Role of oncogenic transcription factor c-Myc in cell cycle regulation, apoptosis and metabolism

被引:31
作者
Dang, CV
Lewis, BC
机构
[1] Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA
[2] Johns Hopkins Univ, Sch Med, Dept Oncol, Baltimore, MD 21205 USA
[3] Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21205 USA
[4] Johns Hopkins Univ, Sch Med, Dept Mol Biol & Genet, Baltimore, MD 21205 USA
[5] Johns Hopkins Univ, Sch Med, Program Human Genet & Mol Biol, Baltimore, MD 21205 USA
基金
美国国家卫生研究院;
关键词
c-Myc; oncogene; transcription; cancer; metabolism; apoptosis;
D O I
10.1007/BF02258350
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The myc gene was initially discovered as a prototypical retrovirally transduced oncogene. Over the decades, abundant evidence has emerged to support a causal role for the activated cellular gene, c-myc, in animal and human tumors. The gene encodes an oncogenic helix-loop-helix leucine zipper transcription factor that acts as a heterodimer with its partner protein, Max, to activate genes regulating the cell cycle machinery as well as critical metabolic enzymes. The additional ability of c-Myc to repress transcription of differentiation-related genes suggest that c-Myc is a central and key molecular integrator of cell proliferation, differentiation and metabolism.
引用
收藏
页码:269 / 278
页数:10
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