肿瘤抑制因子Hamartin和Tuberin信号调控机制  

Regulation of Tumor Suppressors Hamartin and Tuberin Signaling

作　　者：赵蕴玉[1] 楼丽广[1] 

机构地区：[1]中国科学院上海生命科学研究院上海药物研究所,上海201203

出　　处：《细胞生物学杂志》2005年第5期489-492,共4页Chinese Journal of Cell Biology

摘　　要：结节硬化复合症由tsc1、tsc2基因突变引起,这2个基因分别编码hamartin和tuberin,它们均为肿瘤抑制因子,在细胞生长和增殖过程中起关键性的调节作用。生长因子刺激的PI3K/Akt信号通路通过磷酸化tuberin,调控下游效应因子功能,最终影响细胞的生长和增殖。现对hamartin和tuberin信号调控机制的最新进展进行综述,并展望其发展趋势。Tuberous sclerosis is an autosomal dominant disorder caused by mutations in tscl and tsc2 genes. Hamartin and tuberin, encoded by tscl and tsc2 genes, respectively, are tumor suppressors and play critical roles in cell growth and proliferation. Growth factor-stimulated PI3K/Akt signaling leads to tuberin phosphorylation, then regulates downstream effector function and affects cell growth and proliferation. This review summarizes the latest progresses in hamartin-and tuberin-mediated signaling transduction. We hope this review will give some insights into the understanding of the roles of hamartin and tuberin in cellular signaling and the challenge behind them.

关 键 词：肿瘤抑制因子 HAMARTIN TUBERIN 信号调控机制 细胞增殖 结节硬化复合症 

分 类 号：R730.2[医药卫生—肿瘤]