Reduction of apoptosis in Rb-deficient embryos via Abl knockout

被引：7

作者：

Borges, H. L. ^{[1
]}

Hunton, I. C. ^{[1
]}

Wang, J. Y. J. ^{[1
]}

机构：

[1] Univ Calif San Diego, Sch Med, Moores Canc Ctr, Div Hematol Oncol,Dept Med, La Jolla, CA 92093 USA

来源：

ONCOGENE | 2007年 / 26卷 / 26期

关键词：

central nervous system; fetal live; haploid insufficiency; knockout mice; tumor suppressor;

D O I：

10.1038/sj.onc.1210157

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：

The retinoblastoma protein RB regulates cell proliferation, differentiation and apoptosis. Homozygous knockout of Rb in mice causes embryonic lethality owing to placental defects that result in excessive apoptosis. RB binds to a number of cellular proteins including the nuclear Abl protein and inhibits its tyrosine kinase activity. Ex vivo experiments have shown that genotoxic or inflammatory stress can activate Abl kinase to stimulate apoptosis. Employing the Rb-null embryos as an in vivo model of apoptosis, we have shown that the genetic ablation of Abl can reduce apoptosis in the developing central nervous system and the embryonic liver. These results are consistent with the inhibitory interaction between RB and Abl, and provide in vivo evidence for the proapoptotic function of Abl.

引用

页码：3868 / 3877

页数：10

共 50 条

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[2]

Agami R, 1999, NATURE, V399, P809

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