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Description :Recombinant full-length human PTEN was expressed in E. coli cells using an N-terminal GST tag.
Tag :GST tag
Sequence :Full Length
Genbank Number :NM_000314
Purity :Sample Purity Data. For specific information on a given lot, see related technical data sheet.
Storage, Stability and Shipping :Store product at –70oC. For optimal storage, aliquot target into smaller quantities after centrifugation and store at recommended temperature. For most favorable performance, avoid repeated handling and multiple freeze/thaw cycles.
Applications :Western Blot
Molecular Weight :~76 kDa
Gene Aliases :BZS, MHAM, TEP1, MMAC1, PTEN1, MGC11227
Scientific Background :PTEN (phosphatase and tensin homolog) is a tumor suppressor that is frequently mutated in a large number of cancers (1). PTEN has phosphatidylinositol-3,4,5-trisphosphate 3-phosphatase activity and contains a tensin like domain as well as a catalytic domain similar to that of the dual specificity protein tyrosine phosphatases. Unlike most of the protein tyrosine phosphatases, PTEN preferentially dephosphorylates phosphoinositide substrates and is responsible for negatively regulating the intracellular levels of phosphatidylinositol-3,4,5-trisphosphate in cells. PTEN functions as a tumor suppressor by negatively regulating the PI3K/AKT signaling pathway (2).
1. Butler, M.G. et al: Subset of individuals with autism spectrum disorders and extreme macrocephaly associated with germline PTEN tumour suppressor gene mutations. J. Med. Genet. 2005;42(4):318-21.
2. Steck, P.A. et aal: Identification of a candidate tumour suppressor gene, MMAC1, at chromosome 10q23.3 that is mutated in multiple advanced cancers. Nat. Genet. 1997; 15(4):356-62
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Research Areas :Cancer, Neurobiology, Inflammation, Metabolic Disorder, Cardiovascular Disease, AKT/PKB Pathway, NfkB Pathway, WNT Signaling, Apoptosis/Autophagy, Angiogenesis, Invasion/Metastasis, Phosphatases, Cancer, Neurobiology, Inflammation, Metabolic Disorder, Cardiovascular Disease, AKT/PKB Pathway, NfkB Pathway, WNT Signaling, Apoptosis/Autophagy, Angiogenesis, Invasion/Metastasis, Phosphatases