AKT2 (Protein|Antibody|cDNA Clone|ELISA Kit)

All AKT2 reagents are produced in house and quality controlled, including 1 AKT2 Antibody, 45 AKT2 Gene, 1 AKT2 Lysate, 1 AKT2 Protein, 3 AKT2 qPCR. All AKT2 reagents are ready to use.

Recombinant AKT2 proteins are expressed by Baculovirus-Insect Cells with fusion tags as N-his & GST.

AKT2 antibodies are validated with different applications, which are IHC-P.

AKT2 cDNA clones are full length sequence confirmed and expression validated. There are 13 kinds of tags for each AKT2 of different species, especially GFP tag, OFP tag, FLAG tag and so on. There are three kinds of vectors for choice, cloning vector, expression vector and lentivrial expression vector.

AKT2 Protein (1)


AKT2 Protein, Human, Recombinant (His & GST Tag)


Expression host: Baculovirus-Insect Cells

Human AKT2/PKB beta Protein 9098

AKT2 Antibody (1)


Anti-AKT2 Antibody


Specificity: Mouse

Application: IHC-P

Clonality: PAb

Mouse AKT2 Immunohistochemistry(IHC) 19280

AKT2 cDNA Clone (45)


AKT2 qPCR Primer (3)

AKT2 Lysate (1)

AKT (AK mouse plus Transforming or Thymoma) is a frequent oncogene expressed in most tissues which includes three isoforms AKT1, AKT2, and AKT3. Hyperactivation of AKT signaling is a central key in many human cancer progressions, through modulating angiogenesis, tumor growth, and cell migration, invasion, metastasis, and chemoresistance. Among all three isoforms, AKT2 is most related to cancer cell invasion, metastasis, and survival. Amplification and overexpression of AKT2 have been shown in many cancers. Accumulating evidence shows the potential role of different miRNA involvements in cancer progression by activating or suppressing AKT2 expression. The AKT2/NAB1/SPK1 pathway is a novel regulating factor of macrophage migration and cardiac remodeling after myocardial infarction. The novel mechanism of the AKT2-PKM2-STAT3/NF-kappaB axis in the regulation of ovarian cancer progression, that both AKT2 and PKM2 may be potential targets for the treatment of ovarian cancer. AKT1 and AKT2, the AKT isoforms that are highly expressed in skeletal muscle, have distinct and overlapping functions, with AKT2 more important for insulin-stimulated glucose metabolism. In adipocytes, AKT2 versus AKT1 has greater susceptibility for insulin-mediated redistribution from cytosolic to membrane localization, and insulin also causes subcellular redistribution of AKT Substrate of 16 kDa (AS16), an AKT2 substrate and crucial mediator of insulin-stimulated glucose transport.