Protein Kinase B

AKT2
AKT2
	Struktur kristal kompleks Akt-2-inhibitor.
Pengidentifikasi
Simbol	AKT2
Gen NCBI	208
HGNC	392
OMIM	164731
RefSeq	NM_001626
UniProt	P31751
Data lain
Lokus	Chr. 19 q13.1-13.2
Struktur
Pencarian
Struktur	Swiss-model
Domain	InterPro

Pencarian
Struktur	Swiss-model
Domain	InterPro

AKT1
AKT1
	Representasi pita dari struktur kristal kompleks Akt-1-inhibitor.
Pengidentifikasi
Simbol	AKT1
Gen NCBI	207
HGNC	391
OMIM	164730
RefSeq	NM_005163
UniProt	P31749
Data lain
Lokus	Chr. 14 q32.32-32.33
Struktur
Pencarian
Struktur	Swiss-model
Domain	InterPro

AKT3

Pengidentifikasi

Simbol

Data lain

Chr. 1 q43-44

Pencarian
Struktur	Swiss-model
Domain	InterPro

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 lintasan receptor 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 epitelial paru, aktivasi dapat diinduksi oleh simtoma seperti hipoksia, reoksigenasi, iskemia-reperfusi dan stres oksidatif.

Rujukan

^ PDB: 3MV5; Freeman-Cook KD, Autry C, Borzillo G, Gordon D, Barbacci-Tobin E, Bernardo V, et al. (June 2010). "Design of selective, ATP-competitive inhibitors of Akt". Journal of Medicinal Chemistry. 53 (12): 4615–22. doi:10.1021/jm1003842. PMID 20481595.
^ PDB: 3D0E; Heerding DA, Rhodes N, Leber JD, Clark TJ, Keenan RM, Lafrance LV, et al. (September 2008). "Identification of 4-(2-(4-amino-1,2,5-oxadiazol-3-yl)-1-ethyl-7-{[(3S)-3-piperidinylmethyl]oxy}-1H-imidazo[4,5-c]pyridin-4-yl)-2-methyl-3-butyn-2-ol (GSK690693), a novel inhibitor of AKT kinase". Journal of Medicinal Chemistry. 51 (18): 5663–79. doi:10.1021/jm8004527. PMID 18800763.
^ ^a ^b (Inggris) "PROTEIN KINASE B (PKB/AKT) – A COMMON ELEMENT IN MULTIPLE SIGNALING PATHWAYS INVOLVED IN INSULIN SIGNALING, CELL SURVIVALAND CANCER" (PDF). Brian A. Hemmings. Diarsipkan (PDF) dari versi asli tanggal 2004-10-20. Diakses tanggal 2011-07-13.
^ (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.

Artikel bertopik biokimia ini adalah sebuah rintisan. Anda dapat membantu Wikipedia dengan mengembangkannya.

[pmid20481595-1] PDB: 3MV5; Freeman-Cook KD, Autry C, Borzillo G, Gordon D, Barbacci-Tobin E, Bernardo V, et al. (June 2010). "Design of selective, ATP-competitive inhibitors of Akt". Journal of Medicinal Chemistry. 53 (12): 4615–22. doi:10.1021/jm1003842. PMID 20481595.

[pmid18800763-2] PDB: 3D0E; Heerding DA, Rhodes N, Leber JD, Clark TJ, Keenan RM, Lafrance LV, et al. (September 2008). "Identification of 4-(2-(4-amino-1,2,5-oxadiazol-3-yl)-1-ethyl-7-{[(3S)-3-piperidinylmethyl]oxy}-1H-imidazo[4,5-c]pyridin-4-yl)-2-methyl-3-butyn-2-ol (GSK690693), a novel inhibitor of AKT kinase". Journal of Medicinal Chemistry. 51 (18): 5663–79. doi:10.1021/jm8004527. PMID 18800763.

[hem-ref-3] (Inggris) "PROTEIN KINASE B (PKB/AKT) – A COMMON ELEMENT IN MULTIPLE SIGNALING PATHWAYS INVOLVED IN INSULIN SIGNALING, CELL SURVIVALAND CANCER" (PDF). Brian A. Hemmings. Diarsipkan (PDF) dari versi asli tanggal 2004-10-20. Diakses tanggal 2011-07-13.

[4] (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.

[5] (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.

[6] (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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