Anti-PI3K p85β Antibody |产品详情|进口橙子视频旧款采购网

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Anti-PI3K p85β Antibody

品牌：Antibodies

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规格：50µl

货期：

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Anti-PI3K p85β Antibody

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Overview

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.

Target

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 translocations 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).