AKT1 Research Reagents

RAC-alpha serine/threonine-protein kinase is a protein in humans that is encoded by AKT1 gene. AKT1 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. AKT is responsible of the regulation of glucose uptake by mediating insulin-induced translocation of the SLC2A4/GLUT4 glucose transporter to the cell surface.

The following AKT1 reagents supplied by CUSABIO are manufactured under a strict quality control system. Multiple applications have been validated and solid technical support is offered.

AKT1 Antibodies

AKT1 Antibodies for Homo sapiens (Human)

AKT1 Antibodies for Arabidopsis thaliana (Mouse-ear cress)

AKT1 Antibodies for Drosophila melanogaster (Fruit fly)

AKT1 Antibodies for Oryza sativa subsp. indica (Rice)

AKT1 Antibodies for Oryza sativa subsp. japonica (Rice)

AKT1 Proteins

AKT1 Proteins for Homo sapiens (Human)

AKT1 Proteins for Mus musculus (Mouse)

AKT1 Proteins for Rattus norvegicus (Rat)

AKT1 Proteins for Drosophila melanogaster (Fruit fly)

AKT1 Proteins for Xenopus laevis (African clawed frog)

AKT1 Proteins for Oryza sativa subsp. japonica (Rice)

AKT1 Proteins for Arabidopsis thaliana (Mouse-ear cress)

AKT1 Proteins for Oryza sativa subsp. indica (Rice)

AKT1 ELISA Kit

AKT1 ELISA Kit for Homo sapiens (Human)

AKT1 Background

AKT1, encoded by the Akt1 gene, is the predominantly expressed isoform of the AKT family. AKT was named after a cell transforming retrovirus found in a spontaneous thymic lymphoma of an AKR mouse [1]. It is also called RAC-alpha serine/threonine-protein kinase, v-akt murine thymoma viral oncogene homolog, or protein kinase B (PKB). AKT1 mainly localizes at the plasma membrane and cytosol, and it may translocate to the nucleus after growth factor stimulation [2][3]. AKT1 is activated by phosphorylation at two regulatory sites Thr308 and Ser473 through various factors such as insulin, PI3K (phosphatidylinositol 3-kinase), and IGF1 (insulin-like growth factor 1) [4][5]. Activated AKT1 phosphorylates serine or threonine residues on a range of downstream substrates regulating cell growth, metabolism, apoptosis, angiogenesis, and drug responses. AKT1 kinase helps control apoptosis, which is the self-destruction of cells when they become damaged or are no longer needed. Due to its involvement in various cellular processes that promote cell survival and growth, the AKT pathway is a major target for cancer drug discovery. The PI3K/AKT/mammalian target of the rapamycin (mTOR) signaling pathway is hyperactivated or altered in many cancers and regulates a broad range of cellular processes including survival, proliferation, growth, metabolism, angiogenesis, and metastasis [6]. The RAF/MEK/ERK pathway is a main compensatory pathway in the downstream events of the PI3K/AKT/mTOR pathway [7]. Furthermore, activation of AKT and Ras pathways is often implicated in carcinogenesis [7]. AKT1 also stimulates glucose uptake by mediating insulin-induced translocation of Glut-4 (glucose transporter 4) to the plasma membrane of fat and muscle cells [8]. Post-mortem brain studies of schizophrenic patients have identified a reduced level of AKT1 in the frontal cortex [9]. Besides, the AKT1 signaling pathway also mediates FOXO1-dependent autophagy induced by FOXO3 [10].

[1] Staal, S. P. Molecular cloning of the akt oncogene and its human homologues AKT1 and AKT2: amplification of AKT1 in a primary human gastric adenocarcinoma [J]. Proc. Natl. Acad. Sci. USA . 1987, 84:5034.
[2] Andjelkovic M., Alessi D. R., et al. Role of translocation in the activation and function of protein kinase B [J]. J. Biol. Chem. 1997, 272, 31515-31524.
[3] Meier R., Alessi D. R., et al. Mitogenic activation, phosphorylation, and nuclear translocation of protein kinase Bbeta [J]. J. Biol. Chem. 1997, 272, 30491-30497.
[4] Alessi DR, Andjelkovic M, et al. Mechanism of activation of protein kinase B by insulin and IGF-1 [J]. EMBO J. 1996; 15:6541–6551.
[5] Kitamura T, Ogawa W, et al. Requirement for activation of the serine-threonine kinase Akt (protein kinase B) in insulin stimulation of protein synthesis but not of glucose transport [J]. Mol Cell Biol. 1998;18:3708-3717.
[6] Ersahin T, Tuncbag N, et al. The PI3K/AKT/mTOR interactive pathway [J]. Mol Biosyst. 2015 Jul;11(7):1946-54.
[7] Ho C1, Wang C, et al. AKT (v-akt murine thymoma viral oncogene homolog 1) and N-Ras (neuroblastoma ras viral oncogene homolog) coactivation in the mouse liver promotes rapid carcinogenesis by way of mTOR (mammalian target of rapamycin complex 1), FOXM1 (forkhead box M1)/SKP2, and c-Myc pathways [J]. Hepatology. 2012 Mar;55(3):833-45.
[8] Kohn AD, Summers SA, et al. Expression of a constitutively active Akt Ser/Thr kinase in 3T3-L1 adipocytes stimulates glucose uptake and glucose transporter 4 translocation [J]. J Biol Chem. 1996; 271:31372-31378.
[9] Cohen MM Jr. The AKT genes and their roles in various disorders [J]. Am J Med Genet A. 2013 Dec;161A(12):2931-7.
[10] Jingyi Zhou, Wenjuan Liao, et al. FOXO3 induces FOXO1-dependent autophagy by activating the AKT1 signaling pathway [J]. Autophagy vol. 8,12 (2012): 1712-23.

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