Protein Kinase B: Perbedaan antara revisi
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'''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 |
'''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 |
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| url = http://www.cloetta-stiftung.ch/hemmings-ref.pdf |
| url = http://www.cloetta-stiftung.ch/hemmings-ref.pdf |
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| title = PROTEIN KINASE B (PKB/AKT) – A COMMON ELEMENT IN MULTIPLE SIGNALING PATHWAYS INVOLVED IN INSULIN SIGNALING, CELL SURVIVALAND CANCER |
| title = PROTEIN KINASE B (PKB/AKT) – A COMMON ELEMENT IN MULTIPLE SIGNALING PATHWAYS INVOLVED IN INSULIN SIGNALING, CELL SURVIVALAND CANCER |
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|archiveurl=http://web.archive.org/web/20041020071101/http://www.cloetta-stiftung.ch/hemmings-ref.pdf|archivedate=2004-10-20}}</ref> |
|archiveurl=http://web.archive.org/web/20041020071101/http://www.cloetta-stiftung.ch/hemmings-ref.pdf|archivedate=2004-10-20}}</ref> |
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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 |
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 |
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| url = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2826820 |
| url = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2826820 |
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| title = Physiological regulation of Akt activity and stability |
| title = Physiological regulation of Akt activity and stability |
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| accessdate = 2011-07-13 |
| accessdate = 2011-07-13 |
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| 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 |
| 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 |
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}}</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 |
}}</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 |
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| url = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2832988 |
| url = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2832988 |
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| title = A Small Molecule Inhibits Akt through Direct Binding to Akt and Preventing Akt Membrane Translocation |
| title = A Small Molecule Inhibits Akt through Direct Binding to Akt and Preventing Akt Membrane Translocation |
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| accessdate = 2011-07-13 |
| accessdate = 2011-07-13 |
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| 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 |
| 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 |
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}}</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 |
}}</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 |
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| url = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1945105 |
| url = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1945105 |
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| title = Protein kinase B/Akt modulates nephrotoxicant-induced necrosis in renal cells |
| title = Protein kinase B/Akt modulates nephrotoxicant-induced necrosis in renal cells |
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Revisi per 29 November 2019 13.07
Kinase PB (bahasa Inggris: protein kinase b, PKB, RAC, Akt) adalah kinase protein dari golongan kinase AGC yang menyebabkan inaktivasi glikogen sintase kinase-3.[1]
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),[2] dan merupakan substrat utama bagi PI3K.[1] 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.[3] Akt juga teraktivasi oleh obat-obatan, toksin, radikal bebas seperti litium, asam valproat, clostridium difficile toxin, tert-butylhydroquinone, oksigen singlet, dan nitrogen monoksida.[4] Pada sel saraf, miosit jantung, sel epitelial paru, aktivasi dapat diinduksi oleh simtoma seperti hipoksia, reoksigenasi, iskemia-reperfusi dan stres oksidatif.
Rujukan
- ^ 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 dari versi asli (PDF) 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.
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