Anti-GSTM1 Antibody Picoband® Fluoro647 Conjugated

Glutathione S-transferase Mu 1 (gene name GSTM1) is a human glutathione S-transferase. Cytosolic and membrane-bound forms of glutathione S-transferase are encoded by two distinct supergene families. At present, eight distinct classes of the soluble cytoplasmic mammalian glutathione S-transferases have been identified: alpha, kappa, mu, omega, pi, sigma, theta and zeta. This gene encodes a glutathione S-transferase that belongs to the mu class. The mu class of enzymes functions in the detoxification of electrophilic compounds, including carcinogens, therapeutic drugs, environmental toxins and products of oxidative stress, by conjugation with glutathione. The genes encoding the mu class of enzymes are organized in a gene cluster on chromosome 1p13.3 and are known to be highly polymorphic. These genetic variations can change an individual's susceptibility to carcinogens and toxins as well as affect the toxicity and efficacy of certain drugs. Null mutations of this class mu gene have been linked with an increase in a number of cancers, likely due to an increased susceptibility to environmental toxins and carcinogens. Multiple protein isoforms are encoded by transcript variants of this gene.

A synthetic peptide corresponding to a sequence in the middle region of human GSTM1, which shares 70.6% and 73.5% amino acid (aa) sequence identity with mouse and rat GSTM1, respectively.

Cancer, Cell Type Markers, Drug Metabolism, Metabolic Signaling Pathways, Metabolism, Pathways and Processes, Signal Transduction, Tags & Cell Markers, Tumor Associated

1. Carless, M. A., Lea, R. A., Curran, J. E., Appleyard, B., Gaffney, P., Green, A., Griffiths, L. R. TheGSTM1 null genotype confers an increased risk for solar keratosis development in an Australian Caucasian population. J. Invest. Derm. 119: 1373-1378, 2002. 2. Zhong, S., Wyllie, A. H., Barnes, D., Wolf, C. R., Spurr, N. K. Relationship between theGSTM1 genetic polymorphism and susceptibility to bladder, breast and colon cancer.Carcinogenesis 14: 1821-1824, 1993.