Akt2
AKT2 (protein kinase Bβ) is a serine/threonine kinase that functions downstream of phosphoinositide 3-kinase (PI3K) and mediates insulin-dependent regulation of glucose transport, glycogen synthesis, and metabolic homeostasis[1][2]. Mechanistically, AKT2 is a central effector of insulin receptor signaling and controls glucose utilization through phosphorylation networks linked to cellular metabolism and nutrient storage[2][3]. In disease contexts, AKT2 was originally identified as an oncogenic kinase amplified in ovarian carcinoma and later shown to contribute to malignant phenotypes in multiple tumor models through enhanced survival and growth signaling[1]. Genetic studies further established its metabolic importance, as Akt2-deficient mice develop insulin resistance, glucose intolerance, dyslipidemia, adipose tissue loss, and progressive diabetic phenotypes, supporting its essential role in systemic glucose regulation[2][3]. Compared with related isoforms, AKT1 is more strongly associated with organismal growth and developmental regulation, whereas AKT2 displays a more specialized function in insulin-responsive tissues and metabolic control[4][5]. Isoform-specific analyses in skeletal muscle from patients with type 2 diabetes demonstrated impaired insulin-stimulated AKT2 activation and altered phosphorylation patterns, linking defective AKT2 signaling to human metabolic disease[6]. For experimental applications, ATP-competitive AKT inhibitors such as GSK690693 directly target the AKT kinase domain and are widely used to investigate AKT-dependent signaling mechanisms in cancer and metabolic research models[7].
Verweise:
- [1]. Cheng JQ, et al. AKT2, a putative oncogene encoding a member of a subfamily of protein-serine/threonine kinases, is amplified in human ovarian carcinomas. Proc Natl Acad Sci U S A. 1992 Oct 1;89(19):9267-71. [Content Brief]
- [2]. Cho H, et al. Insulin resistance and a diabetes mellitus-like syndrome in mice lacking the protein kinase Akt2 (PKB beta). Science. 2001 Jun 1;292(5522):1728-31. [Content Brief]
- [3]. Garofalo RS, et al. Severe diabetes, age-dependent loss of adipose tissue, and mild growth deficiency in mice lacking Akt2/PKB beta. J Clin Invest. 2003 Jul;112(2):197-208. [Content Brief]
- [4]. Alibardi L. Stimulation of regenerative blastema formation in lizards as a model to analyze limb regeneration in amniotes. Histol Histopathol. 2019 Oct;34(10):1111-1120. doi: 10.14670/HH-18-123. Epub 2019 May 6. PMID: 31058307. et al. Stimulation of regenerative blastema formation in lizards as a model to analyze limb regeneration in amniotes. Histol Histopathol. 2019 Oct;34(10):1111-1120. [Content Brief]
- [5]. Irie HY, et al. Distinct roles of Akt1 and Akt2 in regulating cell migration and epithelial-mesenchymal transition. J Cell Biol. 2005 Dec 19;171(6):1023-34. [Content Brief]
- [6]. Cozzone D, et al. Isoform-specific defects of insulin stimulation of Akt/protein kinase B (PKB) in skeletal muscle cells from type 2 diabetic patients. Diabetologia. 2008 Mar;51(3):512-21. [Content Brief]
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Akt2 Verwandte Produkte (46)
Verwandte Produkte (46)
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Recombinant Proteins (5)
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Pifusertib hydrochloride
0 ImagesSynonyms: TAS-117 hydrochloridePifusertib (TAS-117) hydrochloride is a potent, selective, orally active allosteric Akt inhibitor (with IC50s of 4.8, 1.6, and 44 nM for Akt1, 2, and 3, respectively). Pifusertib hydrochloride triggers anti-myeloma activities and enhances fatal endoplasmic reticulum (ER) stress induced by proteasome inhibition. Pifusertib hydrochloride induces apoptosis and autophagy.
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Vevorisertib trihydrochloride
0 ImagesSynonyms: ARQ 751 trihydrochlorideVevorisertib (ARQ 751) trihydrochloride is a selective, allosteric, pan-AKT and AKT1-E17K mutant inhibitors. Vevorisertib trihydrochloride potently inhibit phosphorylation of AKT. Vevorisertib trihydrochloride has Kd values of 1.2 nM and 8.6 nM for AKT1 and AKT1-E17K, respectively. Vevorisertib trihydrochloride has IC50 values of 0.55, 0.81, and 1.3 nM for AKT1, AKT2, and AKT3, respectively. Vevorisertib trihydrochloride can be used for the research of cancer.
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Sulfabenzamide
0 ImagesSulfabenzamide (N-Sulfanilylbenzamide) is a sulfonamide antibacterial agent. Sulfabenzamide exhibit antibacterial activity against Staphylococcus aureus (ATCC 25923) and Escherichia coli (ATCC 8739). Sulfabenzamide can promote autophagic cell autophagy in breast cancer cells through p53/ DRAM pathway. Sulfabenzamide increases caspase-3 activity, deactivates PARP1 and DNA-PK, downregulates AKT1 and AKT2. Sulfabenzamide can be used for the researches of breast cancer and bacterial infections.
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AKT-IN-6
0 ImagesAKT-IN-6 (Example 13) is a potent Akt inhibitor. AKT-IN-6 inhibits Akt1, Akt2 and Akt3 with IC50s < 500nM, respectively. (patent WO2013056015A1).
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Miransertib hydrochloride
0 ImagesSynonyms: ARQ-092 hydrochlorideMiransertib hydrochloride (ARQ-092 hydrochloride) is a potent, orally active, selective and allosteric Akt inhibitor with IC50s of 2.7 nM, 14 nM and 8.1 nM for Akt1, Akt2, Akt3, respectively. Miransertib hydrochloride is also a potent the AKT1-E17K mutant protein inhibitor and has the potential for PI3K/AKT-driven tumors and Proteus syndrome research. Miransertib hydrochloride is effective against Leishmania.
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Vevorisertib
0 ImagesSynonyms: ARQ 751Vevorisertib (ARQ 751) is an orally active, potent and selective pan-AKT serine/threonine kinase inhibitor against AKT1 (IC50=0.55 nM), AKT2 (IC50=0.81 nM), and AKT3 (IC50=1.31 nM). Vevorisertib, as a single agent or in combination with other anti-cancer agents, can be used for the research of solid tumors with PIK3CA / AKT / PTEN mutations.
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INY-03-041 trihydrochloride
0 ImagesArt. -Nr.: HY-133120AINY-03-041 trihydrochloride is a potent, highly selective and PROTAC-based pan-AKT degrader consisting of the ATP-competitive AKT inhibitor Ipatasertib (HY-15186) conjugated to Lenalidomide (HY-A0003). INY-03-041 trihydrochloride inhibits AKT1, AKT2 and AKT3 with IC50s of 2.0, 6.8 and 3.5 nM, respectively.
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Pifusertib
0 ImagesSynonyms: TAS-117Pifusertib (TAS-117) is a potent, selective, orally active allosteric Akt inhibitor (with IC50s of 4.8, 1.6, and 44 nM for Akt1, 2, and 3, respectively). Pifusertib triggers anti-myeloma activities and enhances fatal endoplasmic reticulum (ER) stress induced by proteasome inhibition. Pifusertib induces apoptosis and autophagy.
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CCT128930 hydrochloride
0 ImagesCCT128930 hydrochloride is a potent and selective inhibitor of AKT (IC50=6 nM). CCT128930 hydrochloride has 28-fold selectivity over the closely related PKA kinase (IC50=168 nM) through the targeting of Met282 of AKT (Met173 of PKA-AKT chimera), as well as 20-fold selectivity over p70S6K (IC50=120 nM). CCT128930 hydrochloride induces cell cycle arrest, DNA damage, and autophagy. Antitumor activity.
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AKT-IN-3
0 ImagesAKT-IN-3 (compound E22) is a potent, orally active low hERG blocking Akt inhibitor, with 1.4 nM, 1.2 nM and 1.7 nM for Akt1, Akt2 and Akt3, respectively. AKT-IN-3 (compound E22) also exhibits good inhibitory activity against other AGC family kinases, such as PKA, PKC, ROCK1, RSK1, P70S6K, and SGK. AKT-IN-3 (compound E22) induces apoptosis and inhibits metastasis of cancer cells.
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MS143
0 ImagesArt. -Nr.: HY-143883CAS. Nr.: 2376137-41-4MS143 is a VHL-recruiting AKT protein PROTAC degrader with a DC50 of 46 nM in PC3 prostate cancer cells. MS143 preferentially binds to AKT1 and AKT3, with weaker binding activity towards AKT2. MS143 degrades AKT and blocks the phosphorylation of downstream signaling molecules in the PI3K/AKT/mTOR pathway. MS143 inhibits cancer cell growth and xenograft tumor growth. MS143 can be used for research on prostate cancer, triple-negative breast cancer, and breast cancer.
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Hu7691 free base
0 ImagesArt. -Nr.: HY-132302ACAS. Nr.: 2241232-43-7
