Activation of Nrf2 by arsenite and monomethylarsonous acid is independent of Keap1-C151: enhanced Keap1-Cul3 interaction (Q24656061)

1

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Zheng Sun

2

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Weimin Chen

3

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Yanjie Li

4

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Nicole F Villeneuve

5

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Donna D Zhang

Toxicology and Applied Pharmacology

6

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language of work or name

English

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publication date

1 August 2008

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published in

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volume

230

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issue

3

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page(s)

383-9

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cites work

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BTB protein Keap1 targets antioxidant transcription factor Nrf2 for ubiquitination by the Cullin 3-Roc1 ligase

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Oxidative stress sensor Keap1 functions as an adaptor for Cul3-based E3 ligase to regulate proteasomal degradation of Nrf2

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Keap1 controls postinduction repression of the Nrf2-mediated antioxidant response by escorting nuclear export of Nrf2

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Nrf2 controls constitutive and inducible expression of ARE-driven genes through a dynamic pathway involving nucleocytoplasmic shuttling by Keap1

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Distinct Cysteine Residues in Keap1 Are Required for Keap1-Dependent Ubiquitination of Nrf2 and for Stabilization of Nrf2 by Chemopreventive Agents and Oxidative Stress

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Nrf2 protects human bladder urothelial cells from arsenite and monomethylarsonous acid toxicity

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Interferon-gamma plays protective roles in sodium arsenite-induced renal injury by up-regulating intrarenal multidrug resistance-associated protein 1 expression.

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