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Autophagy joins the game to regulate NF-κB signaling pathways

机译:自噬参与游戏调节NF-κB信号通路

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摘要

The nuclear factor kappa B (NF-κB) transcription factor coordinates several aspects of innate and adaptive immunity, inflammation, cell survival and proliferation [1, 2]. Dysregulation of the NF-κB pathway has been associated with cancer development and progression as well as with other human diseases including viral infections and a number of inflammatory diseases [1]. NF-κB is formed through the dimerization of 5 subunits, including members of the Rel protein family, namely RelA (p65), c-Rel, RelB, NF-κB 1 (p50 and its precursor p105) and NF-κB2 (p52 and its precursor p100). Two pathways are involved in the activation of NF-κB. In both these pathways, kinase activity and proteasome activity play a major role in freeing NF-κB from cytoplasmic inhibitors to promote its nuclear translo-cation and activation. The classical or canonical pathway is activated by a large range of stimuli (microbial and viral infections, proinflammatory cytokines).
机译:核因子κB(NF-κB)转录因子可协调先天性和适应性免疫,炎症,细胞存活和增殖的多个方面[1、2]。 NF-κB通路的失调与癌症的发展和进程以及其他人类疾病(包括病毒感染和许多炎症性疾病)有关[1]。 NF-κB是通过5个亚基的二聚化形成的,包括Rel蛋白家族的成员,即RelA(p65),c-Rel,RelB,NF-κB1(p50及其前体p105)和NF-κB2(p52和其前身p100)。 NF-κB的激活涉及两个途径。在这两种途径中,激酶活性和蛋白酶体活性在使NF-κB脱离细胞质抑制剂以促进其核转录和活化中起主要作用。经典或经典途径被多种刺激(微生物和病毒感染,促炎细胞因子)激活。

著录项

  • 来源
    《Cell Research》 |2007年第7期|576-577|共2页
  • 作者单位

    Institut National de la Sante et de la Recherche Medicate Unite 756 (INSERM U756);

  • 收录信息 美国《科学引文索引》(SCI);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 细胞生物学;
  • 关键词

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