scholarly journals Negative cross-talk between the human orphan nuclear receptor Nur77/NAK-1/TR3 and nuclear factor- B

2004 ◽  
Vol 32 (17) ◽  
pp. 5280-5290 ◽  
Author(s):  
H. Harant
Keyword(s):  
Nuclear Receptor ◽  
Cross Talk ◽  
Nuclear Factor ◽  
Orphan Nuclear Receptor ◽  
Factor B

Orphan nuclear receptor SHP interacts with and represses hepatocyte nuclear factor-6 (HNF-6) transactivation

2008 ◽  
Vol 413 (3) ◽  
pp. 559-569 ◽  
Author(s):  
Yong-Soo Lee ◽  
Don-Kyu Kim ◽  
Yong Deuk Kim ◽  
Ki Cheol Park ◽  
Minho Shong ◽  
...  
Keyword(s):  
Nuclear Receptor ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Target Genes ◽  
Consensus Sequence ◽  
Nuclear Factor ◽  
Orphan Nuclear Receptor ◽  
Hepatocyte Nuclear Factor ◽  
Mobility Shift ◽  
Endocrine Differentiation

SHP (small heterodimer partner; NR0B2) is an atypical orphan NR (nuclear receptor) that functions as a transcriptional co-repressor by interacting with a diverse set of NRs and transcriptional factors. HNF-6 (hepatocyte nuclear factor-6) is a key regulatory factor in pancreatic development, endocrine differentiation and the formation of the biliary tract, as well as glucose metabolism. In this study, we have investigated the function of SHP as a putative repressor of HNF-6. Using transient transfection assays, we have shown that SHP represses the transcriptional activity of HNF-6. Confocal microscopy revealed that both SHP and HNF-6 co-localize in the nuclei of cells. SHP physically interacted with HNF-6 in protein–protein association assays in vitro. EMSAs (electrophoretic mobility-shift assays) and ChIP (chromatin immunoprecipitation) assays demonstrated that SHP inhibits the DNA-binding activity of HNF-6 to an HNF-6-response element consensus sequence, and the HNF-6 target region of the endogenous G6Pase (glucose 6-phosphatase) promoter respectively. Northern blot analysis of HNF-6 target genes in cells infected with adenoviral vectors for SHP and SHP siRNAs (small inhibitory RNAs) indicated that SHP represses the expression of endogenous G6Pase and PEPCK (phosphoenolpyruvate carboxykinase). Our results suggest that HNF-6 is a novel target of SHP in the regulation of gluconeogenesis.

ERα/E2 signaling suppresses the expression of steroidogenic enzyme genes via cross-talk with orphan nuclear receptor Nur77 in the testes

2012 ◽  
Vol 362 (1-2) ◽  
pp. 91-103 ◽  
Author(s):  
Seung-Yon Lee ◽  
Eunsook Park ◽  
Seung-Chang Kim ◽  
Ryun-Sup Ahn ◽  
CheMyong Ko ◽  
...  
Keyword(s):  
Nuclear Receptor ◽  
Cross Talk ◽  
Orphan Nuclear Receptor ◽  
Steroidogenic Enzyme

scholarly journals Loss of Orphan Receptor Germ Cell Nuclear Factor Function Results in Ectopic Development of the Tail Bud and a Novel Posterior Truncation

2001 ◽  
Vol 21 (2) ◽  
pp. 663-677 ◽  
Author(s):  
Arthur C.-K. Chung ◽  
Deborah Katz ◽  
Fred A. Pereira ◽  
Kathy J. Jackson ◽  
Francesco J. DeMayo ◽  
...  
Keyword(s):  
Germ Cell ◽  
Nuclear Receptor ◽  
Germ Line ◽  
Physiological Role ◽  
Orphan Receptor ◽  
Marker Genes ◽  
Nuclear Factor ◽  
Orphan Nuclear Receptor ◽  
Embryonic Survival ◽  
Germ Cell Nuclear Factor

ABSTRACT The dynamic embryonic expression of germ cell nuclear factor (GCNF), an orphan nuclear receptor, suggests that it may play an important role during early development. To determine the physiological role of GCNF, we have generated a targeted mutation of theGCNF gene in mice. Germ line mutation of theGCNF gene proves that the orphan nuclear receptor is essential for embryonic survival and normal development. GCNF−/− embryos cannot survive beyond 10.5 days postcoitum (dpc), probably due to cardiovascular failure. Prior to death, GCNF−/− embryos suffer significant defects in posterior development. Unlike GCNF+/+ embryos, GCNF−/− embryos do not turn and remain in a lordotic position, the majority of the neural tube remains open, and the hindgut fails to close. GCNF−/− embryos also suffer serious defects in trunk development, specifically in somitogenesis, which terminates by 8.75 dpc. The maximum number of somites in GCNF−/− embryos is 13 instead of 25 as in the GCNF+/+ embryos. Interestingly, the tailbud of GCNF−/− embryos develops ectopically outside the yolk sac. Indeed, alterations in expression of multiple marker genes were identified in the posterior of GCNF−/− embryos, including the primitive streak, the node, and the presomitic mesoderm. These results suggest that GCNF is required for maintenance of somitogenesis and posterior development and is essential for embryonic survival. These results suggest that GCNF regulates a novel and critical developmental pathway involved in normal anteroposterior development.

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