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The finding that overexpression of HIF-1alpha (show HIF1A ELISA Kits) increased the activity of the CYP7A1 (show CYP7A1 ELISA Kits) promoter suggested that hypoxia decreased the expression of CYP7A1 (show CYP7A1 ELISA Kits) in a HIF-1 (show HIF1A ELISA Kits)-independent manner.
Results demonstrated a detrimental effect of Bcl2 (show BCL2 ELISA Kits) and H19 (show NCKAP1 ELISA Kits) associated with cholestatic liver fibrosis and an indispensable role of Shp (show LAMC1 ELISA Kits) to maintain normal liver function.
These findings show that POD-1/TCF21 (show TCF21 ELISA Kits) regulates SF-1 (show NR5A1 ELISA Kits) and LRH-1 (show NR5A2 ELISA Kits) by distinct mechanisms, contributing to the understanding of POD-1 (show TCF21 ELISA Kits) involvement and its mechanisms of action in adrenal and liver tumorigenesis.
Overexpression of SHP (show LAMC1 ELISA Kits) and activation of AMPK (show PRKAA1 ELISA Kits) reverses profibrogenic features of HCV-infected cells by decreasing TGF-beta (show TGFB1 ELISA Kits) and fibrotic gene expression.
Data suggest that LRH1/NR5A2 (show NR5A2 ELISA Kits) (liver receptor homologue-1) exhibits phospholipid-mediated allosteric control of protein-protein binding interface in interactions with TIF2 (show NCOA2 ELISA Kits) (co-activator; transcription intermediary factor 2) and SHP (show LAMC1 ELISA Kits).
At the molecular level, estrogen upregulated hepatic SHP (show LAMC1 ELISA Kits) expression through binding to its proximal promoter. In addition, the roles of estrogen were largely blunted in mice with SHP (show LAMC1 ELISA Kits) deficiency.
These data are suggestive of a role for SHP (show LAMC1 ELISA Kits) in controlling NLRP3 (show NLRP3 ELISA Kits) inflammasome activation through a mechanism involving interaction with NLRP3 (show NLRP3 ELISA Kits) and maintenance of mitochondrial homeostasis.
These results establish SHP (show LAMC1 ELISA Kits) as a novel antihypertrophic regulator that acts by interfering with GATA6 (show GATA6 ELISA Kits) 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 (show LAMC1 ELISA Kits) regulates PDCD5 (show PDCD5 ELISA Kits)-mediated apoptosis in cancer cells
Six novel SNPs, five in ME1 (show ME1 ELISA Kits) and one in NR0B2, were identified as candidates that have effects on meat and carcass quality traits.
Mortality of SHP (show LAMC1 ELISA Kits)-/- mice after ethanol binge feeding was significantly reduced and Aldh2 (show ALDH2 ELISA Kits) mRNA level was higher. After an intoxicating dose of ethanol, SHP (show LAMC1 ELISA Kits)-/- mice exhibited faster blood ethanol clearance.
This study reveals SHP (show LAMC1 ELISA Kits) as a global transcriptional partner of SREBP-2 (show SREBF2 ELISA Kits) in regulation of sterol biosynthetic gene networks and provides a potential mechanism for cholesterol-lowering action of FGF19 (show FGF19 ELISA Kits).
Our results suggest that SHP (show LAMC1 ELISA Kits) is required for both antidiabetic and hypolipidemic effects of TZDs in ob/ob mice through regulation of PPARgamma (show PPARG ELISA Kits) expression.
LSD1 (show KDM1A ELISA Kits) 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 (show LAMC1 ELISA Kits) 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 (show LAMC1 ELISA Kits) and represses CYP2D6 (show CYP2D6 ELISA Kits) expression in Tg-CYP2D6 (show CYP2D6 ELISA Kits) mice in part through ERa transactivation of Shp (show LAMC1 ELISA Kits) promoter.
Neonatal exposure to diethylstilbestrol alters adult hepatic physiology in an SHP (show LAMC1 ELISA Kits)-dependent manner.
Disruption of Shp (show LAMC1 ELISA Kits) in mice alters timing of expression of genes that regulate homocysteine metabolism and the liver responses to ethanol and homocysteine. SHP (show LAMC1 ELISA Kits) inhibits the transcriptional activation of Bhmt (show BHMT ELISA Kits) and cystathionine gamma-lyase (show CTH ELISA Kits) by FOXA1 (show FOXA1 ELISA Kits).
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