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Studied the importance of selenium in bovine female reproductive function. Gene expression analysis revealed selenoprotein gene GPX1 was significantly up-regulated in large healthy follicles.
did not find any significant inhibition of bovine GPx-1 by (S)- or (R)-misonidazole.
Data indicate a positive correlation between GSH-Px activity and serum selenium concentration for all the cows analysed together.
Data indicate mRNA level and activity of GPx1 are regulated by level of selenium supplied to hepatocytes.
homocysteine decreases GPx1 activity by altering the translational mechanism
glutathione peroxidase-1 activity is decreased by aminoglycosides through interference with selenocysteine incorporation
GPx1 plays a key role in blocking the promotion of porcine circovirus type 2 replication
The developmental expression of GPX1 and thioredoxin reductase during fetal development and the effect of maternal selenium consumption on the expression of these proteins are reported.
GPx-1 knockout potentiated methamphetamine-induced cognitive deficits and alterations in phospho-ERK1/2 and phospho-PKCdelta expression.
This repletion study shows that loss of capacity to incorporate Se into Gpx1 in Gpx1 KO mice does not dramatically alter expression of other Se biomarkers, nor the short-term flux of Se from intestine to liver to kidney.
interactive modulations between the GPx-1 gene and Nrf2-dependent glutathione induction are critical for attenuating phencyclidine-induced abnormal behaviors in mice.
Notably, CUEDC2 promoted E3 ubiquitin ligases tripartite motif-containing 33 (TRIM33)-mediated the antioxidant enzyme, glutathione peroxidase 1 (GPX1) ubiquitination, and proteasome-dependent degradation.
GPx1 does not clearly exacerbate hyperoxia-induced increases in oxidative stress or lung injury but may alter pulmonary immune function.
GPx-1 expression deters the unfolded protein response following exposure to cigarette smoke
Glutathione peroxidase 1 (GPx1) knockdown not only induced oxidative stress characterized by the increased production of reactive oxygen species (ROS) but also caused reductive stress indicated by an elevation of glutathione (GSH)/oxidized GSH (GSSG) ratio.
Exposure to far infrared rays significantly protects acute restraint stress oxidative burdens via inhibition of JAK2/STAT3 signaling by induction of GPx-1.
Genetic inhibition of Gpx1 potentiates cocaine-induced renal damage via activation of AT1R by inhibition of PI3K-Akt signaling.
Glutathione peroxidase 1 deficiency attenuates concanavalin A-induced liver injury by induction of T-cell hyporesponsiveness through chronic reactive oxygen species exposure.
GPx1 was found to play a critical role in regulating pro-inflammatory pathways in vascular endothelium.
Plasmalogen enrichment via batyl alcohol supplementation attenuated atherosclerosis in ApoE- and ApoE/GPx1-deficient mice.
Gpx1 expression in the mouse skeletal muscle can be altered by both exercise and dyslipidemia through changes in DNA methylation, leading to a fine regulation of free radical metabolism.
our findings unveil a new metabolic role for Reg3beta in protein nitration and a new biosynthesis control of GPX1 by a completely "unrelated" regenerating protein, Reg3beta, via transcriptional activation of Scly
Rora induces the mRNA level of antioxidant enzymes, superoxide dismutase 2 and glutathione peroxidase 1, through the Rora response elements located in the upstream promoters of Sod2 and Gpx1.
High-fat-fed Gpx1(-/-) mice also exhibited decreased hepatic steatosis and liver damage accompanied by decreased plasma insulin and decreased glucose-induced insulin secretion.
we propose that ileocolitis in the DKO mice is caused by Nox1, which is induced by TNF. The milder disease in female het-TKO intestine is probably due to random or imprinted X-chromosome inactivation, which produces mosaic Nox1 expression.
PD-linked mutations in Parkin and DJ-1 cause dysregulation of neurotransmitter systems beyond the nigrostriatal dopaminergic circuit especially in the context of Gpx1 deficiency.
During early differentiation of embryonic stem (ES) cells, the quick degradation of GPx-1 was mediated by proteasome. Both knockdown of GPx-1 expression with shRNA and inhibiting GPx-1 activity by inhibitor led to the differentiation of ES cells.
Data indicate that he macrophage-colony-stimulating factor (MCSF) and oxLDL-induced proliferation of peritoneal macrophages from GPx-1(-/-)ApoE(-/-) mice was mediated by the ERK1/2 (extracellular-signal regulated kinase 1/2) signaling pathway.
reduction of GPX-1 expression drives epithelial-mesenchymal transition and drug resistance pancreatic ductal adenocarcinoma
The redox balance of a Brazilian healthy population is associated with GPX1 polymorphisms (Pro198Leu and -602A/G) and selenium status.
No significant association between CAT and GPx1 polymorphisms and coronary artery disease risk was observed.
that polymorphisms in GPX1 and GPX4 are significantly associated with episodic memory and AD in a South Brazilian population
there is no correlation between idiopathic male infertility and the GPx1 codon Pro198Leu polymorphism; further studies are needed to investigate other genetic factors that influence the development of idiopathic male infertility
Increased glutathione peroxidase (GPx) activity seemed to compensate for a decrease in GPx1 protein due to enhanced degradation via the proteasome. Mass spectrometry analysis identified Lys-114 as a possible carbonylation target which provides a vestibule for the substrate H2O2 and thus enhances the enzymatic reaction
ESR1 and GPX1 expression levels were found to be significantly down-regulated by 14.7% and 7.4% (respectively) in the tumorous breast tissue when compared to the non-malignant one.
The result of this study suggested that GPX1 Pro198Leu polymorphism could not be a risk factor for breast cancer in Rwanda.
A significant increase in the T allele and TT genotype frequencies was observed in diabetic peripheral neuropathy patients compared to control diabetics. The association remained significant after correction for age, disease duration, HbA1c and BMI.
No significant differences in allelic or genotypic frequencies of GPX1 rs1050450 or GSTP1 rs1695 were detected between Chinese schizophrenia cases and controls.
Genetic variations in selenoprotein genes modulated both GPX1 and SELENOP selenoprotein gene expression and global gene expression in response to Brazil nut supplementation.
Allele-specific interaction between GPX1 and MnSOD affects the levels of Bcl2, Sirt3 and E-cadherin.
GPX1, GPX3 and GPX4 may be upregulated in response to a change in oxidative stress during an acute coronary syndromes
The Pro198Leu polymorphism (rs1050450) to the selenoprotein glutathione peroxidase 1 gene (GPX1), and GSTM1 deletion had no effect on mercury levels in mildly exposed people, suggesting these genetic variants impact mercury levels only in highly exposed populations.
Evaluation of Glutathione Peroxidase and KCNJ11 Gene Polymorphisms in Patients with New Onset Diabetes Mellitus After Renal Transplantation
G/C (rs8179169; Arg5Pro) and T/C (rs4991448; Leu6Pro) polymorphisms significantly associated with vitiligo
Data show that the inflammation of the gallbladder wall (IGW) correlated significantly with plasma GPX1 and hs-CRP (high-sensitivity C-reactive protein) values suggesting that inflammation and oxidative stress are related.
High GPX1 expression is associated with oral squamous cell carcinoma.
GPX1 is a gatekeeper restraining the oncogenic power of mitochondrial ROS generated by SOD2 is presented. Review.
Using lens epithelial cells derived from targeted inactivation of Prdx6(-/-) gene and relative enzymatic and stability assays, we discovered dramatic increases in GSH-peroxidase (30%) and aiPLA2 (37%) activities and stability in the K122/142 R mutant, suggesting Sumo1 destabilized Prdx6 integrity
This gene encodes a member of the glutathione peroxidase family. Glutathione peroxidase functions in the detoxification of hydrogen peroxide, and is one of the most important antioxidant enzymes in humans. This protein is one of only a few proteins known in higher vertebrates to contain selenocysteine, which occurs at the active site of glutathione peroxidase and is coded by UGA, that normally functions as a translation termination codon. In addition, this protein is characterized in a polyalanine sequence polymorphism in the N-terminal region, which includes three alleles with five, six or seven alanine (ALA) repeats in this sequence. The allele with five ALA repeats is significantly associated with breast cancer risk. Two alternatively spliced transcript variants encoding distinct isoforms have been found for this gene.
glutathione peroxidase Gpx1
, glutathione peroxidase
, cellular glutathione peroxidase
, cytosolic glutathione peroxidase
, putative glutathione peroxidase
, selenium-dependent glutathione peroxidase 1
, glutathione peroxidase 1
, glutathione peroxidase 1 S homeolog