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AKT2 Proteins

AKT2 (AKT Serine/Threonine Kinase 2) is a Protein Coding gene. Diseases associated with AKT2 include Hypoinsulinemic Hypoglycemia With Hemihypertrophy and Diabetes Mellitus, Noninsulin-Dependent. Among its related pathways are Signaling by GPCR and Regulation of TP53 Activity. Gene Ontology (GO) annotations related to this gene include transferase activity, transferring phosphorus-containing groups and protein tyrosine kinase activity. An important paralog of this gene is AKT1.

The following recombinant AKT2 proteins are manufactured in house under a complete QC system by CUSABIO. They are expressed by Yeast, E.coli, Baculovirus, Mammalian cell, In Vivo Biotinylation in E.coli. Highlights of these recombinant AKT2 proteins as follow:
High purity, Low endotoxin, Multiple Tags, Animal-free, Wide applications (Cell assay, Protein-protein interaction, Drug-related studies, Enzymatic activity in vitro, Protein structure analysis, etc.)
In addition, various options on sizes, excellent technical support, and recombinant AKT2 proteins custom service will be also offered.

AKT2 Proteins Catalog

AKT2 Proteins for Homo sapiens (Human)

AKT2 Proteins for Rattus norvegicus (Rat)

AKT2 Proteins for Arabidopsis thaliana (Mouse-ear cress)

AKT2 Proteins for Mus musculus (Mouse)

AKT2 Background

RAC-beta serine/threonine-protein kinase (AKT2) is an enzyme that in humans is encoded by the AKT2 gene[1], which is a putative oncogene. AKT2 regulates many processes, including metabolism, proliferation, cell survival, growth, and angiogenesis. All these processes are mediated through serine and/or threonine phosphorylation of a range of downstream substrates. AKT2 might serve as a more direct and specific kinase mediating Glucocorticoid resistance through FoxO3a/Bim signaling pathway. And AKT2 inhibition may be explored as a promising target for treating Glucocorticoids-resistant hematopoietic malignancies[2]. CDK9 acts as a proto-oncogene in cervical cancer and modulates cell proliferation and apoptosis through the AKT2/p53 pathway[3]. AKT2 increases the migration and invasion of ovarian cancer cells in vitro and promotes lung metastasis in nude mice in vivo through PKM2-mediated elevation of STAT3 expression and NF-kappaB activation[4]. Tang Y, et al. provided evidence suggesting that AKT2 drives de novo lipogenesis in adipocytes by stimulating ChREBP beta transcriptional activity. The AKT2-ChREBP pathway in brown adipose tissue could optimize fuel storage and thermogenesis[5]. MiR-92a could inhibit the proliferation and migration of rheumatoid arthritis fibroblast-like synoviocytes (RA-FLSs) by regulating AKT2 expression[6].

[1] Cheng JQ, Godwin AK, et al. AKT2, a putative oncogene encoding a member of a subfamily of protein-serine/threonine kinases, is amplified in human ovarian carcinomas [J]. Proc Natl Acad Sci U S A. November 1992, 89 (19): 9267-71.

[2] Xie M, Yang A, et al. Akt2 mediates glucocorticoid resistance in lymphoid malignancies through FoxO3a/Bim axis and serves as a direct target for resistance reversal [J]. Cell Death Dis. 2019 Jan 1;9(10):1013. doi: 10.1038/s41419-018-1043-6.

[3] Xu J, Xu S,et al. Cyclin-dependent kinase 9 promotes cervical cancer development via AKT2/p53 pathway [J]. IUBMB Life. 2019 Mar;71(3):347-356.

[4] Zheng B, Geng L, et al. AKT2 contributes to increase ovarian cancer cell migration and invasion through the AKT2-PKM2-STAT3/NF-kappaB axis [J]. Cell Signal. 2018 May;45:122-131.

[5] Sanchez-Gurmaches J, Tang Y, et al. Brown Fat AKT2 Is a Cold-Induced Kinase that Stimulates ChREBP-Mediated De Novo Lipogenesis to Optimize Fuel Storage and Thermogenesis [J]. Cell Metab. 2018 Jan 9;27(1):195-209.e6.

[6] Yu FY, Xie CQ, et al. MiR-92a inhibits fibroblast-like synoviocyte proliferation and migration in rheumatoid arthritis by targeting AKT2 [J]. J Biosci. 2018 Dec;43(5):911-919.



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