.bak
Bak
出典: フリー百科事典『ウィキペディア(Wikipedia)』 (2024/07/16 14:34 UTC 版)
Bak(Bcl-2 homologous antagonist/killer)またはBAK1(BCL2 antagonist/killer 1)は、ヒトでは6番染色体のBAK1遺伝子にコードされるタンパク質である[4][5]。この遺伝子にコードされるタンパク質は、Bcl-2タンパク質ファミリーに属する。Bcl-2ファミリーのメンバーはオリゴマーまたはヘテロ二量体を形成し、さまざまな細胞活動に関与して抗アポトーシスまたはアポトーシス促進調節因子として作用する。このタンパク質はミトコンドリアに局在し、アポトーシスを誘導する機能を果たす。ミトコンドリアの電位依存性アニオンチャネル(VDAC)と相互作用して開口を促進し、膜電位の喪失とシトクロムcの放出を引き起こす。また、このタンパク質は細胞ストレスへの曝露後にがん抑制因子であるp53と相互作用する[6]。
- ^ a b c GRCh38: Ensembl release 89: ENSG00000030110 - Ensembl, May 2017
- ^ Human PubMed Reference:
- ^ Mouse PubMed Reference:
- ^ “Induction of apoptosis by the Bcl-2 homologue Bak”. Nature 374 (6524): 733–6. (April 1995). Bibcode: 1995Natur.374..733C. doi:10.1038/374733a0. PMID 7715730.
- ^ “Modulation of apoptosis by the widely distributed Bcl-2 homologue Bak”. Nature 374 (6524): 736–9. (April 1995). Bibcode: 1995Natur.374..736K. doi:10.1038/374736a0. PMID 7715731.
- ^ a b c “Entrez Gene: BAK1 BCL2-antagonist/killer 1”. 2021年9月27日閲覧。
- ^ a b “Building blocks of the apoptotic pore: how Bax and Bak are activated and oligomerize during apoptosis”. Cell Death and Differentiation 21 (2): 196–205. (February 2014). doi:10.1038/cdd.2013.139. PMC 3890949. PMID 24162660 .
- ^ a b c d e “Metaxins 1 and 2, two proteins of the mitochondrial protein sorting and assembly machinery, are essential for Bak activation during TNF alpha triggered apoptosis”. Cellular Signalling 26 (9): 1928–34. (September 2014). doi:10.1016/j.cellsig.2014.04.021. PMID 24794530.
- ^ “Deficiency in apoptotic effectors Bax and Bak reveals an autophagic cell death pathway initiated by photodamage to the endoplasmic reticulum”. Autophagy 2 (3): 238–40. (2006). doi:10.4161/auto.2730. PMID 16874066.
- ^ a b c d “Bioactive lipids and the control of Bax pro-apoptotic activity”. Cell Death & Disease 5 (5): e1266. (May 2014). doi:10.1038/cddis.2014.226. PMC 4047880. PMID 24874738 .
- ^ “BAK/BAX macropores facilitate mitochondrial herniation and mtDNA efflux during apoptosis”. Science 359 (6378): eaao6047. (February 2018). doi:10.1126/science.aao6047. PMID 29472455.
- ^ “BAK overexpression mediates p53-independent apoptosis inducing effects on human gastric cancer cells”. BMC Cancer 4: 33. (July 2004). doi:10.1186/1471-2407-4-33. PMC 481072. PMID 15248898 .
- ^ “Suppression of apoptosis, crypt hyperplasia, and altered differentiation in the colonic epithelia of bak-null mice”. Gastroenterology 136 (3): 943–52. (March 2009). doi:10.1053/j.gastro.2008.11.036. PMID 19185578.
- ^ a b “Casp8p41 generated by HIV protease kills CD4 T cells through direct Bak activation”. The Journal of Cell Biology 206 (7): 867–76. (September 2014). doi:10.1083/jcb.201405051. PMC 4178959. PMID 25246614 .
- ^ Michel Eduardo Beleza Yamagishi (2009). "A simpler explanation to BAK1 gene variation in Aortic and Blood tissues". arXiv:0909.2321 [q-bio.GN]。
- ^ “BAK1 gene variation and abdominal aortic aneurysms”. Human Mutation 30 (7): 1043–7. (July 2009). doi:10.1002/humu.21046. PMID 19514060.
- ^ “BAK1 gene variation and abdominal aortic aneurysms-variants are likely due to sequencing of a processed gene on chromosome 20”. Human Mutation 31 (1): 108–9; author reply 110–1. (January 2010). doi:10.1002/humu.21147. PMID 19847788.
- ^ “Conversion of Bcl-2 from protector to killer by interaction with nuclear orphan receptor Nur77/TR3”. Cell 116 (4): 527–40. (February 2004). doi:10.1016/s0092-8674(04)00162-x. PMID 14980220.
- ^ “Discovery of small-molecule inhibitors of Bcl-2 through structure-based computer screening”. Journal of Medicinal Chemistry 44 (25): 4313–24. (December 2001). doi:10.1021/jm010016f. PMID 11728179.
- ^ “Towards a proteome-scale map of the human protein-protein interaction network”. Nature 437 (7062): 1173–8. (October 2005). Bibcode: 2005Natur.437.1173R. doi:10.1038/nature04209. PMID 16189514.
- ^ “Development of a high-throughput fluorescence polarization assay for Bcl-x(L)”. Analytical Biochemistry 307 (1): 70–5. (August 2002). doi:10.1016/s0003-2697(02)00028-3. PMID 12137781.
- ^ “High-throughput methods to detect dimerization of Bcl-2 family proteins”. Analytical Biochemistry 322 (2): 170–8. (November 2003). doi:10.1016/j.ab.2003.07.014. PMID 14596824.
- ^ a b “Proapoptotic Bak is sequestered by Mcl-1 and Bcl-xL, but not Bcl-2, until displaced by BH3-only proteins”. Genes & Development 19 (11): 1294–305. (June 2005). doi:10.1101/gad.1304105. PMC 1142553. PMID 15901672 .
- ^ “Death by design: the big debut of small molecules”. Nature Cell Biology 3 (2): E43–6. (February 2001). doi:10.1038/35055145. PMID 11175758.
- ^ a b “Fatal liaisons of p53 with Bax and Bak”. Nature Cell Biology 6 (5): 386–8. (May 2004). doi:10.1038/ncb0504-386. PMID 15122264.
- ^ “Specific cleavage of Mcl-1 by caspase-3 in tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis in Jurkat leukemia T cells”. The Journal of Biological Chemistry 280 (11): 10491–500. (March 2005). doi:10.1074/jbc.M412819200. PMID 15637055.
- ^ “MCL-1S, a splicing variant of the antiapoptotic BCL-2 family member MCL-1, encodes a proapoptotic protein possessing only the BH3 domain”. The Journal of Biological Chemistry 275 (33): 25255–61. (August 2000). doi:10.1074/jbc.M909826199. PMID 10837489.
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