NF-κB

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NF-κB作用机制。在此图中,将以Rel与p50蛋白组成的NF-κB异质二聚体为例。当处于激活状态时,NF-κB位于细胞质中且与抑制蛋白IκBα形成复合体。通过内在膜受体的介导,一些胞外信号物质可激活一种称为IκB激酶(IKK)的酶。IKK转而磷酸化IκBα蛋白,这将导致后者的泛素化,使得IκBα从NF-κB上脱离下来,最终IκBα被蛋白酶体所降解。被激活的NF-κB接下来转移到细胞核内,在这里会结合到DNA上被称为反应元件(RE)的特异性序列上。DNA/NF-κB 复合体接下来会招募其它蛋白,如辅激活物RNA聚合酶,这些蛋白将下游的DNA转录为mRNA并转而被翻译为蛋白质,这些蛋白最终导致细胞功能发生改变[1][2][3]

核因子活化B细胞κ轻链增强子英语nuclear factor kappa-light-chain-enhancer of activated B cells,简称为NF-κB)是一种控制DNA转录的蛋白复合体。NF-κB几乎存在于所有类型的动物细胞中并参与细胞对诸多刺激的响应,这些刺激包括应激、细胞因子自由基紫外线照射、氧化LDL及细菌或病毒抗原[1][2][3][4][5]。在针对感染的免疫反应中,NF-κB起到了重要的调节作用(κ轻链是免疫球蛋白的重要组成部分)。NF-κB的调控失常与癌症、炎症和自身免疫病感染性休克、病毒感染以及免疫发育异常有关。NF-κB亦与突触可塑性及记忆过程有着密切关系[6][7][8][9][10]

参考文献[编辑]

  1. ^ 1.0 1.1 Gilmore TD. Introduction to NF-κB: players, pathways, perspectives. Oncogene. 2006, 25 (51): 6680–4. doi:10.1038/sj.onc.1209954. PMID 17072321. 
  2. ^ 2.0 2.1 Brasier AR. The NF-κB regulatory network. Cardiovasc. Toxicol. 2006, 6 (2): 111–30. doi:10.1385/CT:6:2:111. PMID 17303919. 
  3. ^ 3.0 3.1 Perkins ND. Integrating cell-signalling pathways with NF-κB and IKK function. Nat. Rev. Mol. Cell Biol. 2007.January, 8 (1): 49–62. doi:10.1038/nrm2083. PMID 17183360. 
  4. ^ Gilmore TD. The Rel/NF-κB signal transduction pathway: introduction. Oncogene. 1999, 18 (49): 6842–4. doi:10.1038/sj.onc.1203237. PMID 10602459. 
  5. ^ Tian B, Brasier AR. Identification of a nuclear factor κ B-dependent gene network. Recent Prog. Horm. Res. 2003, 58: 95–130. doi:10.1210/rp.58.1.95. PMID 12795416. 
  6. ^ Albensi BC, Mattson MP. Evidence for the involvement of TNF and NF-κB in hippocampal synaptic plasticity. Synapse. 2000, 35 (2): 151–9. doi:10.1002/(SICI)1098-2396(200002)35:2<151::AID-SYN8>3.0.CO;2-P. PMID 10611641. 
  7. ^ Meffert MK, Chang JM, Wiltgen BJ, Fanselow MS, Baltimore D. NF-kappa B functions in synaptic signaling and behavior. Nat. Neurosci. 2003.October, 6 (10): 1072–8. doi:10.1038/nn1110. PMID 12947408. 
  8. ^ Levenson JM, Choi S, Lee SY, Cao YA, Ahn HJ, Worley KC, Pizzi M, Liou HC, Sweatt JD. A bioinformatics analysis of memory consolidation reveals involvement of the transcription factor c-rel. J. Neurosci. 2004.April, 24 (16): 3933–43. doi:10.1523/JNEUROSCI.5646-03.2004. PMID 15102909. 
  9. ^ Freudenthal R, Locatelli F, Hermitte G, Maldonado H, Lafourcade C, Delorenzi A, Romano A. Kappa-B like DNA-binding activity is enhanced after spaced training that induces long-term memory in the crab Chasmagnathus. Neurosci. Lett. 1998.February, 242 (3): 143–6. doi:10.1016/S0304-3940(98)00059-7. PMID 9530926. 
  10. ^ Merlo E, Freudenthal R, Romano A. The IkappaB kinase inhibitor sulfasalazine impairs long-term memory in the crab Chasmagnathus. Neuroscience. 2002, 112 (1): 161–72. doi:10.1016/S0306-4522(02)00049-0. PMID 12044481. 

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