|Target General Information||Top|
T38257 (Former ID: TTDI00078)
Phosphatase and tensin homolog (PTEN)
TEP1; Phosphatidylinositol 3,4,5trisphosphate 3phosphatase and dualspecificity protein phosphatase PTEN; Phosphatidylinositol 3,4,5-trisphosphate 3-phosphatase and dual-specificity protein phosphatase PTEN; Mutated in multiple advanced cancers 1; MMAC1
Acts as a dual-specificity protein phosphatase, dephosphorylating tyrosine-, serine- and threonine-phosphorylated proteins. Also acts as a lipid phosphatase, removing the phosphate in the D3 position of the inositol ring from phosphatidylinositol 3,4,5-trisphosphate, phosphatidylinositol 3,4-diphosphate, phosphatidylinositol 3-phosphate and inositol 1,3,4,5-tetrakisphosphate with order of substrate preference in vitro PtdIns(3,4,5)P3 > PtdIns(3,4)P2 > PtdIns3P > Ins(1,3,4,5)P4. The lipid phosphatase activity is critical for its tumor suppressor function. Antagonizes the PI3K-AKT/PKB signaling pathway by dephosphorylating phosphoinositides and thereby modulating cell cycle progression and cell survival. The unphosphorylated form cooperates with AIP1 to suppress AKT1 activation. Dephosphorylates tyrosine-phosphorylated focal adhesion kinase and inhibits cell migration and integrin-mediated cell spreading and focal adhesion formation. Plays a role as a key modulator of the AKT-mTOR signaling pathway controlling the tempo of the process of newborn neurons integration during adult neurogenesis, including correct neuron positioning, dendritic development and synapse formation. May be a negative regulator of insulin signaling and glucose metabolism in adipose tissue. The nuclear monoubiquitinated form possesses greater apoptotic potential, whereas the cytoplasmic nonubiquitinated form induces less tumor suppressive ability. In motile cells, suppresses the formation of lateral pseudopods and thereby promotes cell polarization and directed movement. Tumor suppressor.
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Phosphoric monoester hydrolase
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|3D Structure||Click to Show 3D Structure of This Target||PDB|
|Target-regulating Transcription Factors|
|Target Profiles in Patients||Top|
|Drug Resistance Mutation (DRM)|
|REF 1||The future therapy of endometrial cancer: microRNA's functionality, capability, and putative clinical application. Arch Gynecol Obstet. 2016 Nov;294(5):889-895.|
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