PTEN Mouse Monoclonal Antibody [4D8]

Function

As human tumors progress to advanced stages, one genetic alteration that occurs at high frequency is a loss of heterozygosity (LOH) at chromosome 10q23.31. Mapping of homozygous deletions on this chromosome led to the isolation of the PTEN gene, also designated MMAC1 (for mutated in multiple advanced cancers) and TEP1. This candidate tumor suppressor gene exhibits a high frequency of mutations in human glioblastomas and is also mutated in other cancers, including sporadic brain, breast, kidney and prostate cancers.PTEN has been associated with Cowden disease, an autosomal dominant cancer predisposition syndrome. The PTEN gene product is a putative protein tyrosine phosphatase that is localized to the cytoplasm, and it shares extensive homology with the cytoskeletal proteins tensin and auxilin. Gene transfer studies have indicated that the phosphatase domain of PTEN is essential for growth suppression of glioma cells.

Background References

1. Huang, J. and Kontos, C.D. 2002. PTEN modulates vascular endothelial growth factor-mediated signaling and angiogenic effects. J. Biol. Chem.277: 10760-10766.

2. Altomare, D.A., et al. 2002. Frequent activation of AKT2 kinase in human pancreatic carcinomas. J. Cell. Biochem. 87: 470-476.

3. Pernicová, Z., et al. 2011. Androgen depletion induces senescence in prostate cancer cells through down-regulation of Skp2. Neoplasia 13:526-536.

4. Lehman, J.A., et al. 2011. Induction of apoptotic genes by a p73-phosphatase and tensin homolog (p73-PTEN) protein complex in response to genotoxic stress. J. Biol. Chem. 286: 36631-36640

Subcellular Location

Cytoplasm, Nucleus

UNIPROT

SwissProt: P60484 Human

Synonyms