NR0B2
Description
The NR0B2 (nuclear receptor subfamily 0 group B member 2) is a protein-coding gene located on chromosome 1.
NR0B2, also known as SHP (Small heterodimer partner), is a protein encoded by the NR0B2 gene in humans. It belongs to the nuclear receptor family of intracellular transcription factors. SHP is unique because it lacks a DNA binding domain, making it technically neither a transcription factor nor a true nuclear receptor. However, it is still classified as such due to its sequence homology with other members of the nuclear receptor family. SHP's primary role is to repress other nuclear receptors by forming non-productive heterodimers. It has also been implicated in the metabolic circadian clock. Research shows that SHP interacts with and inhibits the ligand-dependent transcriptional activation of retinoid and thyroid hormone receptors, as well as estrogen receptors. SHP represses nuclear hormone receptor-mediated transactivation through two mechanisms: competition with coactivators and its own transcriptional repressor function. A crystal structure of the LBD-only SHP, obtained through co-crystallisation with EID1, has been determined.
NR0B2, also known as SHP, is a transcriptional regulator that acts as a negative regulator of receptor-dependent signaling pathways. It specifically inhibits the transactivation of nuclear receptors with which it interacts. SHP inhibits the transcriptional activity of NEUROD1 on E-box-containing promoters by interfering with the coactivation function of the p300/CBP-mediated transcription complex for NEUROD1. It is an essential component of the liver circadian clock, regulating NPAS2-mediated hepatic lipid metabolism through its interactions with NR1D1 and RORG. SHP regulates the circadian expression of cytochrome P450 (CYP) enzymes. It represses NR5A2 and HNF4A to down-regulate CYP2C38, NFLI3 to up-regulate CYP2A5, BHLHE41/HNF1A axis to up-regulate CYP1A2, CYP2E1 and CYP3A11, and NR1D1 to up-regulate CYP2B10, CYP4A10 and CYP4A14.
NR0B2 is also known as SHP, SHP1.
