c-Myc招募P-TEFb用于转录、细胞增殖和凋亡。

c-Myc recruits P-TEFb for transcription, cellular proliferation and apoptosis.

作者信息

Kanazawa Satoshi, Soucek Laura, Evan Gerard, Okamoto Takashi, Peterlin B Matija

机构信息

Departments of Medicine, Microbiology and Immunology, Rosalind Russell Medical Research Center, University of California, San Francisco, CA 94143-0703, USA.

出版信息

Oncogene. 2003 Aug 28;22(36):5707-11. doi: 10.1038/sj.onc.1206800.

DOI:10.1038/sj.onc.1206800

PMID:12944920

Abstract

c-Myc promotes cellular proliferation, sensitizes cells to apoptosis and prevents differentiation. It binds cyclin T1 structurally and functionally from the positive transcription elongation factor b (P-TEFb). The cyclin-dependent kinase 9 (Cdk9) in P-TEFb then phosporylates the C-terminal domain of RNA polymerase II, which is required for the transition from initiation to elongation of eukaryotic transcription. Inhibiting P-TEFb blocks the transcription of its target genes as well as cellular proliferation and apoptosis induced by c-Myc.

摘要

c-Myc促进细胞增殖，使细胞对凋亡敏感并阻止分化。它在结构和功能上与正转录延伸因子b（P-TEFb）中的细胞周期蛋白T1结合。然后，P-TEFb中的细胞周期蛋白依赖性激酶9（Cdk9）使RNA聚合酶II的C末端结构域磷酸化，这是真核转录从起始过渡到延伸所必需的。抑制P-TEFb会阻断其靶基因的转录以及c-Myc诱导的细胞增殖和凋亡。