Caspases 3 and 7: Key mediators of mitochondrial events of apoptosis

被引：996

作者：

Lakhani, SA

Masud, A

Kuida, K

Porter, GA

Booth, CJ

Mehal, WZ

Inayat, I

Flavell, RA

机构：

[1] Yale Univ, Sch Med, Immunobiol Sect, New Haven, CT 06520 USA

[2] Yale Univ, Sch Med, Dept Pediat, New Haven, CT 06520 USA

[3] Yale Univ, Sch Med, Comparat Med Sect, New Haven, CT 06520 USA

[4] Yale Univ, Sch Med, Dept Internal Med, New Haven, CT 06520 USA

[5] Yale Univ, Sch Med, Howard Hughes Med Inst, New Haven, CT 06520 USA

[6] Vertex Pharmaceut, Cambridge, MA 02139 USA

来源：

SCIENCE | 2006年 / 311卷 / 5762期

关键词：

D O I：

10.1126/science.1115035

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

The current model of apoptosis holds that upstream signals lead to activation of downstream effector caspases. We generated mice deficient in the two effectors, caspase 3 and caspase 7, which died immediately after birth with defects in cardiac development. Fibroblasts lacking both enzymes were highly resistant to both mitochondrial and death receptor-mediated apoptosis, displayed preservation of mitochondrial membrane potential, and had defective nuclear translocation of apoptosis-inducing factor (AIF). Furthermore, the early apoptotic events of Bax translocation and cytochrome c release were also delayed. We conclude that caspases 3 and 7 are critical mediators of mitochondrial events of apoptosis.

引用

页码：847 / 851

页数：5

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