Short Heterodimer Partner (SHP) Orphan Nuclear Receptor Inhibits the Transcriptional Activity of Aryl Hydrocarbon Receptor (AHR)/AHR Nuclear Translocator (ARNT)

2001 ◽  
Vol 390 (1) ◽  
pp. 64-70 ◽  
Author(s):  
Carolyn M. Klinge ◽  
Sarah C. Jernigan ◽  
Kelly E. Risinger ◽  
Jennie E. Lee ◽  
Valentyn V. Tyulmenkov ◽  
...  
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
Nuclear Receptor ◽  
Transcriptional Activity ◽  
Orphan Nuclear Receptor ◽  
Aryl Hydrocarbon ◽  
Short Heterodimer Partner

scholarly journals The Role of the Aryl Hydrocarbon Receptor (AHR) in Immune and Inflammatory Diseases

2018 ◽  
Vol 19 (12) ◽  
pp. 3851 ◽  
Author(s):  
Drew Neavin ◽  
Duan Liu ◽  
Balmiki Ray ◽  
Richard Weinshilboum
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
Nuclear Receptor ◽  
Binding Sites ◽  
Inflammatory Responses ◽  
Inflammatory Diseases ◽  
Dependent Manner ◽  
Nucleotide Polymorphisms ◽  
Aryl Hydrocarbon ◽  
Inflammatory Processes ◽  
Targeted Gene Expression

The aryl hydrocarbon receptor (AHR) is a nuclear receptor that modulates the response to environmental stimuli. It was recognized historically for its role in toxicology but, in recent decades, it has been increasingly recognized as an important modulator of disease—especially for its role in modulating immune and inflammatory responses. AHR has been implicated in many diseases that are driven by immune/inflammatory processes, including major depressive disorder, multiple sclerosis, rheumatoid arthritis, asthma, and allergic responses, among others. The mechanisms by which AHR has been suggested to impact immune/inflammatory diseases include targeted gene expression and altered immune differentiation. It has been suggested that single nucleotide polymorphisms (SNPs) that are near AHR-regulated genes may contribute to AHR-dependent disease mechanisms/pathways. Further, we have found that SNPs that are outside of nuclear receptor binding sites (i.e., outside of AHR response elements (AHREs)) may contribute to AHR-dependent gene regulation in a SNP- and ligand-dependent manner. This review will discuss the evidence and mechanisms of AHR contributions to immune/inflammatory diseases and will consider the possibility that SNPs that are outside of AHR binding sites might contribute to AHR ligand-dependent inter-individual variation in disease pathophysiology and response to pharmacotherapeutics.

scholarly journals Complex regulation of orphan nuclear receptor Nur77 (Nr4a1) transcriptional activity by SUMO2 and PIASγ

2021 ◽  
Vol 1868 (2) ◽  
pp. 118908
Author(s):  
Fatéma Dodat ◽  
David Cotnoir-White ◽  
Elham Dianati ◽  
Amandine Vallet ◽  
Sylvie Mader ◽  
...  
Keyword(s):  
Nuclear Receptor ◽  
Transcriptional Activity ◽  
Orphan Nuclear Receptor ◽  
Complex Regulation

scholarly journals The Orphan Nuclear Receptor SHP Inhibits Agonist-dependent Transcriptional Activity of Estrogen Receptors ERα and ERβ

1999 ◽  
Vol 274 (1) ◽  
pp. 345-353 ◽  
Author(s):  
Lotta Johansson ◽  
Jane S. Thomsen ◽  
Anastasios E. Damdimopoulos ◽  
Giannis Spyrou ◽  
Jan-Åke Gustafsson ◽  
...  
Keyword(s):  
Estrogen Receptors ◽  
Nuclear Receptor ◽  
Transcriptional Activity ◽  
Orphan Nuclear Receptor

scholarly journals Orphan nuclear receptor TR3/Nur77 regulates VEGF-A–induced angiogenesis through its transcriptional activity

2006 ◽  
Vol 203 (3) ◽  
pp. 719-729 ◽  
Author(s):  
Huiyan Zeng ◽  
Liuliang Qin ◽  
Dezheng Zhao ◽  
Xiaolian Tan ◽  
Eleanor J. Manseau ◽  
...  
Keyword(s):  
Nuclear Receptor ◽  
Transcriptional Activity ◽  
Umbilical Vein ◽  
Early Response ◽  
Tube Formation ◽  
Orphan Nuclear Receptor ◽  
Dna Binding Domains ◽  
Binding Domains ◽  
Umbilical Vein Endothelial Cells

Vascular endothelial growth factor (VEGF)-A has essential roles in vasculogenesis and angiogenesis, but the downstream steps and mechanisms by which human VEGF-A acts are incompletely understood. We report here that human VEGF-A exerts much of its angiogenic activity by up-regulating the expression of TR3 (mouse homologue Nur77), an immediate-early response gene and orphan nuclear receptor transcription factor previously implicated in tumor cell, lymphocyte, and neuronal growth and apoptosis. Overexpression of TR3 in human umbilical vein endothelial cells (HUVECs) resulted in VEGF-A–independent proliferation, survival, and induction of several cell cycle genes, whereas expression of antisense TR3 abrogated the response to VEGF-A in these assays and also inhibited tube formation. Nur77 was highly expressed in several types of VEGF-A–dependent pathological angiogenesis in vivo. Also, using a novel endothelial cell-selective retroviral targeting system, overexpression of Nur77 DNA potently induced angiogenesis in the absence of exogenous VEGF-A, whereas Nur77 antisense strongly inhibited VEGF-A–induced angiogenesis. B16F1 melanoma growth and angiogenesis were greatly inhibited in Nur77−/− mice. Mechanistic studies with TR3/Nur77 mutants revealed that TR3/Nur77 exerted most of its effects on cultured HUVECs and its pro-angiogenic effects in vivo, through its transactivation and DNA binding domains (i.e., through transcriptional activity).

Sign in / Sign up

Export Citation Format

Share Document