INK potentiates TNF-stimulated necrosis by increasing the production of cytotoxic reactive oxygen species

被引：253

作者：

Ventura, JJ

Cogswell, P

Flavell, RA

Baldwin, AS

Davis, RJ ^{[1
]}

机构：

[1] Univ Massachusetts, Sch Med, Howard Hughes Med Inst, Worcester, MA 01605 USA

[2] Univ Massachusetts, Sch Med, Program Mol Med, Worcester, MA 01605 USA

[3] Univ N Carolina, Lineberger Canc Res Ctr, Chapel Hill, NC 27599 USA

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

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

来源：

GENES & DEVELOPMENT | 2004年 / 18卷 / 23期

关键词：

TNF; necrosis; apoptosis; JNK; reactive oxygen species;

D O I：

10.1101/gad.1223004

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

The c-Jun NH2-terminal kinase (INK) has been implicated in both cell death and survival responses to different stimuli. Here we reexamine the function of INK in tumor necrosis factor (TNF)-stimulated cell death using fibroblasts isolated from wild-type, Mkk4(-/-) Mkk7(-/-), and Jnk1(-/-) Jnk2(-/-) mice. We demonstrate that INK can act to suppress TNF-stimulated apoptosis. However, we find that INK can also potentiate TNF-stimulated necrosis by increasing the production of reactive oxygen species (ROS). Together, these data indicate that INK can shift the balance of TNF-stimulated cell death from apoptosis to necrosis. increased necrosis may represent a contributing factor in stress-induced inflammatory responses mediated by INK.

引用

页码：2905 / 2915

页数：11

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