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GSTM3 Antibody (N-term) Blocking Peptide
Synthetic peptide
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
| Primary Accession | P21266 |
|---|---|
| Clone Names | 90415099 |
| Gene ID | 2947 |
|---|---|
| Other Names | Glutathione S-transferase Mu 3, GST class-mu 3, GSTM3-3, hGSTM3-3, GSTM3, GST5 |
| Format | Peptides are lyophilized in a solid powder format. Peptides can be reconstituted in solution using the appropriate buffer as needed. |
| Storage | Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C. |
| Precautions | This product is for research use only. Not for use in diagnostic or therapeutic procedures. |
| Name | GSTM3 |
|---|---|
| Synonyms | GST5 |
| Function | Conjugation of reduced glutathione to a wide number of exogenous and endogenous hydrophobic electrophiles. May govern uptake and detoxification of both endogenous compounds and xenobiotics at the testis and brain blood barriers. |
| Cellular Location | Cytoplasm. |
| Tissue Location | Testis and brain. |
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Provided below are standard protocols that you may find useful for product applications.
Background
Cytosolic and membrane-bound forms of glutathioneS-transferase are encoded by two distinct supergene families. Atpresent, eight distinct classes of the soluble cytoplasmicmammalian glutathione S-transferases have been identified: alpha,kappa, mu, omega, pi, sigma, theta and zeta. This gene encodes aglutathione S-transferase that belongs to the mu class. The muclass of enzymes functions in the detoxification of electrophiliccompounds, including carcinogens, therapeutic drugs, environmentaltoxins and products of oxidative stress, by conjugation withglutathione. The genes encoding the mu class of enzymes areorganized in a gene cluster on chromosome 1p13.3 and are known tobe highly polymorphic. These genetic variations can change anindividual's susceptibility to carcinogens and toxins as well asaffect the toxicity and efficacy of certain drugs. Mutations ofthis class mu gene have been linked with a slight increase in anumber of cancers, likely due to exposure with environmentaltoxins. Alternative splicing results in multiple transcriptvariants.
References
Bailey, S.D., et al. Diabetes Care 33(10):2250-2253(2010)Malik, M.A., et al. Nutr Cancer 62(6):734-742(2010)Salinas-Souza, C., et al. Pharmacogenet. Genomics 20(8):507-515(2010)Teixeira, D., et al. Braz. J. Med. Biol. Res. 43(7):677-680(2010)Jugessur, A., et al. PLoS ONE 5 (7), E11493 (2010) :
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