Kinase PB (bahasa Inggris: protein kinase b, PKB, RAC, Akt) adalah kinase protein dari golongan kinase AGC yang menyebabkan inaktivasi glikogen sintase kinase-3.[3]
Akt diaktivasi melalui lintasanreceptor tyrosine kinase, seperti platelet-derived growth factor receptor (PDGF-R), insulin, epidermal growth factor (EGF), basic fibroblast growth factor (bFGF), and insulin-like growth factor I (IGF-I),[4] dan merupakan substrat utama bagi PI3K.[3]Senyawa fosfoinositida yang diproduksi oleh PI3K, yaitu fosfatidil inositol 3,4-bifosfat dan fosfatidil inositol 3,4,5-trisfosfat, akan mengikat pada domain pleckstrin homology (PH) dari Akt, hingga memungkinan translokasi Akt ke dalam sitoplasma untuk diaktivasi oleh PDK-1 dengan fosforilasi pada residu Thr-308 dan Ser-473.[5] Akt juga teraktivasi oleh obat-obatan, toksin, radikal bebas seperti litium, asam valproat, clostridium difficile toxin, tert-butylhydroquinone, oksigen singlet, dan nitrogen monoksida.[6] Pada sel saraf, miosit jantung, sel epitelialparu, aktivasi dapat diinduksi oleh simtoma seperti hipoksia, reoksigenasi, iskemia-reperfusi dan stres oksidatif.
^(Inggris)"Physiological regulation of Akt activity and stability". Department of Experimental Therapeutics, Department of Molecular & Cellular Oncology, The University of Texas M. D. Anderson Cancer Center, Center for Molecular Medicine and Graduate Institute of Cancer Biology, China Medical University and Hospital; Yong Liao dan Mien-Chie Hung. Diakses tanggal 2011-07-13.
^(Inggris)"A Small Molecule Inhibits Akt through Direct Binding to Akt and Preventing Akt Membrane Translocation". Departments of ‡Molecular Oncology, Thoracic Oncology, and Drug Discovery, H. Lee Moffitt Cancer Center and Research Institute, Tianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenvironment, Lung Cancer Institute, Tianjin Medical University General Hospital; Donghwa Kim, Mei Sun, Lili He, Qing-Hua Zhou, Jun Chen, Xia-Meng Sun, Gerold Bepler, Said M. Sebti, dan Jin Q. Cheng. Diakses tanggal 2011-07-13.
^(Inggris)"Protein kinase B/Akt modulates nephrotoxicant-induced necrosis in renal cells". Department of Pharmaceutical Sciences, College of Pharmacy, University of Arkansas for Medical Sciences; Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences; Zabeena P. Shaik, E. Kim Fifer, dan Grażyna Nowak. Diakses tanggal 2011-07-14.
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