediated activation. This suggests that KDACs play a significant role in facilitating GR signaling. We have shown that VPA does not impair GR processing and that the inhibitory effects of VPA are due to impaired transcription. We have also determined that apicidin, a structurally distinct class I-selective KDACi, impairs GR-transactivation similar to VPA, while valpromide, a structural analog of VPA without KDACi activity, does not. In addition, siRNA-mediated depletion of KDAC1 fully or partially mimics the effects of VPA at most of the VPA impaired GR-target genes and co-depletion of KDACs 1 and 2 caused full or partial impairment of Dex-activation at a few other genes. Collectively, our results show that class-I KDACs facilitate GR-mediated transcription at most of the GR-target genes and that KDAC1 alone or in co-operation with KDAC2 is required for efficient GR-mediated transactivation. Furthermore, ChIP assays have shown that active KDACs are constitutively present at the gene promoters and that KDAC inhibition does not affect GR binding to the DNA. Thus KDACs could potentially deacetylate the coregulators necessary for transcriptional activation. Finally, KDACs are known targets of a group of drugs either being used or evaluated in the treatment of cancer and other diseases. These results also pose ramifications for the clinical use of these drugs. Advisors/Committee Members: Smith, Catharine L (advisor), Smith, Catharine L. (committeemember), Miesfeld, Roger L. (committeemember), Tsao, Tsu-Shuen (committeemember), Futscher, Bernard (committeemember).

Subjects/Keywords: Lysine deaectylases; Transcription; Chemistry; Glucocorticoid receptor

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Kadiyala, V. (2013). Class I Lysine Deacetylases Facilitate Glucocorticoid Receptor-Mediated Transcriptional Activation . (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/311669

Chicago Manual of Style (16^th Edition):

Kadiyala, Vineela. “Class I Lysine Deacetylases Facilitate Glucocorticoid Receptor-Mediated Transcriptional Activation .” 2013. Doctoral Dissertation, University of Arizona. Accessed January 18, 2021. http://hdl.handle.net/10150/311669.

MLA Handbook (7^th Edition):

Kadiyala, Vineela. “Class I Lysine Deacetylases Facilitate Glucocorticoid Receptor-Mediated Transcriptional Activation .” 2013. Web. 18 Jan 2021.

Vancouver:

Kadiyala V. Class I Lysine Deacetylases Facilitate Glucocorticoid Receptor-Mediated Transcriptional Activation . [Internet] [Doctoral dissertation]. University of Arizona; 2013. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/10150/311669.

Council of Science Editors:

Kadiyala V. Class I Lysine Deacetylases Facilitate Glucocorticoid Receptor-Mediated Transcriptional Activation . [Doctoral Dissertation]. University of Arizona; 2013. Available from: http://hdl.handle.net/10150/311669

15. Vardas, Konstantinos. Η έκφραση των υποδοχέων των γλυκοκορτικοειδών στα περιφερικά μονοπύρηνα αίματος σε συσχέτιση με την διέγερση του άξονα και των πρωτεϊνών στρες hsp70 και hsp90 σε ασθενείς ΜΕΘ με σήψη ή τραύμα.

Degree: 2017, University of Crete (UOC); Πανεπιστήμιο Κρήτης

URL: http://hdl.handle.net/10442/hedi/41231

►

ΑBSTRACT. Purpose: To examine if the human glucocorticoid receptor (hGR) isoform-α mRNA and hGR protein expressions are deficient in the acute phase of sepsis (S)… (more)

▼

ΑBSTRACT. Purpose: To examine if the human glucocorticoid receptor (hGR) isoform-α mRNA and hGR protein expressions are deficient in the acute phase of sepsis (S) compared to systemic inflammatory response syndrome (SIRS) and healthy subjects (H). To evaluate if the hGRα and hGR alterations are associated with cortisol changes, and if they are related to: 1) extracellular and intracellular heat shock proteins (HSP) 72 and 90α; 2) ACTH, prolactin, and interleukins (ILs); 3) the outcome.Methods: Patients consecutively admitted to a University Hospital Intensive Care Unit (ICU) with S (n=48) or SIRS (n=40) were enrolled in the study. Thirty-five H were also included. Total mRNA was isolated from peripheral blood samples and cDNA was prepared. RT-PCR was performed. Intracellular hGR and HSPs expression in monocytes and/or neutrophils was evaluated using 4-colour flow cytometry. Serum prolactin, ACTH and cortisol concentrations were also measured. ELISA was used to evaluate serum ILs and extracellular (e) HSPs (eHSP72, eHSP90α). Results: hGR protein was higher in S compared to H and SIRS; hGRα mRNA was higher in S compared to H (p<0.05). In sepsis, hGR protein and eHSP72 were higher among non-survivors compared to survivors (p<0.05). The hGR MFI and hGRα mRNA fold change were significantly related to each other (rs=0.64, p<0.001). Monocyte hGR protein expression was positively correlated to extracellular and intracellular HSPs, cortisol, and ILs and negatively to organ dysfunction (p<0.05). HSPs, hGR, and cortisol were able to discriminate sepsis from SIRS (AUROC >0.85, p<0.05). In sepsis, monocyte-hGR protein and eHSP72 were strong predictors of mortality (AUROC >0.95 p<0.04).Conclusions: Acute-phase sepsis is associated with increased hGR expression and cortisol concentrations, possibly implying no need for exogenous steroids. At this stage, hGR is able to predict sepsis and outcome, and is related to stress-activated bio-molecules and organ dysfunction.

Εισαγωγή: Ο υποδοχέας γλυκοκορτικοειδών (GR) εκφράζεται υποχρεωτικά σε όλους τους κυτταρικούς πληθυσμούς. Η έλλειψή του από τους ιστούς μπορεί να οδηγήσει σε χαρακτηριστικά παθολογικούς φαινότυπους. Πρόσφατα ερευνητικά δεδομένα παρέχουν ενδείξεις ότι η έκφραση του GR ελαττώνεται προοδευτικά σε πειραματικά μοντέλα σήψης, καθώς και ότι αυτή η διαδικασία οδηγεί σε μειωμένη ικανότητα της δεξαμεθαζόνης να μετακινείται προς τον πυρήνα του κυττάρου. Σκοπός: Nα εξετάσουμε εάν το αγγελιοφόρο RNA (mRNA) της ισομορφής α του ανθρώπινου υποδοχέα των γλυκοκορτικοειδών (hGRα) και η πρωτεϊνη hGR είναι ανεπαρκή σε ασθενείς με πρώιμη σήψη (Σ) σε σχέση με ασθενείς με μη-λοιμώδες σύνδρομο συστηματικής φλεγμονώδους απάντησης (SIRS) και υγιείς εθελοντές (Ε). Να εκτιμήσουμε εάν οι μεταβολές στη γονιδιακή και πρωτεϊνική έκφραση του υποδοχέα των γλυκοκορτικοειδών σχετίζονται με μεταβολές στα επίπεδα της κορτιζόλης και εάν συσχετίζονται με τις α) ενδοκυττάριες και εξωκυττάριες πρωτεϊνες θερμικού σοκ (HSP) 90α και 72 β) την προλακτίνη, ΑCTH και τις ιντερλευκίνες γ) την έκβαση.Μέθοδοι: Η μελέτη…

Subjects/Keywords: Yποδοχέας γλυκοκορτικοειδών; Σήψη; Glucocorticoid receptor (GR); sepsis

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Vardas, K. (2017). Η έκφραση των υποδοχέων των γλυκοκορτικοειδών στα περιφερικά μονοπύρηνα αίματος σε συσχέτιση με την διέγερση του άξονα και των πρωτεϊνών στρες hsp70 και hsp90 σε ασθενείς ΜΕΘ με σήψη ή τραύμα. (Thesis). University of Crete (UOC); Πανεπιστήμιο Κρήτης. Retrieved from http://hdl.handle.net/10442/hedi/41231

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):

Vardas, Konstantinos. “Η έκφραση των υποδοχέων των γλυκοκορτικοειδών στα περιφερικά μονοπύρηνα αίματος σε συσχέτιση με την διέγερση του άξονα και των πρωτεϊνών στρες hsp70 και hsp90 σε ασθενείς ΜΕΘ με σήψη ή τραύμα.” 2017. Thesis, University of Crete (UOC); Πανεπιστήμιο Κρήτης. Accessed January 18, 2021. http://hdl.handle.net/10442/hedi/41231.

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

MLA Handbook (7^th Edition):

Vardas, Konstantinos. “Η έκφραση των υποδοχέων των γλυκοκορτικοειδών στα περιφερικά μονοπύρηνα αίματος σε συσχέτιση με την διέγερση του άξονα και των πρωτεϊνών στρες hsp70 και hsp90 σε ασθενείς ΜΕΘ με σήψη ή τραύμα.” 2017. Web. 18 Jan 2021.

Vancouver:

Vardas K. Η έκφραση των υποδοχέων των γλυκοκορτικοειδών στα περιφερικά μονοπύρηνα αίματος σε συσχέτιση με την διέγερση του άξονα και των πρωτεϊνών στρες hsp70 και hsp90 σε ασθενείς ΜΕΘ με σήψη ή τραύμα. [Internet] [Thesis]. University of Crete (UOC); Πανεπιστήμιο Κρήτης; 2017. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/10442/hedi/41231.

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

Council of Science Editors:

Vardas K. Η έκφραση των υποδοχέων των γλυκοκορτικοειδών στα περιφερικά μονοπύρηνα αίματος σε συσχέτιση με την διέγερση του άξονα και των πρωτεϊνών στρες hsp70 και hsp90 σε ασθενείς ΜΕΘ με σήψη ή τραύμα. [Thesis]. University of Crete (UOC); Πανεπιστήμιο Κρήτης; 2017. Available from: http://hdl.handle.net/10442/hedi/41231

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

University of Sydney

16. Stoner, Shihani Priscilla. The Role of Glucocorticoid Receptor in Mature Osteoblasts and Osteocytes in Bone Modelling and Bone Remodelling .

Degree: 2016, University of Sydney

URL: http://hdl.handle.net/2123/15883

► Endogenous glucocorticoids (GCs) are known for their role in maintaining glucose homeostasis. GCs are also essential for several biological functions including metabolic, immunologic and cardiovascular… (more)

▼ Endogenous glucocorticoids (GCs) are known for their role in maintaining glucose homeostasis. GCs are also essential for several biological functions including metabolic, immunologic and cardiovascular functions. Previous research have shown that the targeted overexpression of 11β-HSD type 2 enzyme resulting in the abrogation of endogenous GC signalling in osteoblasts at the pre-receptor level, is associated with impaired bone acquisition in mice. This study examined the skeletal phenotype of mice with glucocorticoid receptor (GR) deletion in mature osteoblasts and osteocytes, during bone remodelling and modelling. Mature osteoblast and osteocyte specific GR knock-out mice (obGRKO) were generated by crossing GRflox/flox mice with a transgenic mouse line expressing cre recombinase under the control of a type I collagen (Col2.3) truncated rat promoter. At 12-weeks (bone remodelling) and 3-weeks (bone modelling) of age, vertebrae and tibiae from male and female obGRKO mice and their Cre-negative GRflox/flox wildtype (WT) littermates were harvested and examined to observe the effects of the knockout gene. In bone remodelling there was a significant decrease in vertebral bone volume across both male and female obGRKO mice, compared to WT. This was largely due to a reduction in trabecular number, and a corresponding increase in trabecular separation in obGRKO mice. Interestingly, the trabecular bone parameters in the tibia were similar between obGRKO and WT mice, during bone remodelling. Results also revealed that the low vertebral bone mass in obGRKO mice was associated with a significant increase in osteoclast number and surface when compared with WT. In addition, no differences was observed in molecular or bone turnover markers between obGRKO and WT. However, the deletion of GR in osteoblasts/osteocytes during bone modelling demonstrated no apparent effect on the skeleton in postnatal mice. These results indicate that endogenous GC signalling in osteoblasts via the GR pathway is crucial for the accrual and maintenance of vertebral trabecular bone mass, during bone remodelling. Furthermore, GC signalling may have a role in osteoblast-mediated bone resorption specifically in vertebral trabecular bone.

Subjects/Keywords: glucocorticoid; endogenous; receptor; bone; osteoblast; osteoclast

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Stoner, S. P. (2016). The Role of Glucocorticoid Receptor in Mature Osteoblasts and Osteocytes in Bone Modelling and Bone Remodelling . (Thesis). University of Sydney. Retrieved from http://hdl.handle.net/2123/15883

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):

Stoner, Shihani Priscilla. “The Role of Glucocorticoid Receptor in Mature Osteoblasts and Osteocytes in Bone Modelling and Bone Remodelling .” 2016. Thesis, University of Sydney. Accessed January 18, 2021. http://hdl.handle.net/2123/15883.

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

MLA Handbook (7^th Edition):

Stoner, Shihani Priscilla. “The Role of Glucocorticoid Receptor in Mature Osteoblasts and Osteocytes in Bone Modelling and Bone Remodelling .” 2016. Web. 18 Jan 2021.

Vancouver:

Stoner SP. The Role of Glucocorticoid Receptor in Mature Osteoblasts and Osteocytes in Bone Modelling and Bone Remodelling . [Internet] [Thesis]. University of Sydney; 2016. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/2123/15883.

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

Council of Science Editors:

Stoner SP. The Role of Glucocorticoid Receptor in Mature Osteoblasts and Osteocytes in Bone Modelling and Bone Remodelling . [Thesis]. University of Sydney; 2016. Available from: http://hdl.handle.net/2123/15883

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

17. Wilkinson, Legh. Homologous down-regulation of the glucocorticoid receptor is influenced by the dimerization state of the receptor.

Degree: PhD, Biochemistry, 2018, Stellenbosch University

URL: http://hdl.handle.net/10019.1/103838

►

ENGLISH ABSTRACT: Glucocorticoids (GCs) remain the mainstay therapeutic choice for the treatment of inflammation, and exert their potent anti-inflammatory effects via the glucocorticoid receptor (GRα).… (more)

▼

ENGLISH ABSTRACT: Glucocorticoids (GCs) remain the mainstay therapeutic choice for the treatment of inflammation, and exert their potent anti-inflammatory effects via the glucocorticoid receptor (GRα). However, the chronic use of GCs, in addition to generating undesirable side-effects (e.g. hyperglycemia), results in homologous down-regulation of the GRα. This reduction in GRα protein levels has been coupled to a decrease in GC-responsiveness, in a number of psychological and pathological conditions, which may culminate in GC-acquired resistance, a major concern for chronic GC users. The current study investigated whether ligand-induced down-regulation of the GRα is influenced by the dimerization state of the receptor by transfecting human wild type GRα (hGRwt) or a dimerization deficient GRα mutant (hGRdim) into COS-1 cells. In addition, Compound A (CpdA), which abrogates GR dimerization, was used to mimic the effect of the hGRdim in HepG2 cells containing endogenous GRα. Furthermore, the ability of an endogenous mutant, mGRdim, to undergo ligand-induced receptor turnover was compared to that of the wild-type GRα, mGRwt, in MEF-mGRdim and MEF-mGRwt cells, respectively. Whole-cell-binding and Western blotting revealed that the hGRwt, but not the hGRdim, underwent homologous down-regulation following dexamethasone (Dex), a potent synthetic GC, and cortisol (F), an endogenous GC, treatment. In contrast, ligand-induced down-regulation of GRα was abolished by CpdA treatment or the use of hGRdim, suggesting a novel role for GRα dimerization in mediating receptor turnover. These findings from the COS-1 cells were supported by results from the HepG2 cells, and, in part, by results from the MEF cells. Moreover, the dimerization state of the GRα influenced the posttranslational processing of the receptor, impacting its degradation via the proteasome. Specifically, ‘loss’ of GRα dimerization via CpdA treatment or the use of the dimerization deficient GRα mutant, restricted hyper-phosphorylation at Ser404, which has been coupled to increased GRα degradation, as well as restricted the interaction of GRα with the E3 ligase, FBXW7α, thus hampering receptor turnover. Lastly, a model to mimic acquired GC resistance was established and tested. Results from these experiments demonstrated that prolonged GC treatment of mGRwt (i.e. ‘gain’ of GRα dimerization) leads to molecular GC resistance (i.e. GILZ) and clinical GC resistance (FKBP51), whilst maintaining the up-regulation of a metabolic gene (i.e. TAT). In contrast, ‘loss’ of GRα dimerization partially restricts acquired resistance, at a molecular and clinical level, whilst displaying an improved side-effect profile in terms of restricting the expression of a metabolic gene (i.e. TAT). These results expand our understanding of factors that contribute to GC-resistance and may be exploited clinically.

AFRIKAANSE OPSOMMING: Glukokortikoïede (GK's) bly die staatmaker terapeutiese keuse vir die behandeling van inflammasie en oefen hul kragtige…

Advisors/Committee Members: Louw, Ann, Verhoog, Nicolette, Stellenbosch University. Faculty of Science. Dept. of Biochemistry..

Subjects/Keywords: Steroid receptor signalling; Glucocorticoid receptor; CompoundA; Acquired glucocorticoid resistance; Inflammation – Alternative treatment; UCTD

10 more images…

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Wilkinson, L. (2018). Homologous down-regulation of the glucocorticoid receptor is influenced by the dimerization state of the receptor. (Doctoral Dissertation). Stellenbosch University. Retrieved from http://hdl.handle.net/10019.1/103838

Chicago Manual of Style (16^th Edition):

Wilkinson, Legh. “Homologous down-regulation of the glucocorticoid receptor is influenced by the dimerization state of the receptor.” 2018. Doctoral Dissertation, Stellenbosch University. Accessed January 18, 2021. http://hdl.handle.net/10019.1/103838.

MLA Handbook (7^th Edition):

Wilkinson, Legh. “Homologous down-regulation of the glucocorticoid receptor is influenced by the dimerization state of the receptor.” 2018. Web. 18 Jan 2021.

Vancouver:

Wilkinson L. Homologous down-regulation of the glucocorticoid receptor is influenced by the dimerization state of the receptor. [Internet] [Doctoral dissertation]. Stellenbosch University; 2018. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/10019.1/103838.

Council of Science Editors:

Wilkinson L. Homologous down-regulation of the glucocorticoid receptor is influenced by the dimerization state of the receptor. [Doctoral Dissertation]. Stellenbosch University; 2018. Available from: http://hdl.handle.net/10019.1/103838

Queens University

18. Perri, Amelia. Glucocorticoid Receptor (NR3C1) Promoter Methylation as a Circulating Breast Cancer Biomarker and its Role in Tamoxifen Sensitivity .

Degree: Biochemistry, 2014, Queens University

URL: http://hdl.handle.net/1974/12458

► The glucocorticoid receptor (GR) binds glucocorticoids and transcriptionally regulates genes involved in immune response, cellular proliferation, and apoptosis. Previous work in our lab using MeDIP… (more)

Subjects/Keywords: Glucocorticoid Receptor ; Stress ; Estrogen Receptor ; Breast Cancer ; Methylation

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Perri, A. (2014). Glucocorticoid Receptor (NR3C1) Promoter Methylation as a Circulating Breast Cancer Biomarker and its Role in Tamoxifen Sensitivity . (Thesis). Queens University. Retrieved from http://hdl.handle.net/1974/12458

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):

Perri, Amelia. “Glucocorticoid Receptor (NR3C1) Promoter Methylation as a Circulating Breast Cancer Biomarker and its Role in Tamoxifen Sensitivity .” 2014. Thesis, Queens University. Accessed January 18, 2021. http://hdl.handle.net/1974/12458.

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

MLA Handbook (7^th Edition):

Perri, Amelia. “Glucocorticoid Receptor (NR3C1) Promoter Methylation as a Circulating Breast Cancer Biomarker and its Role in Tamoxifen Sensitivity .” 2014. Web. 18 Jan 2021.

Vancouver:

Perri A. Glucocorticoid Receptor (NR3C1) Promoter Methylation as a Circulating Breast Cancer Biomarker and its Role in Tamoxifen Sensitivity . [Internet] [Thesis]. Queens University; 2014. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1974/12458.

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

Council of Science Editors:

Perri A. Glucocorticoid Receptor (NR3C1) Promoter Methylation as a Circulating Breast Cancer Biomarker and its Role in Tamoxifen Sensitivity . [Thesis]. Queens University; 2014. Available from: http://hdl.handle.net/1974/12458

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

Queens University

19. Sellars, Erin. Glucocorticoid Receptor Function and its Role in Tamoxifen Resistance .

Degree: Biochemistry, 2015, Queens University

URL: http://hdl.handle.net/1974/13692

► The function of the glucocorticoid receptor (GR) is crucial for the development and proliferation of normal human breast cells. The primary activity of GR is… (more)

▼ The function of the glucocorticoid receptor (GR) is crucial for the development and proliferation of normal human breast cells. The primary activity of GR is in its binding to glucocorticoids and the subsequent activation of its transcriptional target genes. However, GR is also able to transcriptionally regulate target genes in the absence of ligand in EPH4 mouse mammary cells, which is termed the unliganded activity of GR. Unliganded GR stimulates the activity of the BRCA1 and CH25H promoters and is important in modulating apoptosis and cell growth. The activity of unliganded GR in normal human breast cell lines was investigated in this study in order to validate its regulatory role. Unliganded GR did not upregulate BRCA1 or CH25H expression in the human breast cell lines MCF-10A and 184-hTERT. As well, no novel target genes of unliganded GR were identified in normal human breast cells, however both PRLR and CDKN1A were found to be negatively regulated by liganded and possibly unliganded GR respectively. The second portion of this study focused on the exploration of the role of GR in modulating tamoxifen response in ER+ breast cancer. GR was overexpressed in response to tamoxifen in ER+ breast cancer cells in the ER+ cell lines MCF-7 and T47D. As well, GSTM1 expression was increased by tamoxifen in a GR-dependent manner which suggests that downstream GR signaling is also increased in response to tamoxifen. This is crucial as it suggests that the increase in GR leads to increased GR activity and signaling. The ERα pioneer factor, FOXA1 was overexpressed by tamoxifen as well and may be responsible for activating GR overexpression. Finally, loss of GR may initiate a survival signal in ER+ cells as tamoxifen also increased the expression of cancer stem-like marker genes, EpCAM and ALDH1A3. EpCAM expression was found to be upregulated by tamoxifen and loss of GR expression and ALDH1A3 expression was increased 5-fold by tamoxifen alone. This upregulation of cancer stem-like markers suggests that tamoxifen resistance could occur through the formation of a stem-like chemotherapeutic resistant cell population.

Subjects/Keywords: Breast Cancer ; Tamoxifen Resistance ; Estrogen Receptor ; Glucocorticoid Receptor

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Sellars, E. (2015). Glucocorticoid Receptor Function and its Role in Tamoxifen Resistance . (Thesis). Queens University. Retrieved from http://hdl.handle.net/1974/13692

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):

Sellars, Erin. “Glucocorticoid Receptor Function and its Role in Tamoxifen Resistance .” 2015. Thesis, Queens University. Accessed January 18, 2021. http://hdl.handle.net/1974/13692.

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

MLA Handbook (7^th Edition):

Sellars, Erin. “Glucocorticoid Receptor Function and its Role in Tamoxifen Resistance .” 2015. Web. 18 Jan 2021.

Vancouver:

Sellars E. Glucocorticoid Receptor Function and its Role in Tamoxifen Resistance . [Internet] [Thesis]. Queens University; 2015. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1974/13692.

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

Council of Science Editors:

Sellars E. Glucocorticoid Receptor Function and its Role in Tamoxifen Resistance . [Thesis]. Queens University; 2015. Available from: http://hdl.handle.net/1974/13692

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

University of Ottawa

20. Carrigan, Amanda. Sequence and Effects of Glucocorticoid Receptor Nuclear Retention: An Aid to Understanding Nuclear Retention in Other Proteins? .

Degree: 2011, University of Ottawa

URL: http://hdl.handle.net/10393/19719

► Corticosteroid ligands activate the glucocorticoid receptor (GR). GR plays a role in glucose homeostasis, adipogenesis, inflammation, and mood and cognitive functions. Understanding the interplay of… (more)

▼ Corticosteroid ligands activate the glucocorticoid receptor (GR). GR plays a role in glucose homeostasis, adipogenesis, inflammation, and mood and cognitive functions. Understanding the interplay of diverse forms of receptor regulation (including post-translational modification, cofactor interactions, ligand binding, and receptor localization) and their effects is important for understanding and developing more effective treatment for a variety of conditions. Prior to ligand binding, the naïve GR is primarily cytoplasmic, residing in a chaperone complex containing heat-shock proteins and immunophilins. Upon ligand-binding, alterations to the complex allow the receptor to dimerize and import into the nucleus. Nuclear GR interacts with transcriptional regulatory sequences and recruits cofactors to regulate specific gene expression. Upon hormone withdrawal, the original chaperone complex is reassembled and the receptor is exported to the cytoplasm. Interestingly, while the import of GR into the nucleus occurs very rapidly (t ½ = 5 min), the re-export is significantly slower (t ½ = 12-24h). Previous work by our lab and others has indicated the existence of a nuclear retention signal (NRS) within the GR. The NRS sequence of the GR, its interaction partners, and the role it might play in the activity of the receptor have not yet been fully defined. Work in the Hache lab indicates that mutation of the GR nuclear localization signal 1 (NL1) increases the export rate of nuclear GR to the cytoplasm, as well as compromising receptor import, suggesting that the NL1 overlapped an NRS sequence. In this work, I made a series of GR mutants, based on sequence from the SV40 large T antigen NLS, which lacks nuclear retention activity. Using these mutants, I found that GR nuclear retention is influenced by both specific residues within the hinge region and the location of the sequence within the receptor, as reintroduction of the NLS sequence at the N-terminus of the receptor retention mutant failed to reconstitute the retention activity. Agonist liganded and hormone-withdrawn receptor mutants showed a similar decrease in retention. By contrast, antagonist-withdrawn GR mutants were retained in the nucleus, possibly due to altered receptor configuration and interactions. Assays of GR-responsive promoter activation by receptor retention mutants showed that while no difference in the ability of retention mutants to activate transcription was seen at a simple promoter, activation of a complex promoter was compromised. This impaired transactivation for the SV506-523 mutant correlated with decreased histone H4 acetylation and PolII recruitment, while GR DNA-binding at the target promoter appeared to be unaffected. These results suggested that promoter-specific cofactor interactions might be implicated in GR nuclear retention. Loss of GR hinge interaction with Oct cofactors produced an incomplete loss of retention, suggesting overlapping signals, but not supporting Oct as a primary factor in GR retention. The overlap between important residues…

Subjects/Keywords: glucocorticoid receptor; nuclear retention; steroid hormone receptor; export; NLS; trafficking

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Carrigan, A. (2011). Sequence and Effects of Glucocorticoid Receptor Nuclear Retention: An Aid to Understanding Nuclear Retention in Other Proteins? . (Thesis). University of Ottawa. Retrieved from http://hdl.handle.net/10393/19719

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):

Carrigan, Amanda. “Sequence and Effects of Glucocorticoid Receptor Nuclear Retention: An Aid to Understanding Nuclear Retention in Other Proteins? .” 2011. Thesis, University of Ottawa. Accessed January 18, 2021. http://hdl.handle.net/10393/19719.

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

MLA Handbook (7^th Edition):

Carrigan, Amanda. “Sequence and Effects of Glucocorticoid Receptor Nuclear Retention: An Aid to Understanding Nuclear Retention in Other Proteins? .” 2011. Web. 18 Jan 2021.

Vancouver:

Carrigan A. Sequence and Effects of Glucocorticoid Receptor Nuclear Retention: An Aid to Understanding Nuclear Retention in Other Proteins? . [Internet] [Thesis]. University of Ottawa; 2011. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/10393/19719.

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

Council of Science Editors:

Carrigan A. Sequence and Effects of Glucocorticoid Receptor Nuclear Retention: An Aid to Understanding Nuclear Retention in Other Proteins? . [Thesis]. University of Ottawa; 2011. Available from: http://hdl.handle.net/10393/19719

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

Univerzitet u Beogradu

21. Tešić, Vesna T., 1978-. Uticaj dugotrajne restrikcije hrane na ekspresiju glukokortikoidnog receptora u prednjem mozgu pacova tokom starenja.

Degree: Biološki fakultet, 2016, Univerzitet u Beogradu

URL: https://fedorabg.bg.ac.rs/fedora/get/o:10711/bdef:Content/get

►

Biologija - Molekularna neurobiologija / Biology - Molecular neurobiology

Dugotrajna restrikcija hrane produžava životni vek i odlaže pojavu mnogih bolesti koje se javljaju sa starenjem.… (more)

▼

Biologija - Molekularna neurobiologija / Biology - Molecular neurobiology

Dugotrajna restrikcija hrane produžava životni vek i odlaže pojavu mnogih bolesti koje se javljaju sa starenjem. Brojni literaturni podaci ukazuju da kod životinja kojima je unos hrane smanjen izostaje karakterističan starosno-zavistan pad u kognitivnim funkcijama, međutim, mehanizam ovakvog neuroprotektivnog dejstva restrikcije hrane nije u potpunosti razjašnjen. U isto vreme, kod životinja na dugotrajnoj restrikciji hrane se povećava nivo kortikosterona u plazmi što ukazuje da ovaj tretman deluje kao blagi stresor. Do sada nije ispitivano do kakvih promena u signalnom putu glukokortikoida dovodi smanjeni unos hrane tokom starenja u mozgu. Centralno polje istraživanja procesa starenja neizbežno podrazumeva ispitivanje promena do kojih dolazi u korteksu i hipokampusu, strukturama mozga koje su ključne za kognitivne funkcije. Sa druge strane, iste strukture učestvuju u regulaciji HHA ose kao važni regioni delovanja negativne povratne sprege. Cilj doktorske disertacije je da se ispita uloga signalnog puta glukokortikoida u korteksu i hipokampusu pacova tokom starenja i pod uticajem dugotrajne restrikcije hrane. Eksperimentalne životinje (mužjaci pacova soja Wistar) starosti 6 meseci su podeljene u dve grupe. Prva grupa, označena kao ad libitum (AL), je imala neograničen pristup hrani, dok je druga grupa (označena kao DR) podvrgnuta režimu redukovane ishrane koji je podrazumevao dobijanje 100% dnevnog unosa hrane AL životinja svakog drugog dana. Životinje su analizirane kada su dostigle starost od 18 i 24 meseca. Životinje stare 6 meseci su predstavljale kontrolnu grupu. Glukokortikoidna signalizacija u ispitivanim strukturama je praćena na prereceptorskom nivou, kao i na nivou ekspresije i aktivacije glukokortikoidnog receptora primenom imunoesej, imunoblot i PCR metoda, kao i imunohistohemijske analize. Rezultati doktorske disertacije pokazuju da tokom starenja dolazi do povećanja koncentracije kortikosterona u korteksu pacova, dok dugotrajna restrikcija hrane povećava nivo kortikosterona u obe ispitivane strukture. Utvrđeno je da nivo ključnog enzima koji u moždanom tkivu reguliše dostupnost kortikosterona za receptore, 11β-HSD1, raste u hipokampusu pacova koji imaju neograničen pristup hrani. Tretman dugotrajnom restrikcijom hrane dovodi do povećanja nivoa 11β-HSD1 u korteksu, dok u hipokampusu izostaje efekat na nivo ovog enzima...

Advisors/Committee Members: Perović, Milka.

Subjects/Keywords: long-term food restriction; aging; glucocorticoid hormones; 11β-HSD1; glucocorticoid receptor; cortex; hippocampus

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Tešić, Vesna T., 1. (2016). Uticaj dugotrajne restrikcije hrane na ekspresiju glukokortikoidnog receptora u prednjem mozgu pacova tokom starenja. (Thesis). Univerzitet u Beogradu. Retrieved from https://fedorabg.bg.ac.rs/fedora/get/o:10711/bdef:Content/get

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):

Tešić, Vesna T., 1978-. “Uticaj dugotrajne restrikcije hrane na ekspresiju glukokortikoidnog receptora u prednjem mozgu pacova tokom starenja.” 2016. Thesis, Univerzitet u Beogradu. Accessed January 18, 2021. https://fedorabg.bg.ac.rs/fedora/get/o:10711/bdef:Content/get.

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

MLA Handbook (7^th Edition):

Tešić, Vesna T., 1978-. “Uticaj dugotrajne restrikcije hrane na ekspresiju glukokortikoidnog receptora u prednjem mozgu pacova tokom starenja.” 2016. Web. 18 Jan 2021.

Vancouver:

Tešić, Vesna T. 1. Uticaj dugotrajne restrikcije hrane na ekspresiju glukokortikoidnog receptora u prednjem mozgu pacova tokom starenja. [Internet] [Thesis]. Univerzitet u Beogradu; 2016. [cited 2021 Jan 18]. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:10711/bdef:Content/get.

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

Council of Science Editors:

Tešić, Vesna T. 1. Uticaj dugotrajne restrikcije hrane na ekspresiju glukokortikoidnog receptora u prednjem mozgu pacova tokom starenja. [Thesis]. Univerzitet u Beogradu; 2016. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:10711/bdef:Content/get

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

University of California – San Francisco

22. Schiller, Benjamin Joseph. Data Biology: A quantitative exploration of gene regulation and underlying mechanisms.

Degree: Biochemistry and Molecular Biology, 2013, University of California – San Francisco

URL: http://www.escholarship.org/uc/item/2rc2q811

► Regulation of gene expression is a fundamental biological process required to adapt the full set of hereditary information (i.e., the genome) to the varied environments… (more)

▼ Regulation of gene expression is a fundamental biological process required to adapt the full set of hereditary information (i.e., the genome) to the varied environments that any organism encounters. Here, we elucidate two distinct forms of gene regulation – of endogenous genes by binding of transcription factors to information-containing genomic sequences and of selfish genes (“transposons”) by targeting of small RNAs to repetitive genomic sequences – using a wide array of approaches.To study regulation by transcription factors, we used glucocorticoid receptor (GR), a hormone-activated, DNA-binding protein that controls inflammation, metabolism, stress responses and other physiological processes. In vitro, GR binds as an inverted dimer to two imperfectly palindromic “half sites” separated by a “spacer”. Moreover, GR binds different sequences with distinct conformations, as demonstrated by nuclear magnetic resonance spectroscopy (NMR) and other biophysical methods.In vivo, GR employs different functional surfaces when regulating different genes. We investigated whether sequences bound by GR in vivo might be a composite of several motifs, each biased toward utilization of a particular pattern of functional surfaces of GR. Using microarrays and deep sequencing, we characterized gene expression and genomic occupancy by GR, with and without glucocorticoid treatment, of cells expressing GR alleles bearing differences in three known functional surfaces. We found a “sub-motif”, the GR “half site”, that relates to utilization of the dimerization interface and directs genomic binding by GR in a distinct conformation.To study repression of tranposons, we characterized the production and function of small RNAs in the yeast Cryptococcus neoformans. We found that target transcripts are distinguished by suboptimal introns and inefficient splicing. We identified a complex, SCANR, required for synthesis of small RNAs and demonstrate that it physically associates with the spliceosome. We propose that recognition of gene products by SCANR is in kinetic competition with splicing, thereby further promoting small RNA production from target transcripts.To achieve these results, we developed new bioinformatics tools: twobitreader, a small Python package for efficient extraction of genomic sequences; scripter, a flexible back-end for easily creating scripts and pipeline; and seriesoftubes, a pipeline built upon scripter for the analysis of deep sequencing data.

Subjects/Keywords: Molecular biology; Bioinformatics; Biochemistry; gene regulation; glucocorticoid receptor; glucocorticoid response element; GR; motif; transcriptional regulation

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Schiller, B. J. (2013). Data Biology: A quantitative exploration of gene regulation and underlying mechanisms. (Thesis). University of California – San Francisco. Retrieved from http://www.escholarship.org/uc/item/2rc2q811

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):

Schiller, Benjamin Joseph. “Data Biology: A quantitative exploration of gene regulation and underlying mechanisms.” 2013. Thesis, University of California – San Francisco. Accessed January 18, 2021. http://www.escholarship.org/uc/item/2rc2q811.

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

MLA Handbook (7^th Edition):

Schiller, Benjamin Joseph. “Data Biology: A quantitative exploration of gene regulation and underlying mechanisms.” 2013. Web. 18 Jan 2021.

Vancouver:

Schiller BJ. Data Biology: A quantitative exploration of gene regulation and underlying mechanisms. [Internet] [Thesis]. University of California – San Francisco; 2013. [cited 2021 Jan 18]. Available from: http://www.escholarship.org/uc/item/2rc2q811.

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

Council of Science Editors:

Schiller BJ. Data Biology: A quantitative exploration of gene regulation and underlying mechanisms. [Thesis]. University of California – San Francisco; 2013. Available from: http://www.escholarship.org/uc/item/2rc2q811

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

University of Toronto

23. Hunter, Sarah Rachel. Induction of the Rat Hepatic Aryl Hydrocarbon Receptor Nuclear Translocator by Glucocorticoids.

Degree: 2014, University of Toronto

URL: http://hdl.handle.net/1807/73165

►

The aryl hydrocarbon receptor (AHR) nuclear translocator (ARNT), a partner in the hypoxia and AHR signaling pathways, is induced in rat liver by dexamethasone (DEX),… (more)

Subjects/Keywords: aryl hydrocarbon receptor nuclear translocator; glucocorticoid receptor; glucocorticoids; pregnane X receptor; rat; signaling pathway; 0419

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Hunter, S. R. (2014). Induction of the Rat Hepatic Aryl Hydrocarbon Receptor Nuclear Translocator by Glucocorticoids. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/73165

Chicago Manual of Style (16^th Edition):

Hunter, Sarah Rachel. “Induction of the Rat Hepatic Aryl Hydrocarbon Receptor Nuclear Translocator by Glucocorticoids.” 2014. Masters Thesis, University of Toronto. Accessed January 18, 2021. http://hdl.handle.net/1807/73165.

MLA Handbook (7^th Edition):

Hunter, Sarah Rachel. “Induction of the Rat Hepatic Aryl Hydrocarbon Receptor Nuclear Translocator by Glucocorticoids.” 2014. Web. 18 Jan 2021.

Vancouver:

Hunter SR. Induction of the Rat Hepatic Aryl Hydrocarbon Receptor Nuclear Translocator by Glucocorticoids. [Internet] [Masters thesis]. University of Toronto; 2014. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1807/73165.

Council of Science Editors:

Hunter SR. Induction of the Rat Hepatic Aryl Hydrocarbon Receptor Nuclear Translocator by Glucocorticoids. [Masters Thesis]. University of Toronto; 2014. Available from: http://hdl.handle.net/1807/73165

University of Bristol

24. Paul, Susana N. Mineralocorticoid and glucocorticoid receptor interactive complexes and their cellular localisation.

Degree: PhD, 2020, University of Bristol

URL: http://hdl.handle.net/1983/c6ba7afd-413d-4c7a-afd8-cc8515dc306a

► Adrenal glucocorticoids (GCs) released into circulation exhibit circadian and ultradian profiles, which are important in regulating homeostasis and physiological pathways. GCs induce gene expression changes… (more)

▼ Adrenal glucocorticoids (GCs) released into circulation exhibit circadian and ultradian profiles, which are important in regulating homeostasis and physiological pathways. GCs induce gene expression changes in targeted cells via ligand activated transcription factors, the mineralocorticoid receptor (MR) and the glucocorticoid receptor (GR), which produce both physiological and adaptive responses to stress. MR and GR are highly abundant in the hippocampus, an area vital for learning and memory, and effective responses to stressful events involve modification of cognitive processes in the brain to improve coping mechanisms to future stressors. MR and GR regulate transcription of GC targets, often as homodimers, but the existence and significance of MR/GR heteromers in gene regulation remains unclear. Using a proximity ligation assay (PLA) for the first time, MR and GR have been shown to be in very close proximity and are consequently likely to be interacting together. MR:GR complexes were detected both in cultured cells (3617 and Neuro-2A) transfected with MR/GR expression vectors and in rat hippocampal tissue where endogenous MR and GR are co-expressed. Nuclear MR:GR complexes were localised to heterochromatic regions, in proximity to the nuclear lamina. The interaction appears to require neither the DNA binding domain, nor the dimerization interface, indicating another mode of MR:GR interaction. In the absence of ligand, MR:GR complexes were unexpectedly detected in the cytoplasm, predominantly at the nuclear envelope. Using RT-qPCR, the transcriptional consequences of MR/GR alone or together with ‘physiological’ levels of CORT suggested cooperative regulation of some GC target genes. An optimised protocol for in situ PLA and the modular image analysis (MIA) pipeline are presented, for the detection and analysis of MR:GR complexes in Neuro-2A cells and hippocampal tissue, which are applicable to other receptor-receptor interaction studies in order to reveal dynamic spatio-temporal protein-protein interactions.

Subjects/Keywords: glucocorticoids; glucocorticoid receptor; mineralocorticoid receptor; transcription factors; protein interactions; proximity ligation assay; protein co-localisation

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Paul, S. N. (2020). Mineralocorticoid and glucocorticoid receptor interactive complexes and their cellular localisation. (Doctoral Dissertation). University of Bristol. Retrieved from http://hdl.handle.net/1983/c6ba7afd-413d-4c7a-afd8-cc8515dc306a

Chicago Manual of Style (16^th Edition):

Paul, Susana N. “Mineralocorticoid and glucocorticoid receptor interactive complexes and their cellular localisation.” 2020. Doctoral Dissertation, University of Bristol. Accessed January 18, 2021. http://hdl.handle.net/1983/c6ba7afd-413d-4c7a-afd8-cc8515dc306a.

MLA Handbook (7^th Edition):

Paul, Susana N. “Mineralocorticoid and glucocorticoid receptor interactive complexes and their cellular localisation.” 2020. Web. 18 Jan 2021.

Vancouver:

Paul SN. Mineralocorticoid and glucocorticoid receptor interactive complexes and their cellular localisation. [Internet] [Doctoral dissertation]. University of Bristol; 2020. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1983/c6ba7afd-413d-4c7a-afd8-cc8515dc306a.

Council of Science Editors:

Paul SN. Mineralocorticoid and glucocorticoid receptor interactive complexes and their cellular localisation. [Doctoral Dissertation]. University of Bristol; 2020. Available from: http://hdl.handle.net/1983/c6ba7afd-413d-4c7a-afd8-cc8515dc306a

University of Bristol

25. Paul, Susana N. Mineralocorticoid and glucocorticoid receptor interactive complexes and their cellular localisation.

Degree: PhD, 2020, University of Bristol

URL: https://research-information.bris.ac.uk/en/studentTheses/c6ba7afd-413d-4c7a-afd8-cc8515dc306a ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.809867

► Adrenal glucocorticoids (GCs) released into circulation exhibit circadian and ultradian profiles, which are important in regulating homeostasis and physiological pathways. GCs induce gene expression changes… (more)

▼ Adrenal glucocorticoids (GCs) released into circulation exhibit circadian and ultradian profiles, which are important in regulating homeostasis and physiological pathways. GCs induce gene expression changes in targeted cells via ligand activated transcription factors, the mineralocorticoid receptor (MR) and the glucocorticoid receptor (GR), which produce both physiological and adaptive responses to stress. MR and GR are highly abundant in the hippocampus, an area vital for learning and memory, and effective responses to stressful events involve modification of cognitive processes in the brain to improve coping mechanisms to future stressors. MR and GR regulate transcription of GC targets, often as homodimers, but the existence and significance of MR/GR heteromers in gene regulation remains unclear. Using a proximity ligation assay (PLA) for the first time, MR and GR have been shown to be in very close proximity and are consequently likely to be interacting together. MR:GR complexes were detected both in cultured cells (3617 and Neuro-2A) transfected with MR/GR expression vectors and in rat hippocampal tissue where endogenous MR and GR are co-expressed. Nuclear MR:GR complexes were localised to heterochromatic regions, in proximity to the nuclear lamina. The interaction appears to require neither the DNA binding domain, nor the dimerization interface, indicating another mode of MR:GR interaction. In the absence of ligand, MR:GR complexes were unexpectedly detected in the cytoplasm, predominantly at the nuclear envelope. Using RT-qPCR, the transcriptional consequences of MR/GR alone or together with ‘physiological’ levels of CORT suggested cooperative regulation of some GC target genes. An optimised protocol for in situ PLA and the modular image analysis (MIA) pipeline are presented, for the detection and analysis of MR:GR complexes in Neuro-2A cells and hippocampal tissue, which are applicable to other receptor-receptor interaction studies in order to reveal dynamic spatio-temporal protein-protein interactions.

Subjects/Keywords: glucocorticoids; glucocorticoid receptor; mineralocorticoid receptor; transcription factors; protein interactions; proximity ligation assay; protein co-localisation

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Paul, S. N. (2020). Mineralocorticoid and glucocorticoid receptor interactive complexes and their cellular localisation. (Doctoral Dissertation). University of Bristol. Retrieved from https://research-information.bris.ac.uk/en/studentTheses/c6ba7afd-413d-4c7a-afd8-cc8515dc306a ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.809867

Chicago Manual of Style (16^th Edition):

Paul, Susana N. “Mineralocorticoid and glucocorticoid receptor interactive complexes and their cellular localisation.” 2020. Doctoral Dissertation, University of Bristol. Accessed January 18, 2021. https://research-information.bris.ac.uk/en/studentTheses/c6ba7afd-413d-4c7a-afd8-cc8515dc306a ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.809867.

MLA Handbook (7^th Edition):

Paul, Susana N. “Mineralocorticoid and glucocorticoid receptor interactive complexes and their cellular localisation.” 2020. Web. 18 Jan 2021.

Vancouver:

Paul SN. Mineralocorticoid and glucocorticoid receptor interactive complexes and their cellular localisation. [Internet] [Doctoral dissertation]. University of Bristol; 2020. [cited 2021 Jan 18]. Available from: https://research-information.bris.ac.uk/en/studentTheses/c6ba7afd-413d-4c7a-afd8-cc8515dc306a ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.809867.

Council of Science Editors:

Paul SN. Mineralocorticoid and glucocorticoid receptor interactive complexes and their cellular localisation. [Doctoral Dissertation]. University of Bristol; 2020. Available from: https://research-information.bris.ac.uk/en/studentTheses/c6ba7afd-413d-4c7a-afd8-cc8515dc306a ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.809867

26. Borbhuiya, Md. Monsur Ahmed. Physicochemical changes in the glucocorticoid receptor during development of mice; -.

Degree: Biochemistry, 1997, North-Eastern Hill University

URL: http://shodhganga.inflibnet.ac.in/handle/10603/54913

Abstract not available newline newline

Summary p. 80-83, Bibliography p. 84-92, Appendix p. 93-95

Advisors/Committee Members: Sharma, R.

Subjects/Keywords: Physicochemical; Glucocorticoid Receptor; Development; Mice

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Borbhuiya, M. M. A. (1997). Physicochemical changes in the glucocorticoid receptor during development of mice; -. (Thesis). North-Eastern Hill University. Retrieved from http://shodhganga.inflibnet.ac.in/handle/10603/54913

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):

Borbhuiya, Md Monsur Ahmed. “Physicochemical changes in the glucocorticoid receptor during development of mice; -.” 1997. Thesis, North-Eastern Hill University. Accessed January 18, 2021. http://shodhganga.inflibnet.ac.in/handle/10603/54913.

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

MLA Handbook (7^th Edition):

Borbhuiya, Md Monsur Ahmed. “Physicochemical changes in the glucocorticoid receptor during development of mice; -.” 1997. Web. 18 Jan 2021.

Vancouver:

Borbhuiya MMA. Physicochemical changes in the glucocorticoid receptor during development of mice; -. [Internet] [Thesis]. North-Eastern Hill University; 1997. [cited 2021 Jan 18]. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/54913.

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

Council of Science Editors:

Borbhuiya MMA. Physicochemical changes in the glucocorticoid receptor during development of mice; -. [Thesis]. North-Eastern Hill University; 1997. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/54913

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

University of Toronto

27. Bryushkova, Lyubov. The Role of Genes Regulating the Hypothalamic-pituitary-adrenal Response in Childhood Aggression and Co-morbid Anxiety.

Degree: 2014, University of Toronto

URL: http://hdl.handle.net/1807/68550

►

Childhood aggression is associated with a variety of negative outcomes and is frequently accompanied by increased internalizing problems. The co-morbid group is at a high… (more)

Subjects/Keywords: Aggression; Anxiety; Childhood behavior problems; FKBP5; Glucocorticoid receptor; HPA Axis; 0384

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Bryushkova, L. (2014). The Role of Genes Regulating the Hypothalamic-pituitary-adrenal Response in Childhood Aggression and Co-morbid Anxiety. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/68550

Chicago Manual of Style (16^th Edition):

Bryushkova, Lyubov. “The Role of Genes Regulating the Hypothalamic-pituitary-adrenal Response in Childhood Aggression and Co-morbid Anxiety.” 2014. Masters Thesis, University of Toronto. Accessed January 18, 2021. http://hdl.handle.net/1807/68550.

MLA Handbook (7^th Edition):

Bryushkova, Lyubov. “The Role of Genes Regulating the Hypothalamic-pituitary-adrenal Response in Childhood Aggression and Co-morbid Anxiety.” 2014. Web. 18 Jan 2021.

Vancouver:

Bryushkova L. The Role of Genes Regulating the Hypothalamic-pituitary-adrenal Response in Childhood Aggression and Co-morbid Anxiety. [Internet] [Masters thesis]. University of Toronto; 2014. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1807/68550.

Council of Science Editors:

Bryushkova L. The Role of Genes Regulating the Hypothalamic-pituitary-adrenal Response in Childhood Aggression and Co-morbid Anxiety. [Masters Thesis]. University of Toronto; 2014. Available from: http://hdl.handle.net/1807/68550

University of Toronto

28. Manwani, Neetu. Role of Distal Airway Epithelial Glucocorticoid-Glucocorticoid Receptor Signalling in Mouse Lung in Late Gestation.

Degree: 2009, University of Toronto

URL: http://hdl.handle.net/1807/17697

►

Glucocorticoid (GC) signalling via the GC receptor (GR) regulates many aspects of lung development. To determine the need for epithelial GC-GR signalling, triple transgenic (TT)… (more)

Subjects/Keywords: Lung; Development; Glucocorticoid Receptor; 0758

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Manwani, N. (2009). Role of Distal Airway Epithelial Glucocorticoid-Glucocorticoid Receptor Signalling in Mouse Lung in Late Gestation. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/17697

Chicago Manual of Style (16^th Edition):

Manwani, Neetu. “Role of Distal Airway Epithelial Glucocorticoid-Glucocorticoid Receptor Signalling in Mouse Lung in Late Gestation.” 2009. Masters Thesis, University of Toronto. Accessed January 18, 2021. http://hdl.handle.net/1807/17697.

MLA Handbook (7^th Edition):

Manwani, Neetu. “Role of Distal Airway Epithelial Glucocorticoid-Glucocorticoid Receptor Signalling in Mouse Lung in Late Gestation.” 2009. Web. 18 Jan 2021.

Vancouver:

Manwani N. Role of Distal Airway Epithelial Glucocorticoid-Glucocorticoid Receptor Signalling in Mouse Lung in Late Gestation. [Internet] [Masters thesis]. University of Toronto; 2009. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1807/17697.

Council of Science Editors:

Manwani N. Role of Distal Airway Epithelial Glucocorticoid-Glucocorticoid Receptor Signalling in Mouse Lung in Late Gestation. [Masters Thesis]. University of Toronto; 2009. Available from: http://hdl.handle.net/1807/17697

University of Toronto

29. Lopez, Ana Sofia. Exploring the Suitability of a Specifici Glucocorticoid Receptor Antagonist as a Tool in the Study of the Regulation of Rat Lung Alveolarization by Glucocorticoids.

Degree: 2010, University of Toronto

URL: http://hdl.handle.net/1807/25774

►

Background: Intracellular glucocorticoid receptors (GRs) mediate the regulation of lung development, including alveolarization, by glucocorticoids (GCs). One potential approach to determining the role of GC-GR… (more)

Subjects/Keywords: alveolarization; glucocorticoids; rat lung development; glucocorticoid receptor antagonist; 0719

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Lopez, A. S. (2010). Exploring the Suitability of a Specifici Glucocorticoid Receptor Antagonist as a Tool in the Study of the Regulation of Rat Lung Alveolarization by Glucocorticoids. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/25774

Chicago Manual of Style (16^th Edition):

Lopez, Ana Sofia. “Exploring the Suitability of a Specifici Glucocorticoid Receptor Antagonist as a Tool in the Study of the Regulation of Rat Lung Alveolarization by Glucocorticoids.” 2010. Masters Thesis, University of Toronto. Accessed January 18, 2021. http://hdl.handle.net/1807/25774.

MLA Handbook (7^th Edition):

Lopez, Ana Sofia. “Exploring the Suitability of a Specifici Glucocorticoid Receptor Antagonist as a Tool in the Study of the Regulation of Rat Lung Alveolarization by Glucocorticoids.” 2010. Web. 18 Jan 2021.

Vancouver:

Lopez AS. Exploring the Suitability of a Specifici Glucocorticoid Receptor Antagonist as a Tool in the Study of the Regulation of Rat Lung Alveolarization by Glucocorticoids. [Internet] [Masters thesis]. University of Toronto; 2010. [cited 2021 Jan 18]. Available from: http://hdl.handle.net/1807/25774.

Council of Science Editors:

Lopez AS. Exploring the Suitability of a Specifici Glucocorticoid Receptor Antagonist as a Tool in the Study of the Regulation of Rat Lung Alveolarization by Glucocorticoids. [Masters Thesis]. University of Toronto; 2010. Available from: http://hdl.handle.net/1807/25774

Univerzitet u Beogradu

30. Jovičić, Milica J., 1985-. Značaj regulacije glukokortikoidnog receptora u strukturalnom modelu podložnosti za depresiju.

Degree: Medicinski fakultet, 2016, Univerzitet u Beogradu

URL: https://fedorabg.bg.ac.rs/fedora/get/o:14049/bdef:Content/get

►

medicina -neuronauke / medicine - neuroscience

Uvod. Iskustvo i istraţivanja pokazuju da podloţnost za depresiju nastaje na bazi sloţenih interakcija bioloških i psiholoških činilaca, kao… (more)

▼

medicina -neuronauke / medicine - neuroscience

Uvod. Iskustvo i istraţivanja pokazuju da podloţnost za depresiju nastaje na bazi sloţenih interakcija bioloških i psiholoških činilaca, kao i faktora sredine. MeĎutim, precizni markeri ove predispozicije i dinamika meĎusobnih relacija još uvek nisu dovoljno proučeni. Kada je reč o biološkim faktorima podloţnosti za depresiju, jedan od konzistentnijih nalaza u literaturi je odstupanje koncentracije perifernog kortizola. Ovaj hormon ostvaruje efekte vezivanjem za glukokortikoidni receptor (GR), a poremećaj signalizacije GR-a dovodi do prekomerne sekrecije kortizola u perifernoj krvi, što uslovljava delimičnu glukokortikoidnu rezistenciju kod osoba sa depresijom. MeĎutim, pokazalo se da merenje koncentracije perifernog kortizola nije pouzdan marker depresije i zbog toga je sledeći vaţan korak u istraţivanju ispitivanje sloţenih unutarćelijskih mehanizama koji regulišu aktivnost samog receptora. U ovom istraţivanju su ispitivana dva mehanizma regulacije i modulacije aktivnosti GR-a za koje se od nedavno pretpostavlja da mogu imati značaja u etiopatogenezi depresivnog poremećaja. Prvi mehanizam je vezivanje FKB506-vezujućeg proteina (FKB506-binding protein 51 − FKBP51) za kompleks GR-a (u citoplazmi), a drugi je fosforilacija GR-a (jedro). Konkretno, akcenat je stavljen na fosforilaciju GR-a na serinu 226 (pGR-226) i 211 (pGR-211), zbog prethodno uočene povezanosti sa depresijom u istraţivanjima naše grupe. Pored molekularnih mehanizama, zna se i da faktori psihološke prirode, kao što su neuroticizam i ekstroverzija (dimenzije ličnosti za koje je dokazano da modifikuju predispoziciju za depresiju), ali i faktori sredine, npr. skorašnji nepovoljni ţivotni dogaĎaji, utiču na rizik od depresivnog poremećaja. Svi navedeni elementi bio-psiho-socijalnog kontinuuma nedvosmisleno stupaju u odreĎene interakcije. Ma koliko one bile sloţene, vaţno je traţiti načine da se ove interakcije analiziraju i interpretiraju, jer jednostavni modeli bazirani na konceptu linearne kauzalnosti nisu dovoljni da bi se razumela etiopatogeneza depresije, unapredila prevencija i usavršila terapija...

Advisors/Committee Members: Marić-Bojović, Nađa.

Subjects/Keywords: depression; stress; HPA axis; glucocorticoid receptor; phosphorylation; neuroticism; affective disorders

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Jovičić, Milica J., 1. (2016). Značaj regulacije glukokortikoidnog receptora u strukturalnom modelu podložnosti za depresiju. (Thesis). Univerzitet u Beogradu. Retrieved from https://fedorabg.bg.ac.rs/fedora/get/o:14049/bdef:Content/get

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):

Jovičić, Milica J., 1985-. “Značaj regulacije glukokortikoidnog receptora u strukturalnom modelu podložnosti za depresiju.” 2016. Thesis, Univerzitet u Beogradu. Accessed January 18, 2021. https://fedorabg.bg.ac.rs/fedora/get/o:14049/bdef:Content/get.

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

MLA Handbook (7^th Edition):

Jovičić, Milica J., 1985-. “Značaj regulacije glukokortikoidnog receptora u strukturalnom modelu podložnosti za depresiju.” 2016. Web. 18 Jan 2021.

Vancouver:

Jovičić, Milica J. 1. Značaj regulacije glukokortikoidnog receptora u strukturalnom modelu podložnosti za depresiju. [Internet] [Thesis]. Univerzitet u Beogradu; 2016. [cited 2021 Jan 18]. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:14049/bdef:Content/get.

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

Council of Science Editors:

Jovičić, Milica J. 1. Značaj regulacije glukokortikoidnog receptora u strukturalnom modelu podložnosti za depresiju. [Thesis]. Univerzitet u Beogradu; 2016. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:14049/bdef:Content/get

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

		in
And / Or
		in
And / Or
		in
And / Or
		in

Open Access Theses and Dissertations