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Validated All-in-One™ qPCR Primer for NR0B2(NM_021969.2) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Summary
The protein encoded by this gene is an unusual orphan receptor that contains a putative ligand-binding domain but lacks a conventional DNA-binding domain. The gene product is a member of the nuclear hormone receptor family, a group of transcription factors regulated by small hydrophobic hormones, a subset of which do not have known ligands and are referred to as orphan nuclear receptors. The protein has been shown to interact with retinoid and thyroid hormone receptors, inhibiting their ligand-dependent transcriptional activation. In addition, interaction with estrogen receptors has been demonstrated, leading to inhibition of function.
Gene References into function
- polymorphisms in the human SHP1 gene; found no rare SHP1 coding sequence variants that were exclusive to patients with lipodystrophy
- SHP is able to interact with LXR and to modulate its transcriptional activity.
- SHP has a role in modulating hepatic glucocorticoid action
- the relation between genetic variation in SHP and birth weight, adiposity, and insulin levels in three independent populations
- orphan receptor small heterodimer partner expression is regulated by estrogen receptor alpha
- Modulation of SHP expression and/or activity in adipose tissue may therefore have significant effects on aromatase expression and estrogen production in breast adipose tissue.
- basic helix-loop-helix (bHLH) transcription factors, the E2A proteins (E47, E12 and E2/5), activated the human but not the mouse SHP promoter
- results suggest that bile acids negatively regulate the human angiotensinogen gene through the inhibitory effect of small heterodimer partner on hepatocyte nuclear factor-4
- Acts as a novel corepressor for basic helix-loop-helix transcription factor BETA2/NeuroD
- At diagnosis, methylation of SHP1 occurred more frequently in acute myeloid leukaemia than acute lymphoblastic leukaemia. Frequent methylation of SHP1, but not SOCS1, may be important in the pathogenesis, but not prognosis, of acute leukaemias
- orphan nuclear receptor small heterodimer partner promoter is regulated by sterol regulatory element binding protein-1
- PGC-1alpha mediates the ligand-dependent activation of FXR and transcription of SHP gene.
- SHP-1 tyrosine phosphatase is regulated in human platelets by serine phosphorylation at its C terminus
- c-Jun works to activate the expression of SHP genes associated with the cascade regulation of monocytic differentiation.
- Results suggest that SHP mediates recruitment of mSin3A-Swi/Snf to the CYP7A1 promoter, resulting in chromatin remodeling and gene repression.
- NR0B2 is involved in the regulation of G6Pase, CYP7A1, and PEPCK gene expression via novel mechanism of inhibition of HNF3 activity and expand the role of NR0B2 as a coregulator of other family of transcription factors in addition to nuclear receptors.
- SHP mutations found in obese Danish men
- crystal structure at 1.9 A resoluation of the ligand-binding domain of hLRH-1 in complex with the NR box 1 motif of human SHP, which contacts the AF-2 region of hLRH-1 using selective structural motifs
- SHP affects genes involved in diverse biological pathways, e.g., several key genes involved in consecutive steps of cholesterol degradation, bile acid conjugation, transport and lipogenic pathways.
- The GR/dexamethasone activation of the hNTCP promoter is counteracted by bile acids and small heterodimer partner, providing a negative feedback mechanism for bile acid uptake in human hepatocytes.
- LRH-1 and SHP1 regulate 3-hydroxy-3-methylglutaryl coenzyme A reductase promoter and have a role in regulation of cholesterol synthesis and uptake
- DAX1 and small heterodimer partner (SHP) form homodimers individually, as well as DAX1-SHP heterodimers suggesting the possibility of novel functions independent of their coregulator roles.
- both SHP-1 and SHP-2 have a positive role in epidermal growth factor-induced ERK1/2 activation and they act cooperatively rather than antagonistically.
- SHP deficiency leads to improvement in insulin sensitivity and secretion.
- Loss of SHP1 enhances JAK3/STAT3 signaling and decreases proteosome degradation of JAK3 and NPM-ALK in ALK+ anaplastic large-cell lymphoma.
- SHP is a novel co-regulator of Smad3 that regulates TGF-beta signaling
- results suggest that SHP might regulate a level of hepatic gluconeogenesis driven by C/EBPalpha activation
- These studies establish a critical role for G9a methyltransferase, histone deacetylases, and the Swi/Snf-Brm complex in the SHP-mediated inhibition of hepatic bile acid synthesis via coordinated chromatin modification at target genes.
- New roles for SHP in testicular androgen and retinoic acid metabolism, making SHP a testicular gatekeeper of the timing of male sexual maturation.
- LRH-1 stimulation of the FAS LXR response is blocked by the addition of small heterodimer partner (SHP) and that FAS mRNA
- The repressive functions of SHP and DAX-1 have been conserved in fish and mammals although with different transcriptional targets and mechanisms.
- LRH-1/phospholipid and LRH-1/SHP (fragments) interactions are analyzed by counting atomic contact number, identifying hydrogen bonds, and estimating binding free energies
- Small heterodimer partner (SHP), an orphan nuclear hormone receptor lacking a DNA binding domain, inhibits nuclear hormone receptor-mediated hepatitis B viral transcription and replication.
- SHP-1 acts as a sensor for hydroxynonenal and is responsible for an adaptive response to oxidative stress in respiratory epithetlium.
- These results indicate that bile acid performs a critical function in the regulation of the induction of inflammatory-related genes in gastric cells
- Propose that SHP functions as a novel tumor suppressor in the development of heptaocellular carcinoma.
- PGC-1alpha is an important co-activator for LRH-1 and that SHP targets the interaction between LRH-1 and PGC-1alpha to inhibit CYP7A1 expression.
- Data have shown that SHP represses the transcriptional activity of hepatocyte nuclear factor-6 that serves as a novel target in the regulation of gluconeogenesis.
- These results indicate that SMILE isoforms regulate the inhibition of estrogen receptor transactivation by SHP in a cell-type-specific manner and act as a novel transcriptional co-regulator in ER signalling.
- bile acid induces an increase in the gene expression of COX-2 via the sequential transcriptional induction of SHP and CDX1 in precancerous lesions of human gastric cancer.
- Mutations in SHP associated with mild obesity in childhood increase susceptibility to type 2 diabetes in later life in Japanese patients.
- p300 acts as a critical coactivator of FXR induction of SHP by acetylating histones at the promoter and FXR itself
