Succination of Keap1 and Activation of Nrf2-Dependent Antioxidant Pathways in FH-Deficient Papillary Renal Cell Carcinoma Type 2

被引：95

作者：

Kinch, Lisa ^{[2
]}

Grishin, Nick V. ^{[2
]}

Brugarolas, James ^{[1
,3
,4
]}

机构：

[1] Univ Texas SW Med Ctr Dallas, Dept Internal Med, Dallas, TX 75390 USA

[2] Univ Texas SW Med Ctr Dallas, Dept Biochem, Dallas, TX 75390 USA

[3] Univ Texas SW Med Ctr Dallas, Dept Dev Biol, Dallas, TX 75390 USA

[4] Univ Texas SW Med Ctr Dallas, Simmons Comprehens Canc Ctr, Dallas, TX 75390 USA

来源：

CANCER CELL | 2011年 / 20卷 / 04期

关键词：

CANCER; MECHANISMS;

D O I：

10.1016/j.ccr.2011.10.005

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Fumarate hydratase (FH) is a tumor suppressor, but how it acts is unclear. Two reports in this issue of Cancer Cell reveal that FH deficiency leads to succination of Keap1, stabilization of Nrf2, and induction of stress-response genes including HMOX1, which is important for the survival of FH-deficient cells.

引用

页码：418 / 420

页数：3

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