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Anti-PI3K p85β Antibody

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产品名称: Anti-PI3K p85β Antibody
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Anti-PI3K p85β Antibody


Anti-PI3K p85β Antibody  的详细介绍
Name: Anti-PI3K p85β Antibody
See all PI3K p85β primary antibodies
Description: Rabbit monoclonal antibody to PI3K p85β
Specificity: This antibody detects endogenous levels of PI3K p85β and does not cross-react with related proteins.
Applications: WB, ICC/IF, IHC, FC
Reactivity: Human, Rat
Immunogen: Recombinant antibody.
Host: Rabbit
Clonality: Monoclonal
Conjugate: Unconjugated
Molecular Weight: ~ 85 kDa
Purity: Protein A affinity purified
Product Form: Recombinant Rabbit Monoclonal Antibody. 1*TBS (pH7.4), 1%BSA, 40%Glycerol. Preservative: 0.05% Sodium Azide.
Function: Regulatory subunit of phosphoinositide-3-kinase (PI3K), a kinase that phosphorylates PtdIns(4,5)P2 (Phosphatidylinositol 4,5-bisphosphate) to generate phosphatidylinositol 3,4,5-trisphosphate (PIP3). PIP3 plays a key role by recruiting PH domain-containing proteins to the membrane, including AKT1 and PDPK1, activating signaling cascades involved in cell growth, survival, proliferation, motility and morphology. Binds to activated (phosphorylated) protein-tyrosine kinases, through its SH2 domain, and acts as an adapter, mediating the association of the p110 catalytic unit to the plasma membrane. Indirectly regulates autophagy (PubMed:23604317). Promotes nuclear translocation of XBP1 isoform 2 in a ER stress- and/or insulin-dependent manner during metabolic overloading in the liver and hence plays a role in glucose tolerance improvement (By similarity).
Involvement in Disease: Megalencephaly-polymicrogyria-polydactyly-hydrocephalus syndrome 1: A syndrome characterized by megalencephaly, hydrocephalus, and polymicrogyria; polydactyly may also be seen. There is considerable phenotypic similarity between this disorder and the megalencephaly-capillary malformation syndrome.
Sequence Similarities: Belongs to the PI3K p85 subunit family.
Post-Translational Modification: Phosphorylated in response to signaling from activated receptor-type protein kinases (PubMed:19690332, PubMed:20068231). Dephosphorylated by PTPRJ (PubMed:18348712). Dephosphorylated at Tyr-655 by PTPN13. Phosphorylation of Tyr-655 impairs while its dephosphorylation promotes interaction with FBXL2 and SCF(FBXL2)-mediated polyubiquitination (PubMed:23604317).
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