SHP/NR0B2/Nuclear Receptor SHP Products

Description

SHP (short heterodimer partner) is a bile acid-dependent orphan NR0 Knirps-Like receptor with dimerization and ligand-binding domains but not the conventional DNA-binding domain. SHP has been shown to inhibit the transcriptional activity of other nuclear receptors, including thyroid hormone receptor, constitutive androstane receptor, and retinoic acid receptors. SHP affects hepatic cholesterol catabolism based on a two-step mechanism dependent on both coactivator competition and direct transcriptional repression by mediating the repression of CYP7A1, the rate-limiting enzyme for bile acid synthesis. Mutations in the SHP gene contribute to increased body weight, indicating a possible role of SHP in the development of early-onset diabetes (maturity-onset diabetes of the young, MODY). Loss of SHP in mice caused abnormal accumulation and increased synthesis of bile acids due to derepression of rate-limiting CYP7A1 and CYP8B1 hydroxylase enzymes in the biosynthetic pathway. SHP expression has been documented in human liver, adrenal, spleen, and pancreas. ESTs have been isolated from cancerous human kidney, lung, and stomach, as well as normal human heart, kidney, liver, and liver/spleen. Caution: The nuclear receptor SHP should not be confused with the tyrosine phosphatases SHP-1 and SHP-2.

Bioinformatics

Uniprot	AAH30207 Human AAH30207.1 Human NM_021969 Human Q15466 Human
Product By Gene ID	8431
Alternate Names	FLJ17090 nuclear receptor subfamily 0 group B member 2 nuclear receptor subfamily 0, group B, member 2 Orphan nuclear receptor SHP SHPSHP1 Small heterodimer partner

Research Areas for SHP/NR0B2/Nuclear Receptor SHP

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GPCR