Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.5.1.18 (glutathione S-transferase)
 22,582 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have isolated, by differential library screening, eight cDNAs representing genes that are specifically expressed in the embryonal stem cell line IMT-11, when compared to the parietal endoderm-like cell line PYS-2 or to NIH3T3 fibroblasts. One of these genes, embryonal stem cell gene 1 (esg-1), was analyzed in detail. esg-1 mRNA is found at high levels in both IMT-11 and F9 embryonal carcinoma cells and disappears during the differentiation of the stem cells. Furthermore, expression of the gene was found to be extremely low in, or absent from, oocytes and fertilized eggs, but it is strongly induced at the 2-cell stage, reaching maximum levels at the 4-cell stage. In contrast, esg-1 expression is detectable neither in midgestation embryos nor in neonatal tissues. These results strongly suggest that esg-1 is expressed specifically or at least predominantly in embryonal stem cells. Antibodies directed against a glutathione S-transferase-esg-1 fusion product detect a protein of M(r) approximately 14,000 in F9 embryonal carcinoma cells, but not in differentiated cells. Apart from the esg-1 gene, which contains two introns, there are at least seven esg-1-related pseudogenes in the mouse genome that differ from the esg-1 gene by the presence of multiple point mutations, by the lack of intervening sequences, and/or by the presence of a polyadenylated stretch at the 3' end. The esg-1 gene is under stringent transcriptional control in differentiating and differentiated cells, as shown by both nuclear run-on assays and the transient F9 stem cell-specific expression of constructs consisting of esg-1 upstream sequences fused to a luciferase reporter gene.
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PMID:Cloning of embryonal stem cell-specific genes: characterization of the transcriptionally controlled gene esg-1. 812 91

We hypothesize that smokers with the null genotype for GSTM1 (GSTM1-0), who thus lack the detoxification enzyme glutathione S-transferase mu-1, develop atherosclerosis at an increased rate compared to smokers with the positive genotype (GSTM1-1). We used data from a 2-year randomized placebo-controlled trial on the effect of vitamin E on atherosclerosis among 189 male smokers. Progression of atherosclerosis was measured by 2-year change of the common carotid intima media thickness (CCA-IMT) as measured by B-mode ultrasonography. The frequency of GSTM1-0 genotype was 0.5 in both the placebo and the vitamin E group. Smokers with GSTM1-0 genotype had a tendency to higher baseline CCA-IMT values than those with GSTM1-1 (0.97 versus 0.92 mm, P=0.09). Within the placebo group, more CCA-IMT progression was found for smokers with the GSTM1-0 than for smokers with the GSTM1-1 genotype after adjustment for baseline IMT and major CVD risk factors (0.050 versus -0.002 mm, P=0.046). In the vitamin E group no effect of GSTM1 genotype on atherosclerosis progression was found. Overall, smokers with GSTM1-0 genotype had a higher mean 2-year progression compared to those with GSTM1-1 as shown by a difference in increase of 0.042 mm (95% CI 0.006; 0.078, P=0.02). In conclusion, our data suggest that smokers lacking the detoxifying enzyme GST mu-1 develop progression of atherosclerosis at an increased rate.
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PMID:Effect of glutathione S-transferase M1 genotype on progression of atherosclerosis in lifelong male smokers. 1150 Jan 95