scholarly journals Nuclear Receptor Corepressor 1

2020 ◽  
Author(s):  
Keyword(s):  
Nuclear Receptor ◽  
Nuclear Receptor Corepressor

Localization of the Human Nuclear Receptor Corepressor (hN-CoR) Gene between the CMT1A and the SMS Critical Regions of Chromosome 17p11.2

Genomics ◽  
1999 ◽  
Vol 59 (3) ◽  
pp. 339-341
Author(s):  
Takashi Nagaya ◽  
Ken-Shiung Chen ◽  
Miyuki Fujieda ◽  
Sachiko Ohmori ◽  
Jennifer K. Richer ◽  
...  
Keyword(s):  
Nuclear Receptor ◽  
Nuclear Receptor Corepressor ◽  
Critical Regions

scholarly journals Nuclear Receptor Corepressor 1 Expression and Output Declines with Prostate Cancer Progression

2016 ◽  
Vol 22 (15) ◽  
pp. 3937-3949 ◽  
Author(s):  
Sandra M. Lopez ◽  
Alexander I. Agoulnik ◽  
Manqi Zhang ◽  
Leif E. Peterson ◽  
Egla Suarez ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Nuclear Receptor ◽  
Cancer Progression ◽  
Prostate Cancer Progression ◽  
Nuclear Receptor Corepressor

scholarly journals Recruitment of β-Catenin by Wild-Type or Mutant Androgen Receptors Correlates with Ligand-Stimulated Growth of Prostate Cancer Cells

2004 ◽  
Vol 18 (10) ◽  
pp. 2388-2401 ◽  
Author(s):  
David Masiello ◽  
Shao-Yong Chen ◽  
Youyuan Xu ◽  
Manon C. Verhoeven ◽  
Eunis Choi ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Nuclear Receptor ◽  
Specific Antigen ◽  
Prostate Cancer Cells ◽  
Prostate Cell ◽  
Nuclear Receptor Corepressor ◽  
Prostate Cancers

Abstract Prostate cancers respond to treatments that suppress androgen receptor (AR) function, with bicalutamide, flutamide, and cyproterone acetate (CPA) being AR antagonists in clinical use. As CPA has substantial agonist activity, it was examined to identify AR coactivator/corepressor interactions that may mediate androgen-stimulated prostate cancer growth. The CPA-liganded AR was coactivated by steroid receptor coactivator-1 (SRC-1) but did not mediate N-C terminal interactions or recruit β-catenin, indicating a nonagonist conformation. Nonetheless, CPA did not enhance AR interaction with nuclear receptor corepressor, whereas the AR antagonist RU486 (mifepristone) strongly stimulated AR-nuclear receptor corepressor binding. The role of coactivators was further assessed with a T877A AR mutation, found in LNCaP prostate cancer cells, which converts hydroxyflutamide (HF, the active flutamide metabolite) into an agonist that stimulates LNCaP cell growth. The HF and CPA-liganded T877A ARs were coactivated by SRC-1, but only the HF-liganded T877A AR was coactivated by β-catenin. L-39, a novel AR antagonist that transcriptionally activates the T877A AR, but still inhibits LNCaP growth, similarly mediated recruitment of SRC-1 and not β-catenin. In contrast, β-catenin coactivated a bicalutamide-responsive mutant AR (W741C) isolated from a bicalutamide-stimulated LNCaP subline, further implicating β-catenin recruitment in AR-stimulated growth. Androgen-stimulated prostate-specific antigen gene expression in LNCaP cells could be modulated by β-catenin, and endogenous c-myc expression was repressed by dihydrotestosterone, but not CPA. These results indicate that interactions between AR and β-catenin contribute to prostate cell growth in vivo, although specific growth promoting genes positively regulated by AR recruitment of β-catenin remain to be identified.

B565 Downregulation of Nuclear Receptor Corepressor 2 Enhances the Resistance Against Bortezomib in U26

2009 ◽  
Vol 9 ◽  
pp. S152
Author(s):  
KS Ahn ◽  
J Park ◽  
C Lee ◽  
EK Bae ◽  
BS Kim ◽  
...  
Keyword(s):  
Nuclear Receptor ◽  
Nuclear Receptor Corepressor

scholarly journals Nuclear Hormone Receptors for Heme: REV-ERBα and REV-ERBβ Are Ligand-Regulated Components of the Mammalian Clock

2008 ◽  
Vol 22 (7) ◽  
pp. 1509-1520 ◽  
Author(s):  
Thomas P. Burris
Keyword(s):  
Nuclear Receptor ◽  
Cellular Differentiation ◽  
Target Gene ◽  
Hormone Receptors ◽  
Activation Function ◽  
Nuclear Hormone Receptors ◽  
Gene Promoters ◽  
Nuclear Receptor Corepressor ◽  
Small Molecule Ligands ◽  
Target Gene Transcription

Abstract The nuclear hormone receptors (NHRs), REV-ERBα and REV-ERBβ, regulate a number of physiological functions including the circadian rhythm, lipid metabolism, and cellular differentiation. These two receptors lack the activation function-2 region that is associated with the ability of NHRs to recruit coactivators and activate target gene transcription. These NHRs have been characterized as constitutive repressors of transcription due to their lack of an identified ligand and their strong ability to recruit the corepressor, nuclear receptor corepressor. Recently, the porphyrin heme was demonstrated to function as a ligand for both REV-ERBs. Heme binds directly to the ligand-binding domain and regulates the ability of these NHRs to recruit nuclear receptor corepressor to target gene promoters. This review focuses on the physiological roles that these two receptors play and the implications of heme functioning as their ligand. The prospect that these NHRs, now known to be regulated by small molecule ligands, may be targets for development of drugs for treatment of diseases associated with aberrant circadian rhythms including metabolic and psychiatric disorders as well as cancer is also addressed.

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