作者: Gabriela Hernández-Puga , Pamela Navarrete-Ramírez , Arturo Mendoza , Aurora Olvera , Patricia Villalobos
DOI: 10.1016/J.MCE.2016.01.023
关键词:
摘要: T3 and cortisol activate or repress gene expression in virtually every vertebrate cell mainly by interacting with their nuclear hormone receptors. In contrast to the mechanisms for activation, involved repression remain elusive. teleosts, thyroid receptor beta thrb produces two isoforms of TRβ1 that differ nine amino acids ligand-binding domain long-TRβ1, whereas short-TRβ1 lacks insert. Previous reports have shown genomic effects exerted 3,5-T2, a product outer-ring deiodination, are mediated long-TRβ1. Furthermore, 3,5-T2 down-regulate long-TRβ1 short-TRβ1, respectively. contrast, has been up-regulate thrb. To understand molecular modulation hormones cortisol, we used an silico approach identify thyroid- cortisol-response elements within proximal promoter from tilapia. We then characterized identified response EMSA correlated our observations THs upon Our data show represses impairs its up-regulation possibly through transrepression mechanism. propose down-regulation, ligands other than required orchestrate pleiotropic vertebrates.