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

Lisa Kinch; Nick V. Grishin; James Brugarolas

doi:10.1016/j.ccr.2011.10.005

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

Lisa Kinch, Nick V. Grishin, James Brugarolas

Research output: Contribution to journal › Short survey › peer-review

88 Scopus citations

Abstract

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.

Original language	English (US)
Pages (from-to)	418-420
Number of pages	3
Journal	Cancer Cell
Volume	20
Issue number	4
DOIs	https://doi.org/10.1016/j.ccr.2011.10.005
State	Published - Oct 18 2011

ASJC Scopus subject areas

Oncology
Cell Biology
Cancer Research

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10.1016/j.ccr.2011.10.005

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abstract = "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.",

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AU - Brugarolas, James

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AB - 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.

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

Abstract

ASJC Scopus subject areas

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