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GSTK1 encodes a member of the kappa class of the glutathione transferase superfamily of enzymes that function in cellular detoxification. De plus, nous expédions GSTK1 Anticorps (119) et GSTK1 Protéines (16) et beaucoup plus de produits pour cette protéine.
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Several biological properties of the GST-hNdCTR1 fusion protein were assessed. It was demonstrated that in cells, the protein was prone to oligomerization, formed inclusion bodies and displayed no toxicity. Treatment of E. coli cells with copper and silver ions reduced cell viability in a dose- and time-dependent manner
we confirmed several existing chemoinformatic filters and more importantly extended them as well as added novel filters that specify compounds with anti-GST/GSH activity. Selected compounds were also tested using different antibody-based GST detection technologies and exhibited no interference clearly demonstrating specificity toward their GST/GSH interaction.
Our findings indicate that the medical staff exposed to low IR levels were under risk of significant oxidative stress that was enhanced by their glutathione S-transferase (GST (Montrer GSTA1 Kits ELISA)) polymorphisms.
GSTK1 T/T genotype may be a novel risk factor for the prediction of overweight status in SCZ male patients.
High glutathione-S-transferase (Montrer GSTa2 Kits ELISA) is associated with type 2 diabetes mellitus.
DsbA-L is localized in both the mitochondria and the endoplasmic reticulum (ER) in adipocytes; its ER localization plays a critical role in suppressing ER stress and promoting adiponectin biosynthesis and secretion.
we have optimized the GST-Nck1-SH2 pull-down procedure to obtain tyrosine-phosphorylated proteins in tumor tissues
This study does not give evidence of interaction between the GST polymorphisms and smoking may although this study provided sufficient statistical power to detect modest interaction.
SNP-1308G/T (rs1917760) genotypes of DsbA-L gene might participate in insulin (Montrer INS Kits ELISA) secretion and body fat distribution. It is possible that polymorphisms of DsbA-L gene associated with metabolic diseases[DsbA-L]
structure and function characterization of a GST from human breast
DsbA-L prevents obesity-induced inflammation and insulin (Montrer INS Kits ELISA) resistance by suppressing the mtDNA release-activated cGAS-cGAMP-STING pathway.
These results identify DsbA-L as a critical regulator of mitochondrial function, and its down-regulation in the liver may contribute to obesity-induced hepatosteatosis and whole body insulin (Montrer INS Kits ELISA) resistance.
Results identify Sp1 (Montrer SP1 Kits ELISA) as an inhibitor of DsbA-L gene transcription, and the Sp1 (Montrer SP1 Kits ELISA)-mediated inhibition of DsbA-L gene expression may provide a mechanism underlying obesity-induced adiponectin downregulation and insulin (Montrer INS Kits ELISA) resistance.
Data suggest DsbA-L plays a role in promoting adiponectin multimerization and function (sufficient to suppress obesity-induced insulin (Montrer INS Kits ELISA) resistance and liver damage).
This gene encodes a member of the kappa class of the glutathione transferase superfamily of enzymes that function in cellular detoxification. The encoded protein is localized to the peroxisome and catalyzes the conjugation of glutathione to a wide range of hydrophobic substates facilitating the removal of these compounds from cells. Alternative splicing results in multiple transcript variants.
glutathione S-transferase, mitochondrial
, glutathione S-transferase kappa 1
, Glutathione S-transferase kappa 1
, GST class-kappa
, glutathione S-transferase k1
, glutathione S-transferase subunit 13 homolog
, GST 13-13
, glutathione S-transferase class kappa
, glutathione S-transferase subunit 13