プロテインキナーゼBとは？ わかりやすく解説

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ウィキペディア
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プロテインキナーゼB

出典: フリー百科事典『ウィキペディア（Wikipedia）』 (2024/01/20 08:20 UTC 版)

プロテインキナーゼB （英: protein kinase B、略称: PKB）は、グルコースの代謝やアポトーシス、細胞増殖（英語版）、転写、細胞遊走といった複数の細胞プロセスにおいて重要な役割を果たすセリン/スレオニンキナーゼで、Aktとしても知られる。


出典
  1. ^ PDB: 3MV5​; 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 (June 2010). “Design of selective, ATP-competitive inhibitors of Akt”. J. Med. Chem. 53 (12): 4615–22. doi:10.1021/jm1003842. PMID 20481595. 
  2. ^ PDB: 3D0E​; 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 (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”. J. Med. Chem. 51 (18): 5663–79. doi:10.1021/jm8004527. PMID 18800763. 
  3. ^ Chen WS, Xu PZ, Gottlob K, Chen ML, Sokol K, Shiyanova T, Roninson I, Weng W, Suzuki R, Tobe K, Kadowaki T, Hay N (September 2001). “Growth retardation and increased apoptosis in mice with homozygous disruption of the Akt1 gene.”. Genes & Development (Cold Spring Harbor Laboratory Press) 15 (17): 2203–2208. doi:10.1101/gad.913901. PMC 312770. PMID 11544177. http://genesdev.cshlp.org/content/15/17/2203.long. 
  4. ^ Staal SP, Hartley JW, Rowe WP (July 1977). “Isolation of transforming murine leukemia viruses from mice with a high incidence of spontaneous lymphoma”. Proc. Natl. Acad. Sci. U.S.A. 74 (7): 3065–7. doi:10.1073/pnas.74.7.3065. PMC 431413. PMID 197531. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC431413/. 
  5. ^ Garofalo RS, Orena SJ, Rafidi K, Torchia AJ, Stock JL, Hildebrandt AL, Coskran T, Black SC, Brees DJ, Wicks JR, McNeish JD, Coleman KG (July 2003). “Severe diabetes, age-dependent loss of adipose tissue, and mild growth deficiency in mice lacking Akt2/PKB beta”. J. Clin. Invest. 112 (2): 197–208. doi:10.1172/JCI16885. PMC 164287. PMID 12843127. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC164287/. 
  6. ^ Hill MM, Hemmings BA (2002). “Inhibition of protein kinase B/Akt. implications for cancer therapy”. Pharmacol. Ther. 93 (2–3): 243–51. doi:10.1016/S0163-7258(02)00193-6. PMID 12191616. 
  7. ^ Mitsiades CS, Mitsiades N, Koutsilieris M (2004). “The Akt pathway: molecular targets for anti-cancer drug development”. Curr Cancer Drug Targets 4 (3): 235–56. doi:10.2174/1568009043333032. PMID 15134532. 
  8. ^ Yang ZZ, Tschopp O, Baudry A, Dümmler B, Hynx D, Hemmings BA (April 2004). “Physiological functions of protein kinase B/Akt”. Biochem. Soc. Trans. 32 (Pt 2): 350–4. doi:10.1042/BST0320350. PMID 15046607. 
  9. ^ Franke TF, Kaplan DR, Cantley LC, Toker A (January 1997). “Direct regulation of the Akt proto-oncogene product by phosphatidylinositol-3,4-bisphosphate”. Science 275 (5300): 665–8. doi:10.1126/science.275.5300.665. PMID 9005852. 
  10. ^ Sarbassov DD, Guertin DA, Ali SM, Sabatini DM (February 2005). “Phosphorylation and regulation of Akt/PKB by the rictor-mTOR complex”. Science 307 (5712): 1098–101. doi:10.1126/science.1106148. PMID 15718470. 
  11. ^ Jacinto E, Facchinetti V, Liu D, Soto N, Wei S, Jung SY, Huang Q, Qin J, Su B (October 2006). “SIN1/MIP1 maintains rictor-mTOR complex integrity and regulates Akt phosphorylation and substrate specificity”. Cell 127 (1): 125–37. doi:10.1016/j.cell.2006.08.033. PMID 16962653. 
  12. ^ Persad, S.; Attwell, S.; Gray, V.; Mawji, N.; Deng, J. T.; Leung, D.; Yan, J.; Sanghera, J. et al. (2001-07-20). “Regulation of protein kinase B/Akt-serine 473 phosphorylation by integrin-linked kinase: critical roles for kinase activity and amino acids arginine 211 and serine 343”. The Journal of Biological Chemistry 276 (29): 27462–27469. doi:10.1074/jbc.M102940200. ISSN 0021-9258. PMID 11313365. https://www.ncbi.nlm.nih.gov/pubmed/11313365. 
  13. ^ Rane, M. J.; Coxon, P. Y.; Powell, D. W.; Webster, R.; Klein, J. B.; Pierce, W.; Ping, P.; McLeish, K. R. (2001-02-02). “p38 Kinase-dependent MAPKAPK-2 activation functions as 3-phosphoinositide-dependent kinase-2 for Akt in human neutrophils”. The Journal of Biological Chemistry 276 (5): 3517–3523. doi:10.1074/jbc.M005953200. ISSN 0021-9258. PMID 11042204. https://www.ncbi.nlm.nih.gov/pubmed/11042204. 
  14. ^ a b Mahajan K, Coppola D, Challa S, Fang B, Chen YA, Zhu W, Lopez AS, Koomen J, Engelman RW, Rivera C, Muraoka-Cook RS, Cheng JQ, Schönbrunn E, Sebti SM, Earp HS, Mahajan NP (March 2010). “Ack1 mediated AKT/PKB tyrosine 176 phosphorylation regulates its activation”. PLoS ONE 5 (3): e9646. doi:10.1371/journal.pone.0009646. PMC 2841635. PMID 20333297. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2841635/. 
  15. ^ Stuenaes JT, Bolling A, Ingvaldsen A, Rommundstad C, Sudar E, Lin FC, Lai YC, Jensen J (May 2010). “Beta-adrenoceptor stimulation potentiates insulin-stimulated PKB phosphorylation in rat cardiomyocytes via cAMP and PKA”. Br. J. Pharmacol. 160 (1): 116–29. doi:10.1111/j.1476-5381.2010.00677.x. PMC 2860212. PMID 20412069. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2860212/. 
  16. ^ Fan CD, Lum MA, Xu C, Black JD, Wang X (November 2012). “Ubiquitin-dependent regulation of phospho-AKT dynamics by the ubiquitin E3 ligase, NEDD4-1, in the IGF-1 response”. J. Biol. Chem. 288 (3): 1674–84. doi:10.1074/jbc.M112.416339. PMC 3548477. PMID 23195959. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3548477/. 
  17. ^ Cooper, Geoffrey M. (2000). “Figure 15.37: PTEN and PI3K”. The cell: a molecular approach. Washington, D.C: ASM Press. ISBN 0-87893-106-6. https://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=cooper.figgrp.2669 
  18. ^ Li, Hongzhao; Marshall, Aaron J. (2015-9). “Phosphatidylinositol (3,4) bisphosphate-specific phosphatases and effector proteins: A distinct branch of PI3K signaling”. Cellular Signalling 27 (9): 1789–1798. doi:10.1016/j.cellsig.2015.05.013. ISSN 1873-3913. PMID 26022180. https://www.ncbi.nlm.nih.gov/pubmed/26022180. 
  19. ^ Malek, Mouhannad; Kielkowska, Anna; Chessa, Tamara; Anderson, Karen E.; Barneda, David; Pir, Pınar; Nakanishi, Hiroki; Eguchi, Satoshi et al. (2017-11-02). “PTEN Regulates PI(3,4)P2 Signaling Downstream of Class I PI3K”. Molecular Cell 68 (3): 566–580.e10. doi:10.1016/j.molcel.2017.09.024. ISSN 1097-4164. PMC 5678281. PMID 29056325. https://www.ncbi.nlm.nih.gov/pubmed/29056325. 
  20. ^ Newton, Alexandra C.; Trotman, Lloyd C. (2014). “Turning off AKT: PHLPP as a drug target”. Annual Review of Pharmacology and Toxicology 54: 537–558. doi:10.1146/annurev-pharmtox-011112-140338. ISSN 1545-4304. PMC 4082184. PMID 24392697. https://www.ncbi.nlm.nih.gov/pubmed/24392697. 
  21. ^ Song G, Ouyang G, Bao S (2005). “The activation of Akt/PKB signaling pathway and cell survival”. J. Cell. Mol. Med. 9 (1): 59–71. doi:10.1111/j.1582-4934.2005.tb00337.x. PMID 15784165. 
  22. ^ Alberts B, Johnson A, Lewis J, Raff M, Roberts K, Walter P (2002). “Figure 15-60: BAD phosphorylation by Akt”. Molecular biology of the cell. New York: Garland Science. ISBN 0-8153-3218-1. https://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=mboc4.figgrp.2865 
  23. ^ Lodish H, Berk A, Zipursky LS, Matsudaira P, Baltimore D, Darnell J (1999). “Figure 23-50: BAD interaction with Bcl-2”. Molecular cell biology. New York: Scientific American Books. ISBN 0-7167-3136-3. https://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=mcb.figgrp.6902 
  24. ^ Faissner A, Heck N, Dobbertin A, Garwood J (2006). “DSD-1-Proteoglycan/Phosphacan and receptor protein tyrosine phosphatase-beta isoforms during development and regeneration of neural tissues”. Adv. Exp. Med. Biol. 557: 25–53, Figure 2: regulation of NF-κB. doi:10.1007/0-387-30128-3_3. PMID 16955703. https://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=eurekah.figgrp.997. 
  25. ^ Ramaswamy S, Nakamura N, Vazquez F, Batt DB, Perera S, Roberts TM, Sellers WR (March 1999). “Regulation of G1 progression by the PTEN tumor suppressor protein is linked to inhibition of the phosphatidylinositol 3-kinase/Akt pathway”. Proc. Natl. Acad. Sci. U.S.A. 96 (5): 2110–5. doi:10.1073/pnas.96.5.2110. PMC 26745. PMID 10051603. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC26745/. 
  26. ^ Kandel ES, Skeen J, Majewski N, Di Cristofano A, Pandolfi PP, Feliciano CS, Gartel A, Hay N (November 2002). “Activation of Akt/protein kinase B overcomes a G(2)/m cell cycle checkpoint induced by DNA damage”. Mol. Cell. Biol. 22 (22): 7831–41. doi:10.1128/MCB.22.22.7831-7841.2002. PMC 134727. PMID 12391152. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC134727/. 
  27. ^ Ng, Yvonne; Ramm, Georg; Lopez, Jamie A.; James, David E. (2008-4). “Rapid activation of Akt2 is sufficient to stimulate GLUT4 translocation in 3T3-L1 adipocytes”. Cell Metabolism 7 (4): 348–356. doi:10.1016/j.cmet.2008.02.008. ISSN 1550-4131. PMID 18396141. https://www.ncbi.nlm.nih.gov/pubmed/18396141. 
  28. ^ Park, Chul-Yong; Jun, Hyun-Jeong; Wakita, Takaji; Cheong, Jae Hun; Hwang, Soon B. (2009-04-03). “Hepatitis C virus nonstructural 4B protein modulates sterol regulatory element-binding protein signaling via the AKT pathway”. The Journal of Biological Chemistry 284 (14): 9237–9246. doi:10.1074/jbc.M808773200. ISSN 0021-9258. PMC 2666576. PMID 19204002. https://www.ncbi.nlm.nih.gov/pubmed/19204002. 
  29. ^ Sardiello M, Palmieri M, di Ronza A, Medina DL, Valenza M, Gennarino VA, Di Malta C, Donaudy F, Embrione V, Polishchuk RS, Banfi S, Parenti G, Cattaneo E, Ballabio A (Jul 2009). “A gene network regulating lysosomal biogenesis and function”. Science 325 (5939): 473–7. doi:10.1126/science.1174447. PMID 19556463. 
  30. ^ a b c Palmieri M, Pal R, Nelvagal HR, Lotfi P, Stinnett GR, Seymour ML, Chaudhury A, Bajaj L, Bondar VV, Bremner L, Saleem U, Tse DY, Sanagasetti D, Wu SM, Neilson JR, Pereira FA, Pautler RG, Rodney GG, Cooper JD, Sardiello M (Feb 2017). “mTORC1-independent TFEB activation via Akt inhibition promotes cellular clearance in neurodegenerative storage diseases”. Nature Communications 8: 14338. doi:10.1038/ncomms14338. PMC 5303831. PMID 28165011. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5303831/. 
  31. ^ Chen J, Somanath PR, Razorenova O, Chen WS, Hay N, Bornstein P, Byzova TV (November 2005). “Akt1 regulates pathological angiogenesis, vascular maturation and permeability in vivo”. Nat. Med. 11 (11): 1188–96. doi:10.1038/nm1307. PMC 2277080. PMID 16227992. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2277080/. 
  32. ^ Somanath PR, Razorenova OV, Chen J, Byzova TV (March 2006). “Akt1 in endothelial cell and angiogenesis”. Cell Cycle 5 (5): 512–8. doi:10.4161/cc.5.5.2538. PMC 1569947. PMID 16552185. http://www.landesbioscience.com/journals/cc/article/2538/. 
  33. ^ Lindhurst MJ, Sapp JC, Teer JK, Johnston JJ, Finn EM, Peters K, Turner J, Cannons JL, Bick D, Blakemore L, Blumhorst C, Brockmann K, Calder P, Cherman N, Deardorff MA, Everman DB, Golas G, Greenstein RM, Kato BM, Keppler-Noreuil KM, Kuznetsov SA, Miyamoto RT, Newman K, Ng D, O'Brien K, Rothenberg S, Schwartzentruber DJ, Singhal V, Tirabosco R, Upton J, Wientroub S, Zackai EH, Hoag K, Whitewood-Neal T, Robey PG, Schwartzberg PL, Darling TN, Tosi LL, Mullikin JC, Biesecker LG (August 2011). “A mosaic activating mutation in AKT1 associated with the Proteus syndrome”. N. Engl. J. Med. 365 (7): 611–9. doi:10.1056/NEJMoa1104017. PMC 3170413. PMID 21793738. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3170413/. 
  34. ^ “VioQuest Pharmaceuticals Announces Phase I/IIa Trial For Akt Inhibitor VQD-002”. (2007年4月). http://www.emaxhealth.com/95/11480.html 
  35. ^ Ghobrial IM, Roccaro A, Hong F, Weller E, Rubin N, Leduc R, Rourke M, Chuma S, Sacco A, Jia X, Azab F, Azab AK, Rodig S, Warren D, Harris B, Varticovski L, Sportelli P, Leleu X, Anderson KC, Richardson PG (February 2010). “Clinical and translational studies of a phase II trial of the novel oral Akt inhibitor perifosine in relapsed or relapsed/refractory Waldenstrom's macroglobulinemia”. Clin. Cancer Res. 16 (3): 1033–41. doi:10.1158/1078-0432.CCR-09-1837. PMC 2885252. PMID 20103671. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2885252/. 
  36. ^ “Aeterna Zentaris Regains North American Rights to Akt Inhibitor from Keryx” (英語). GEN - Genetic Engineering and Biotechnology News (2012年5月7日). 2019年2月1日閲覧。
  37. ^ Yap TA, Yan L, Patnaik A, Fearen I, Olmos D, Papadopoulos K, Baird RD, Delgado L, Taylor A, Lupinacci L, Riisnaes R, Pope LL, Heaton SP, Thomas G, Garrett MD, Sullivan DM, de Bono JS, Tolcher AW. “First-in-man clinical trial of the oral pan-AKT inhibitor MK-2206 in patients with advanced solid tumors”. J Clin Oncol 29: 4688–95. doi:10.1200/JCO.2011.35.5263. PMID 22025163. 
  38. ^ MK-2206 phase-2 trials
  39. ^ AKT inhibitor AZD5363 well tolerated, yielded partial response in patients with advanced solid tumors
  40. ^ PARP/AKT Inhibitor Combination Active in Multiple Tumor Types. April 2016
  41. ^ Ipatasertib plus paclitaxel versus placebo plus paclitaxel as first-line therapy for metastatic triple-negative breast cancer (LOTUS): a multicentre, randomised, double-blind, placebo-controlled, phase 2 trial. 2017
  42. ^ Cheshenko N, Trepanier JB, Stefanidou M, Buckley N, Gonzalez P, Jacobs W, Herold BC (March 2013). “HSV activates Akt to trigger calcium release and promote viral entry: novel candidate target for treatment and suppression”. FASEB J. 27 (7): 2584–99. doi:10.1096/fj.12-220285. PMC 3688744. PMID 23507869. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3688744/. 非専門家向けの内容要旨 – Sci-News. 
  43. ^ Sykes SM, Lane SW, Bullinger L, Kalaitzidis D, Yusuf R, Saez B, Ferraro F, Mercier F, Singh H, Brumme KM, Acharya SS, Scholl C, Schöll C, Tothova Z, Attar EC, Fröhling S, DePinho RA, Armstrong SA, Gilliland DG, Scadden DT (September 2011). “AKT/FOXO signaling enforces reversible differentiation blockade in myeloid leukemias”. Cell 146 (5): 697–708. doi:10.1016/j.cell.2011.07.032. PMID 21884932. 
  44. ^ Bessière L, Todeschini AL, Auguste A, Sarnacki S, Flatters D, Legois B, Sultan C, Kalfa N, Galmiche L, Veitia RA (March 2015). “A Hot-spot of In-frame Duplications Activates the Oncoprotein AKT1 in Juvenile Granulosa Cell Tumors”. EBioMedicine 2 (5): 421–31. doi:10.1016/j.ebiom.2015.03.002. PMC 4485906. PMID 26137586. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4485906/. 
  45. ^ Auguste A, Bessière L, Todeschini AL, Caburet S, Sarnacki S, Prat J, D'angelo E, De La Grange P, Ariste O, Lemoine F, Legois B, Sultan C, Zider A, Galmiche L, Kalfa N, Veitia RA (Dec 2015). “Molecular analyses of juvenile granulosa cell tumors bearing AKT1 mutations provide insights into tumor biology and therapeutic leads”. Hum Mol Genet 24 (23): 6687–98. doi:10.1093/hmg/ddv373. PMID 26362254. 

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プロテインキナーゼBのお隣キーワード

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プロテインキナーゼR

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