Keine Produkte auf Ihrer Vergleichsliste.
Ihr Warenkorb ist leer.
Weitere Synonyme anzeigen
Wählen Sie die gewünschte Spezies
Loss of SHP expression is associated with nonalcoholic steatohepatitis.
results suggest that NR0B2 is a tumor suppressor gene in ccRCC, and that the hypermethylation of promoter region is the main mechanism of its downregulation.
DDX3 regulates MTP gene expression and lipid homeostasis through interplay with HNF4 and SHP.
The miR-141 was significantly up-regulated in the samples of metastatic tumors compared to localized tumor samples. Tumor samples showed lower SHP mRNA expression levels than BPH samples.
The impact of these variants on transactivation of the NR0B2 promoter by NRs known to be regulators of SHP1 expression was assessed in a cell-based reporter gene assay, showing that transactivation by hepatocyte nuclear factor 4alpha and liver receptor homolog-1 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 gene is a target gene of DEC1. Cotransfection demonstrated that DEC1 repressed the SHP promoter and attenuated the transactivation of the classic circadian activator complex of Clock/Bmal1.
The molecular dynamics and structural analysis of the small heterodimer partner in complex with glucocorticoid receptor is described.
The finding that overexpression of HIF-1alpha increased the activity of the CYP7A1 promoter suggested that hypoxia decreased the expression of CYP7A1 in a HIF-1-independent manner.
Results demonstrated a detrimental effect of Bcl2 and H19 associated with cholestatic liver fibrosis and an indispensable role of Shp to maintain normal liver function.
These findings show that POD-1/TCF21 regulates SF-1 and LRH-1 by distinct mechanisms, contributing to the understanding of POD-1 involvement and its mechanisms of action in adrenal and liver tumorigenesis.
Overexpression of SHP and activation of AMPK reverses profibrogenic features of HCV-infected cells by decreasing TGF-beta and fibrotic gene expression.
Data suggest that LRH1/NR5A2 (liver receptor homologue-1) exhibits phospholipid-mediated allosteric control of protein-protein binding interface in interactions with TIF2 (co-activator; transcription intermediary factor 2) and SHP.
At the molecular level, estrogen upregulated hepatic SHP expression through binding to its proximal promoter. In addition, the roles of estrogen were largely blunted in mice with SHP deficiency.
These data are suggestive of a role for SHP in controlling NLRP3 inflammasome activation through a mechanism involving interaction with NLRP3 and maintenance of mitochondrial homeostasis.
These results establish SHP as a novel antihypertrophic regulator that acts by interfering with GATA6 signaling.
E2F1 transcription factor activates early growth response (Egr)-1 promoter which is repressed by SHP and EIA-like inhibitor of differentiation (EID)1.
SHP regulates PDCD5-mediated apoptosis in cancer cells
Activation of the VDR represses hepatic SHP to increase levels of CYP7A1 and reduce cholesterol.
SHP repressed HNF4alpha transactivation of CYP2D6 promoter.
Six novel SNPs, five in ME1 and one in NR0B2, were identified as candidates that have effects on meat and carcass quality traits.
Postprandial FGF19 and SHP inhibit SREBF2, which leads to repression of intestinal NPC1L1 expression and cholesterol absorption.
ChREBP and SHP control the regulation of hepatic microsomal triglyceride transfer protein expression and VLDL Secretion. Adenoviral Overexpression of ChREBP and SHP Respectively Increased and Decreased Mttp Expression
These results demonstrate a function of RanBP2-mediated SUMOylation of SHP in maintaining bile acids (BA) homoeostasis and protecting from the BA hepatotoxicity.
Data indicate aryl hydrocarbon receptor (AhR) and small heterodimer partner (SHP) as new physiological regulators of phosphatidylcholines (PC) and S-adenosylmethionine (SAM) 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.
deletion sufficient to protect against fatty liver
SHP 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 target genes Fgf15 and Shp in ileum after long-term colonization. We show that a human microbiota can change BA composition and induce FXR signaling in colonized mice, but the levels of secondary BAs produced are lower than in mice colonized with a mouse microbiota
SHP and REV-ERBalpha play a critical role in controlling rhythmic CHOP expression in alcoholic fatty liver
our results suggest that SHP upregulation upon high-fat feeding leads to lipid accumulation, insulin resistance and inflammation in cardiomyocytes.
Mortality of SHP-/- mice after ethanol binge feeding was significantly reduced and Aldh2 mRNA level was higher. After an intoxicating dose of ethanol, SHP-/- mice exhibited faster blood ethanol clearance.
This study reveals SHP as a global transcriptional partner of SREBP-2 in regulation of sterol biosynthetic gene networks and provides a potential mechanism for cholesterol-lowering action of FGF19.
Our results suggest that SHP is required for both antidiabetic and hypolipidemic effects of TZDs in ob/ob mice through regulation of PPARgamma expression.
LSD1 is a novel histone-modifying enzyme in the orchestrated regulation mediated by the farnesoid X receptor and small heterodimer partner that reduces hepatic bile acid levels and protects the liver against bile acid toxicity.
SHP ablation creates a proinflammatory phenotype which is exacerbated after sleeve gastrectomy despite weight loss. These inflammatory alterations are possibly related to factors extrinsic to a direct manifestation of Non-alcoholic fatty liver.
Data indicate that EE2-induced cholestasis increases SHP and represses CYP2D6 expression in Tg-CYP2D6 mice in part through ERa transactivation of Shp promoter.
Neonatal exposure to diethylstilbestrol alters adult hepatic physiology in an SHP-dependent manner.
Disruption of Shp in mice alters timing of expression of genes that regulate homocysteine metabolism and the liver responses to ethanol and homocysteine. SHP inhibits the transcriptional activation of Bhmt and cystathionine gamma-lyase by FOXA1.
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