|Application ||WB, IP|
|Reactivity||Human, Mouse, Rat|
|Calculated MW||47166 Da|
|Application & Usage||Western blotting (1-2 µg/ml) and immunoprecipitation (10-20 µg/ml). However, the optimal concentrations should be determined individually.|
|Other Names||PTEN, 137800 , P60484 , BZS , MGC11227 , MHAM , MMAC1 , PTEN1 , TEP1|
|Formulation||100 µg (0.5 mg/ml) antigen affinity purified rabbit polyclonal antibody in phosphate-buffered saline (PBS) containing 50% glycerol, 1% BSA, and 0.02% thimerosal.|
|Handling||The antibody solution should be gently mixed before use.|
|Reconstitution & Storage||-20 °C|
|Precautions||PTEN Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Tumor suppressor. 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 (PubMed:26504226). 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.|
|Cellular Location||Cytoplasm. Nucleus Nucleus, PML body Note=Monoubiquitinated form is nuclear. Nonubiquitinated form is cytoplasmic. Colocalized with PML and USP7 in PML nuclear bodies (PubMed:18716620). XIAP/BIRC4 promotes its nuclear localization (PubMed:19473982).|
|Tissue Location||Expressed at a relatively high level in all adult tissues, including heart, brain, placenta, lung, liver, muscle, kidney and pancreas.|
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Provided below are standard protocols that you may find useful for product applications.
PTEN (phosphatase and tensin homologue deleted on chromosome ten) phosphatase is a tumor suppressor gene implicated in a wide variety of human cancers. PTEN encodes the 403 amino acid polypeptide originally described as a dual-specificity protein phosphatase. The main substrates of PTEN are inositol phospholipids generated by the activation of the phosphoinositide 3 kinase (PI3K). PTEN is a major negative regulator of the PI3K/Akt signaling pathway.
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