AKT3 Antibody (Center) [APR05837G]

Product Specifications

Background

Tissue Location: In adult tissues, it is highly expressed in brain, lung and kidney, but weakly in heart, testis and liver. In fetal tissues, it is highly expressed in heart, liver and brain and not at all in kidney

Overview

We constantly strive to ensure we provide our customers with the best antibodies. As a result of this work we offer this antibody in purified format. We are in the process of updating our datasheets. If you have any questions regarding this update, please feel free to contact our technical support team. This product is a high quality AKT3 Antibody (Center) [APR05837G].

Synonyms

RAC-gamma serine/threonine-protein kinase, Protein kinase Akt-3, Protein kinase B gamma, PKB gamma, RAC-PK-gamma, STK-2, AKT3, PKBG

Gene Name

AKT3

Gene ID

10000

UniProt

Q9Y243

Chromosomal Location

Nucleus. Cytoplasm. Membrane; Peripheral membrane protein Note=Membrane-associated after cell stimulation leading to its translocation

Applications

IHC-P, WB

Dilution

WB--1:1000 IHC-P--1:100~500

Form

Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein G column, eluted with high and low pH buffers and neutralized immediately, followed by dialysis against PBS.

Function

AKT3 is one of 3 closely related serine/threonine-protein kinases (AKT1, AKT2 and AKT3) called the AKT kinase, and which regulate many processes including metabolism, proliferation, cell survival, growth and angiogenesis. This is mediated through serine and/or threonine phosphorylation of a range of downstream substrates. Over 100 substrate candidates have been reported so far, but for most of them, no isoform specificity has been reported. AKT3 is the least studied AKT isoform. It plays an important role in brain development and is crucial for the viability of malignant glioma cells. AKT3 isoform may also be the key molecule in up-regulation and down-regulation of MMP13 via IL13. Required for the coordination of mitochondrial biogenesis with growth factor-induced increases in cellular energy demands. Down- regulation by RNA interference reduces the expression of the phosphorylated form of BAD, resulting in the induction of caspase- dependent apoptosis.