Protein Kinase B: Perbedaan antara revisi
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{{Redirect|AKT}}
{{infobox protein
|Name=[[AKT1]]
|image=Crystal structure of Akt-1-inhibitor complexes.png
|caption=Representasi pita dari struktur kristal kompleks ''Akt-1-inhibitor''.<ref name="pmid20481595">{{PDB|3MV5}}; {{cite journal | vauthors = Freeman-Cook KD, Autry C, Borzillo G, Gordon D, Barbacci-Tobin E, Bernardo V, Briere D, Clark T, Corbett M, Jakubczak J, Kakar S, Knauth E, Lippa B, Luzzio MJ, Mansour M, Martinelli G, Marx M, Nelson K, Pandit J, Rajamohan F, Robinson S, Subramanyam C, Wei L, Wythes M, Morris J | display-authors = 6 | title = Design of selective, ATP-competitive inhibitors of Akt | journal = Journal of Medicinal Chemistry | volume = 53 | issue = 12 | pages = 4615–22 | date = June 2010 | pmid = 20481595 | doi = 10.1021/jm1003842 }}</ref>
|width=
|HGNCid=391
|Symbol=[[AKT1]]
|AltSymbols=
|EntrezGene=207
|OMIM=164730
|RefSeq=NM_005163
|UniProt=P31749
|PDB=
|ECnumber=
|Chromosome=14
|Arm=q
|Band=32.32
|LocusSupplementaryData=-32.33
}}
{{infobox protein
|Name=[[AKT2]]
|image=3D0E Ribbon.png
|caption=Struktur kristal kompleks ''Akt-2-inhibitor''.<ref name="pmid18800763">{{PDB|3D0E}}; {{cite journal | vauthors = Heerding DA, Rhodes N, Leber JD, Clark TJ, Keenan RM, Lafrance LV, Li M, Safonov IG, Takata DT, Venslavsky JW, Yamashita DS, Choudhry AE, Copeland RA, Lai Z, Schaber MD, Tummino PJ, Strum SL, Wood ER, Duckett DR, Eberwein D, Knick VB, Lansing TJ, McConnell RT, Zhang S, Minthorn EA, Concha NO, Warren GL, Kumar R | display-authors = 6 | title = 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 = Journal of Medicinal Chemistry | volume = 51 | issue = 18 | pages = 5663–79 | date = September 2008 | pmid = 18800763 | doi = 10.1021/jm8004527 | url = https://figshare.com/articles/Identification_of_4_2_4_Amino_1_2_5_oxadiazol_3_yl_1_ethyl_7_3_i_S_i_3_piperidinylmethyl_oxy_1_i_H_i_imidazo_4_5_i_c_i_pyridin_4_yl_2_methyl_3_butyn_2_ol_GSK690693_a_Novel_Inhibitor_of_AKT_Kinase/2911615 }}</ref>
|HGNCid=392
|Symbol=[[AKT2]]
|AltSymbols=
|EntrezGene=208
|OMIM=164731
|RefSeq=NM_001626
|UniProt=P31751
|PDB=
|ECnumber=
|Chromosome=19
|Arm=q
|Band=13.1
|LocusSupplementaryData=-13.2
}}
{{infobox protein
|Name=[[AKT3]]
|caption=
|image=
|width=
|HGNCid=393
|Symbol=[[AKT3]]
|AltSymbols=
|EntrezGene=10000
|OMIM=611223
|RefSeq=NM_181690
|UniProt=Q9Y243
|PDB=
|ECnumber=
|Chromosome=1
|Arm=q
|Band=43
|LocusSupplementaryData=-44
}}
'''Kinase PB''' ({{lang-en|protein kinase b, PKB, RAC, Akt}}) adalah [[kinase protein]] dari golongan [[kinase AGC]] yang menyebabkan inaktivasi [[glikogen sintase kinase-3]].<ref name="hem-ref">{{en}} {{cite web|url=http://www.cloetta-stiftung.ch/hemmings-ref.pdf|title=PROTEIN KINASE B (PKB/AKT) – A COMMON ELEMENT IN MULTIPLE SIGNALING PATHWAYS INVOLVED IN INSULIN SIGNALING, CELL SURVIVALAND CANCER|accessdate=2011-07-13|work=Brian A. Hemmings|archiveurl=https://web.archive.org/web/20041020071101/http://www.cloetta-stiftung.ch/hemmings-ref.pdf|archivedate=2004-10-20|dead-url=no}}</ref>
Akt diaktivasi melalui [[lintasan metabolisme|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),<ref>{{en}} {{cite web
| url = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2826820
| title = Physiological regulation of Akt activity and stability
| accessdate = 2011-07-13
| work = 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
}}</ref> dan merupakan [[substrat]] utama bagi [[kinase fosfatidil inositol-3|PI3K]].<ref name="hem-ref" /> [[Senyawa organik|Senyawa]] [[fosfoinositida]] yang diproduksi oleh [[kinase fosfatidil inositol-3|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 [[treonina|Thr]]-308 dan [[serina|Ser]]-473.<ref>{{en}} {{cite web
| url = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2832988
| title = A Small Molecule Inhibits Akt through Direct Binding to Akt and Preventing Akt Membrane Translocation
| accessdate = 2011-07-13
| work = 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
}}</ref> Akt juga teraktivasi oleh [[obat|obat-obatan]], [[toksin]], [[radikal bebas]] seperti [[litium]], [[asam valproat]], ''clostridium difficile toxin'', ''tert-butylhydroquinone'', [[oksigen]] singlet, dan [[nitrogen monoksida]].<ref>{{en}} {{cite web
| url = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1945105
| title = Protein kinase B/Akt modulates nephrotoxicant-induced necrosis in renal cells
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