scholarly journals Pharmacologic Repression of Retinoic Acid Receptor-Related Orphan Nuclear Receptor γ Is Therapeutic in the Collagen-Induced Arthritis Experimental Model

2014 ◽  
Vol 66 (3) ◽  
pp. 579-588 ◽  
Author(s):  
Mi Ra Chang ◽  
Brent Lyda ◽  
Theodore M. Kamenecka ◽  
Patrick R. Griffin
Immunity ◽  
2012 ◽  
Vol 37 (3) ◽  
pp. 463-474 ◽  
Author(s):  
Timotheus Y.F. Halim ◽  
Aric MacLaren ◽  
Mark T. Romanish ◽  
Matthew J. Gold ◽  
Kelly M. McNagny ◽  
...  

2000 ◽  
Vol 20 (23) ◽  
pp. 8731-8739 ◽  
Author(s):  
Mime Kobayashi ◽  
Ruth T. Yu ◽  
Kunio Yasuda ◽  
Kazuhiko Umesono

ABSTRACT Malformations in the eye can be caused by either an excess or deficiency of retinoids. An early target gene of the retinoid metabolite, retinoic acid (RA), is that encoding one of its own receptors, the retinoic acid receptor β (RARβ). To better understand the mechanisms underlying this autologous regulation, we characterized the chick RARβ2 promoter. The region surrounding the transcription start site of the avian RARβ2 promoter is over 90% conserved with the corresponding region in mammals and confers strong RA-dependent transactivation in primary cultured embryonic retina cells. This response is selective for RAR but not retinoid X receptor-specific agonists, demonstrating a principal role for RAR(s) in retina cells. Retina cells exhibit a far higher sensitivity to RA than do fibroblasts or osteoblasts, a property we found likely due to expression of the orphan nuclear receptor TLX. Ectopic expression of TLX in fibroblasts resulted in increased sensitivity to RA induction, an effect that is conserved between chick and mammals. We have identified a cis element, the silencing element relieved by TLX (SET), within the RARβ2 promoter region which confers TLX- and RA-dependent transactivation. These results indicate an important role for TLX in autologous regulation of the RARβ gene in the eye.


Obesity ◽  
2012 ◽  
Vol 20 (3) ◽  
pp. 488-497 ◽  
Author(s):  
Francisco J. Tinahones ◽  
Inmaculada Moreno-Santos ◽  
Joan Vendrell ◽  
M. R. Chacon ◽  
Lourdes Garrido-Sanchez ◽  
...  

Author(s):  
Ji Min Lee ◽  
Hyunkyung Kim ◽  
Sung Hee Baek

AbstractRetinoic acid receptor-related orphan receptor-α (RORα) is a member of the orphan nuclear receptor family and functions as a transcriptional activator in response to circadian changes. Circadian rhythms are complex cellular mechanisms regulating diverse metabolic, inflammatory, and tumorigenic gene expression pathways that govern cyclic cellular physiology. Disruption of circadian regulators, including RORα, plays a critical role in tumorigenesis and facilitates the development of inflammatory hallmarks. Although RORα contributes to overall fitness among anticancer, anti-inflammatory, lipid homeostasis, and circadian clock mechanisms, the molecular mechanisms underlying the mode of transcriptional regulation by RORα remain unclear. Nonetheless, RORα has important implications for pharmacological prevention of cancer, inflammation, and metabolic diseases, and understanding context-dependent RORα regulation will provide an innovative approach for unraveling the functional link between cancer metabolism and rhythm changes.


1995 ◽  
Vol 92 (6) ◽  
pp. 2096-2100 ◽  
Author(s):  
M. Teboul ◽  
E. Enmark ◽  
Q. Li ◽  
A. C. Wikstrom ◽  
M. Pelto-Huikko ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document