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The impact of these variants on transactivation of the NR0B2 promoter by NRs (show SPNS1 Proteins) known to be regulators of SHP1 (show PTPN6 Proteins) expression was assessed in a cell-based reporter gene assay, showing that transactivation by hepatocyte nuclear factor 4alpha and liver receptor homolog-1 (show NR5A2 Proteins) was significantly decreased in the presence of the genetic variant NR0B2:c.-594T>
Data indicate a functional interaction between small heterodimer partner protein SHP1 and hepatitis C virus (HCV) NS5A protein.
This study was performed to test the hypothesis that the SHP (show LAMC1 Proteins) gene is a target gene of DEC1 (show BHLHE40 Proteins). Cotransfection demonstrated that DEC1 (show BHLHE40 Proteins) repressed the SHP (show LAMC1 Proteins) promoter and attenuated the transactivation of the classic circadian activator complex of Clock/Bmal1 (show ARNTL Proteins).
The molecular dynamics and structural analysis of the small heterodimer partner in complex with glucocorticoid receptor (show NR3C1 Proteins) is described.
The finding that overexpression of HIF-1alpha (show HIF1A Proteins) increased the activity of the CYP7A1 (show CYP7A1 Proteins) promoter suggested that hypoxia decreased the expression of CYP7A1 (show CYP7A1 Proteins) in a HIF-1 (show HIF1A Proteins)-independent manner.
Results demonstrated a detrimental effect of Bcl2 (show BCL2 Proteins) and H19 (show NCKAP1 Proteins) associated with cholestatic liver fibrosis and an indispensable role of Shp (show LAMC1 Proteins) to maintain normal liver function.
These findings show that POD-1/TCF21 (show TCF21 Proteins) regulates SF-1 (show NR5A1 Proteins) and LRH-1 (show NR5A2 Proteins) by distinct mechanisms, contributing to the understanding of POD-1 (show TCF21 Proteins) involvement and its mechanisms of action in adrenal and liver tumorigenesis.
Overexpression of SHP (show LAMC1 Proteins) and activation of AMPK (show PRKAA1 Proteins) reverses profibrogenic features of HCV-infected cells by decreasing TGF-beta (show TGFB1 Proteins) and fibrotic gene expression.
Data suggest that LRH1/NR5A2 (show NR5A2 Proteins) (liver receptor homologue-1) exhibits phospholipid-mediated allosteric control of protein-protein binding interface in interactions with TIF2 (show NCOA2 Proteins) (co-activator; transcription intermediary factor 2) and SHP (show LAMC1 Proteins).
At the molecular level, estrogen upregulated hepatic SHP (show LAMC1 Proteins) expression through binding to its proximal promoter. In addition, the roles of estrogen were largely blunted in mice with SHP (show LAMC1 Proteins) deficiency.
Six novel SNPs, five in ME1 (show ME1 Proteins) and one in NR0B2, were identified as candidates that have effects on meat and carcass quality traits.
These results demonstrate a function of RanBP2-mediated SUMOylation of SHP (show LAMC1 Proteins) in maintaining bile acids (BA) homoeostasis and protecting from the BA hepatotoxicity.
Data indicate aryl hydrocarbon receptor (AhR (show AHR Proteins)) and small heterodimer partner (SHP) as new physiological regulators of phosphatidylcholines (PC) and S-adenosylmethionine (SAM (show TTN Proteins)) levels.
Data confirm that hepatic stellate cell activation and alteration in hepatic gene expression observed in offspring of dames on vitamin A-deficient diet from mid-gestation are dependent on retinol and Shp/Nr0b2; these alterations in the offspring are reversed by high-fat diet.
SHP (show LAMC1 Proteins) deficiency protects myocardia from lipid accumulation in high fat diet-fed mice.
human microbiota was able to reduce the levels of tauro-beta-muricholic acid and induce expression of FXR (show NR1H4 Proteins) target genes Fgf15 and Shp (show LAMC1 Proteins) in ileum after long-term colonization. We show that a human microbiota can change BA composition and induce FXR (show NR1H4 Proteins) signaling in colonized mice, but the levels of secondary BAs produced are lower than in mice colonized with a mouse microbiota
SHP (show LAMC1 Proteins) and REV-ERBalpha (show NR1D1 Proteins) play a critical role in controlling rhythmic CHOP (show DDIT3 Proteins) expression in alcoholic fatty liver
our results suggest that SHP (show LAMC1 Proteins) upregulation upon high-fat feeding leads to lipid accumulation, insulin (show INS Proteins) resistance and inflammation in cardiomyocytes.
Mortality of SHP (show LAMC1 Proteins)-/- mice after ethanol binge feeding was significantly reduced and Aldh2 (show ALDH2 Proteins) mRNA level was higher. After an intoxicating dose of ethanol, SHP (show LAMC1 Proteins)-/- mice exhibited faster blood ethanol clearance.
This study reveals SHP (show LAMC1 Proteins) as a global transcriptional partner of SREBP-2 (show SREBF2 Proteins) in regulation of sterol biosynthetic gene networks and provides a potential mechanism for cholesterol-lowering action of FGF19 (show FGF19 Proteins).
Our results suggest that SHP (show LAMC1 Proteins) is required for both antidiabetic and hypolipidemic effects of TZDs in ob/ob mice through regulation of PPARgamma (show PPARG Proteins) expression.
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. Studies suggest that the protein represses nuclear hormone receptor-mediated transactivation via two separate steps: competition with coactivators and the direct effects of its transcriptional repressor function.
short heterodimer partner
, nuclear receptor subfamily 0 group B member 2
, nuclear receptor SHP
, orphan nuclear receptor SHP
, small heterodimer partner
, small heterodimer partner homologue