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

被引：146
作者：
Kanazawa, S
Soucek, L
Evan, G
Okamoto, T
Peterlin, BM
机构：
[1] Univ Calif San Francisco, Rosalind Russell Med Res Ctr, Dept Med, San Francisco, CA 94143 USA
[2] Univ Calif San Francisco, Rosalind Russell Med Res Ctr, Dept Microbiol & Immunol, San Francisco, CA 94143 USA
[3] Univ Calif San Francisco, Canc Res Inst, San Francisco, CA 94143 USA
[4] Nagoya City Univ, Sch Med, Dept Mol Genet, Nagoya, Aichi 467, Japan
来源：
ONCOGENE | 2003年 / 22卷 / 36期
基金：
美国国家卫生研究院;
关键词：
c-Myc; P-TEFb; CycT1; apoptosis; proliferation; transcription;
D O I：
10.1038/sj.onc.1206800
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
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.
引用
收藏
页码：5707 / 5711
页数：5
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