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Stanniocalcin 1 downregulation is responsible for sorafenib-induced cardiotoxicity through activated ROS (show ROS1 Proteins) generation.
the results suggest that the CaSR (show CASR Proteins) is critical for Ca(2 (show CA2 Proteins)+) homeostasis in larval zebrafish exposed to low environmental Ca(2 (show CA2 Proteins)+) levels, possibly owing to its modulation of stanniocalcin (show LOC100135946 Proteins) mRNA expression.
This study showed that stanniocalcin 1 (stc1)modulates cation levels in trpm7 (show TRPM7 Proteins) mutants and in the wild type; levels of cations are restored to normal in trpm7 (show TRPM7 Proteins) mutants when stc1 activity is blocked.
STC-1 negatively regulates epithelial Ca(2 (show CA2 Proteins)+) channel gene expression to reduce Ca(2 (show CA2 Proteins)+) uptake in zebrafish embryos
Ssecretory STC1 enhances metastatic potential of hepatocellular carcinomas via JNK (show MAPK8 Proteins) signaling.
Glycolysis from glucose is regulated by hSTC-1, decreasing the adequate supply of glycerol-3-phosphate (G3P) needed for fatty acid esterification and triacylglycerol (TG) storage in brown adipose tissue (BAT (show BAAT Proteins)). The decrease of TG capacity synthesis from glucose by hSTC-1 compromises the BAT (show BAAT Proteins) thermogenic capacity.
Increased STC1 plasma level represents a hallmark of late-onset preeclampsia; STC1 gene variants modulate placental gene expression and maternal hormone levels.
Latanoprost-induced reduction of intraocular pressure is mediated through the downstream signaling molecule STC-1. When used by itself, STC-1 exhibits ocular hypotensive properties.
Study demonstrates that STC1 is overexpressed in the prostate carcinoma cell lines and suggests that it promotes prostate carcinoma cell proliferation via cyclin E1 (show CCNE1 Proteins)/CDK2 (show CDK2 Proteins).
In the fed state, STC1 increases the incorporation of (14)C from glucose into lipids in the white retroperitoneal adipose tissue (WRAT). STC1 is one of the hormonal factors that control glucose metabolism in WRAT in the fed state.
STC1 protein is significantly up-regulated in midsecretory endometrial fluid and is dysregulated in eutopic endometrial tissue from women with endometriosis. It is likely regulated by cAMP and may be involved in the pathogenesis of decidualization defects.
STC1 expression is significantly upregulated in human masticatory mucosa during wound healing
elevated STC-1 expression is associated with poor clinical outcome in triple-negative breast cancer (TNBC) patients, and STC-1 is directly involved in the invasiveness of TNBC cells
we demonstrated that aberrant STC1 expression is associated with poor prognosis and stimulates the invasiveness of triplenegative breast cancer cells
The temporal and cell type-specific expression of STC1 makes this gene a unique marker for implantation in pigs.
The effect of STC1 on the steroidogenetic pathway in cultured granulosa cells is reported.
Over-expression of STC-1 up-regulated Bcl-2 (show BCL2 Proteins) protein expression and slightly down-regulated caspase-3 (show CASP3 Proteins) production in the damaged cells. Findings from this study suggest that STC-1 plays a protective role in intestinal cells through an antioxidant mechanism.
theca cell-derived big STC is targeted to the cholesterol/lipid storage droplets of luteal cells to regulate steroidogenesis.
once removed from their normal context within the ovary, luteal cells are capable of synthesizing and secreting big STC.
STC-1 in milk is increased following milk stasis
STC-1 maybe improve anti-inflammation, anti-oxidant and anti-apoptosis activities by affecting reactive oxygen species -mediated pathways, especially the phospho-modifications of the respective proteins, resulting in the increase of Superoxide dismutase (show SOD1 Proteins) and reduce of capase-3, p53 (show TP53 Proteins), IL-6 (show IL6 Proteins) and IFN-gamma (show IFNG Proteins).
STC1 blunts bleomycin-induced rise in thrombin protein and activity, diminishes thrombin (show F2 Proteins)-induced signaling through PAR1 (show F2R Proteins) to ERK (show EPHB2 Proteins), and inhibits bleomycin-induced pneumonitis.
Stanniocalcin 1 is expressed in thyroid side population cells and thyroid cancer cells.
Mesenchymal stem cells correct inappropriate epithelial-mesenchyme relation in pulmonary fibrosis using Stc1.
Stanniocalcin-1 inhibits renal ischemia/reperfusion injury via an AMP-activated protein kinase (show PRKAA2 Proteins)-dependent pathway.
STC1 is an endogenous stress protein that may counteract LPS (show TLR4 Proteins)-induced lung injury by inhibiting the inflammatory cascade and inducing antioxidant and antiapoptotic mechanisms.
Remarkably, X-linked genes are not overexpressed in female Stc1(-/-) mice, revealing the existence of a mechanism(s) that can compensate for a persistent XCI deficiency to regulate X-linked gene expression.
Overexpression of stanniocalcin-1 inhibits reactive oxygen species and renal ischemia/reperfusion injury.
STC1 was not crucial for the development of ischemic tolerance triggered by hypoxic preconditioning, or for preserving blood-brain barrier integrity but may be involved in functional recovery after stroke.
This gene encodes a secreted, homodimeric glycoprotein that is expressed in a wide variety of tissues and may have autocrine or paracrine functions. The gene contains a 5' UTR rich in CAG trinucleotide repeats. The encoded protein contains 11 conserved cysteine residues and is phosphorylated by protein kinase C exclusively on its serine residues. The protein may play a role in the regulation of renal and intestinal calcium and phosphate transport, cell metabolism, or cellular calcium/phosphate homeostasis. Overexpression of human stanniocalcin 1 in mice produces high serum phosphate levels, dwarfism, and increased metabolic rate. This gene has altered expression in hepatocellular, ovarian, and breast cancers.