The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)



Gene Review

Gstz1  -  glutathione transferase zeta 1...

Mus musculus

Synonyms: GSTZ1-1, Glutathione S-transferase zeta 1, MAAI, Maai, Maleylacetoacetate isomerase, ...
Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.

Disease relevance of Gstz1


High impact information on Gstz1


Biological context of Gstz1

  • In this study we have deleted the Gstz1 gene in BALB/c mice and characterized their phenotype [1].
  • It is significant that diminished glutathione concentrations were also observed in the liver of Gstz1(-/-) mice, which supports the conclusion that under normal dietary conditions, the accumulation of electrophilic intermediates such as maleylacetoacetate and MA results in a high level of oxidative stress [2].
  • Therefore, no alternative pathways for DCA clearance appear to exist in mice other than by MAAI-mediated biotransformation [6].
  • We also investigated the pharmacokinetics of DCA in the recently developed MAAI knockout (MAAI-KO) mouse [6].
  • Expression of GSTzeta/MAAI mRNA and protein was induced during the terminal phase of adipogenesis in 3T3-L1 preadipocytes [7].

Anatomical context of Gstz1

  • These data suggest a role for GSTzeta/MAAI in mature adipocytes that may be responsive to the thiazolidinedione class of insulin sensitizing PPARgamma ligands [7].
  • Ectopic expression of PPARgamma2 in NIH-3T3 fibroblasts exposed to insulin and troglitazone-induced perilipin production, but was incapable of activating GSTzeta/MAAI unless C/EBPalpha was also expressed [7].

Associations of Gstz1 with chemical compounds


Analytical, diagnostic and therapeutic context of Gstz1


  1. Mice deficient in glutathione transferase zeta/maleylacetoacetate isomerase exhibit a range of pathological changes and elevated expression of alpha, mu, and pi class glutathione transferases. Lim, C.E., Matthaei, K.I., Blackburn, A.C., Davis, R.P., Dahlstrom, J.E., Koina, M.E., Anders, M.W., Board, P.G. Am. J. Pathol. (2004) [Pubmed]
  2. Deficiency of glutathione transferase zeta causes oxidative stress and activation of antioxidant response pathways. Blackburn, A.C., Matthaei, K.I., Lim, C., Taylor, M.C., Cappello, J.Y., Hayes, J.D., Anders, M.W., Board, P.G. Mol. Pharmacol. (2006) [Pubmed]
  3. Perturbation of maleylacetoacetic acid metabolism in rats with dichloroacetic Acid-induced glutathione transferase zeta deficiency. Lantum, H.B., Cornejo, J., Pierce, R.H., Anders, M.W. Toxicol. Sci. (2003) [Pubmed]
  4. Glutathione transferases. Hayes, J.D., Flanagan, J.U., Jowsey, I.R. Annu. Rev. Pharmacol. Toxicol. (2005) [Pubmed]
  5. Maleylacetoacetate isomerase (MAAI/GSTZ)-deficient mice reveal a glutathione-dependent nonenzymatic bypass in tyrosine catabolism. Fernández-Cañón, J.M., Baetscher, M.W., Finegold, M., Burlingame, T., Gibson, K.M., Grompe, M. Mol. Cell. Biol. (2002) [Pubmed]
  6. Pharmacologic or genetic ablation of maleylacetoacetate isomerase increases levels of toxic tyrosine catabolites in rodents. Ammini, C.V., Fernandez-Canon, J., Shroads, A.L., Cornett, R., Cheung, J., James, M.O., Henderson, G.N., Grompe, M., Stacpoole, P.W. Biochem. Pharmacol. (2003) [Pubmed]
  7. C/EBPalpha-dependent induction of glutathione S-transferase zeta/maleylacetoacetate isomerase (GSTzeta/MAAI) expression during the differentiation of mouse fibroblasts into adipocytes. Qiang, L., Farmer, S.R. Biochem. Biophys. Res. Commun. (2006) [Pubmed]
WikiGenes - Universities