Escape from Cbl-mediated downregulation: A recurrent theme for oncogenic deregulation of receptor tyrosine kinases

被引：181

作者：

Peschard, P

Park, M ^{[1
]}

机构：

[1] McGill Univ, Ctr Hlth, Mol Oncol Grp, Dept Biochem, Montreal, PQ H3A 1A1, Canada

[2] McGill Univ, Ctr Hlth, Mol Oncol Grp, Dept Med, Montreal, PQ H3A 1A1, Canada

[3] McGill Univ, Ctr Hlth, Mol Oncol Grp, Dept Oncol, Montreal, PQ H3A 1A1, Canada

来源：

CANCER CELL | 2003年 / 3卷 / 06期

基金：

加拿大健康研究院;

关键词：

D O I：

10.1016/S1535-6108(03)00136-3

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Deregulation of growth factor receptor tyrosine kinases (RTKs) is linked to a large number of malignancies. This occurs through a variety of mechanisms that result in enhanced activity of the receptor. Considerable evidence now supports the idea that loss of negative regulation plays an important role in receptor deregulation. RTKs are removed from the cell surface via endocytosis and many are subsequently degraded in the lysosome. Lysosomal targeting has recently been linked with receptor ubiquitination. We review here molecular alterations that uncouple RTKs from ubiquitination and implicate loss of ubiquitination as a process that plays a significant role in the pathogenesis of cancer.

引用

页码：519 / 523

页数：5

共 33 条

[1] Src promotes destruction of c-Cbl: Implications for oncogenic synergy between Src and growth factor receptors [J].