Conjugation of reduced glutathione to a wide number of exogenous and endogenous hydrophobic electrophiles. Involved in the formation of glutathione conjugates of both prostaglandin A2 (PGA2) and prostaglandin J2 (PGJ2) (PubMed:9084911). Participates in the formation of novel hepoxilin regioisomers (PubMed:21046276). (updated: June 17, 2020)
The data and differentiation stages presented below come from the proteomic study and analysis performed by our partners of the GReX consortium, more details are available in their published work.
No sequence conservation computed yet.
Total structural coverage: 100%
No model available.
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The reference OMIM entry for this protein is 138350
Glutathione s-transferase, mu-1; gstm1
Glutathione s-transferase m1
Glutathione transferase, class mu, 1
Gst1
Liver and fibroblast gst1
DESCRIPTION
The glutathione S-transferases (GST; EC 2.5.1.18) are a family of enzymes responsible for the metabolism of a broad range of xenobiotics and carcinogens (Mannervik, 1985). This enzyme catalyzes the reaction of glutathione with a wide variety of organic compounds to form thioethers, a reaction that is sometimes a first step in a detoxification process leading to mercapturic acid formation. Based on amino acid sequence similarities and antibody cross-reactivities, the mammalian cytosolic GSTs are divided into several classes, including alpha (e.g.,
138359), mu, kappa (
602321), theta (e.g.,
600436), pi (
134660), omega (
605482), and zeta (
603758). In addition, there is a class of microsomal GSTs (e.g.,
138330). Each class is encoded by a single gene or a gene family.
CLONING
Board (1981) showed that the most active GSTs of liver are the products of 2 autosomal loci, GST1 (GSTM1) and GST2 (GSTA2;
138360), both of which are polymorphic. Strange et al. (1984) reported that GST1 is easily demonstrable in adult liver, kidney, adrenal and stomach but is only weakly expressed in skeletal and cardiac muscle and not at all in fetal liver, fibroblasts, erythrocytes, lymphocytes and platelets. GST2 is not detectable in the last 4 tissues but is found in many other tissues including fetal liver. GST3 (GSTP1;
134660) is found in every tissue except adult liver. DeJong et al. (1988) isolated a cDNA clone that encodes a human liver GST H(b) subunit representing GST1.
MAPPING
By in situ hybridization, DeJong et al. (1988) mapped the GST1 gene to chromosome 1p31. Zhong et al. (1992) used oligonucleotide primers specific for intron 5 sequences in the GSTM1 gene to amplify a unique 718-bp fragment. They confirmed the assignment to 1p by analysis of DNA from a panel of somatic cell hybrids and refined the localization to 1p13 by linkage analysis in 3-generation CEPH families. Pearson et al. (1993) used locus-specific PCR primer pairs spanning exon 6, intron 6, and exon 7 as probes on DNA from human/hamster somatic cell hybrids to map 5 glutathione transferase genes to chromosome 1: GSTM1, GSTM2 (
138380), GSTM3 (
138390), GSTM4 (
138333), and GSTM5 (
138385). For GSTM1, the assignment was confirmed by Southern blot hybridization. The organization of the 5 genes was confirmed by the isolation of a YAC clone that contained all 5. With this clone, the location of this cluster on chromosome 1 was confirmed by fluorescence in situ hybridization and regionalized to a point in or near 1p13.3. Xu et al. (1998) reported that 4 mu GST genes are tightly clustered. These genes are spaced approximately 20 kb apart and are arranged in the following order: 5-prime--GSTM4--GSTM2--GSTM1--GSTM5--3-prime. Islam et al. (1989) mapped a GST mu gene to human chromosome 3 (
138385).
NOMENCLATURE
Mannervik et al. (1992) gave recommendations on nomenclature for human glutathione transferases.
MOLECULAR GENETICS
Data on gene frequencies of allelic variants were tabulated by Roychoudhury and Nei (1988). A null allele at the GSTM1 locus has a high frequency of about 0.7 (Board et al., 1990). The GST1 null phenotype has a frequency of greater than 50% among Caucasian, Chinese, and Indian populations (Board, 1981; Board et al., 1990). The GSTM1 null phenotype appears to be caused by the deletion of the GSTM1 gene (Seidegard et al., 1988, 1990). The close physical proximity of the GSTM1 and GSTM2 loci, which share 99% nucleotide s ...
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Subscribe to this protein entry history
June 29, 2020: Protein entry updated
Automatic update: Entry updated from uniprot information.
Oct. 19, 2018: Additional information
Initial protein addition to the database. This entry was referenced in Bryk and co-workers. (2017).
Oct. 19, 2018: Protein entry updated
Automatic update: OMIM entry 138350 was added.