Open AccessFormation of retinoid X receptor homodimers leads to repression of T3 response: hormonal cross talk by ligand-induced squelching.
Author(s) -
J. Lehmann,
Xiaokun Zhang,
Gerhart Graupner,
MiOck Lee,
T Hermann,
Birgit Hoffmann,
Magnus Pfahl
Publication year - 1993
Publication title -
molecular and cellular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.14
H-Index - 327
eISSN - 1067-8824
pISSN - 0270-7306
DOI - 10.1128/mcb.13.12.7698
Subject(s) - retinoid x receptor , nuclear receptor , thyroid hormone receptor , retinoid x receptor alpha , biology , retinoic acid , psychological repression , retinoid , receptor , repressor , ligand (biochemistry) , hormone , microbiology and biotechnology , biochemistry , bexarotene , retinoid x receptor gamma , transcription factor , gene , gene expression
Thyroid hormone receptors (TRs) form heterodimers with retinoid X receptors (RXRs). Heterodimerization is required for efficient TR DNA binding to most response elements and transcriptional activation by thyroid hormone. RXRs also function as auxiliary proteins for several other receptors. In addition, RXR alpha can be induced by specific ligands to form homodimers. Here we report that RXR-specific retinoids that induce RXR homodimers are effective repressors of the T3 response. We provide evidence that this repression by RXR-specific ligands occurs by sequestering of RXR from TR-RXR heterodimers into RXR homodimers. This ligand-induced squelching may represent an important mechanism by which RXR-specific retinoids and 9-cis retinoic acid mediate hormonal cross talk among a subfamily of nuclear receptors activated by structurally unrelated ligands.