Oncogene-Stimulated Congestion at the KEAP1 Stress Signaling Hub Allows Bypass of NRF2 and Induction of NRF2-Target Genes that Promote Tumor Survival

John D. Hayes; Albena T. Dinkova-Kostova

doi:10.1016/j.ccell.2017.10.009

Oncogene-Stimulated Congestion at the KEAP1 Stress Signaling Hub Allows Bypass of NRF2 and Induction of NRF2-Target Genes that Promote Tumor Survival

John D. Hayes, Albena T. Dinkova-Kostova (Lead / Corresponding author)

Research output: Contribution to journal › Article › peer-review

24 Citations (Scopus)

299 Downloads (Pure)

Abstract

In this issue of Cancer Cell, Ge et al. show that overexpression of the oncoprotein iASPP in cancer cells provokes NRF2-mediated induction of cytoprotective genes, because it logjams the ubiquitin ligase substrate adaptor function of KEAP1 by virtue of the fact that it possesses a novel DLT-containing KEAP1-interaction motif.

Original language	English
Pages (from-to)	539-541
Number of pages	3
Journal	Cancer Cell
Volume	32
Issue number	5
Early online date	13 Nov 2017
DOIs	https://doi.org/10.1016/j.ccell.2017.10.009
Publication status	Published - Nov 2017

ASJC Scopus subject areas

Oncology
Cell Biology
Cancer Research

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.ccell.2017.10.009

Author Accepted ManuscriptAccepted author manuscript, 185 KBLicence: CC BY-NC-ND
Author Accepted Manuscript - Figure1Accepted author manuscript, 208 KBLicence: CC BY-NC-ND

Cite this

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title = "Oncogene-Stimulated Congestion at the KEAP1 Stress Signaling Hub Allows Bypass of NRF2 and Induction of NRF2-Target Genes that Promote Tumor Survival",

abstract = "In this issue of Cancer Cell, Ge et al. show that overexpression of the oncoprotein iASPP in cancer cells provokes NRF2-mediated induction of cytoprotective genes, because it logjams the ubiquitin ligase substrate adaptor function of KEAP1 by virtue of the fact that it possesses a novel DLT-containing KEAP1-interaction motif.",

author = "Hayes, {John D.} and Dinkova-Kostova, {Albena T.}",

note = "The authors are supported by grant MR/N009851/1 from the Medical Research Council of the UK and grant C20953/A18644 from Cancer Research UK.",

year = "2017",

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AU - Hayes, John D.

AU - Dinkova-Kostova, Albena T.

N1 - The authors are supported by grant MR/N009851/1 from the Medical Research Council of the UK and grant C20953/A18644 from Cancer Research UK.

PY - 2017/11

Y1 - 2017/11

N2 - In this issue of Cancer Cell, Ge et al. show that overexpression of the oncoprotein iASPP in cancer cells provokes NRF2-mediated induction of cytoprotective genes, because it logjams the ubiquitin ligase substrate adaptor function of KEAP1 by virtue of the fact that it possesses a novel DLT-containing KEAP1-interaction motif.

AB - In this issue of Cancer Cell, Ge et al. show that overexpression of the oncoprotein iASPP in cancer cells provokes NRF2-mediated induction of cytoprotective genes, because it logjams the ubiquitin ligase substrate adaptor function of KEAP1 by virtue of the fact that it possesses a novel DLT-containing KEAP1-interaction motif.

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U2 - 10.1016/j.ccell.2017.10.009

DO - 10.1016/j.ccell.2017.10.009

M3 - Article

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SN - 1535-6108

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SP - 539

EP - 541

JO - Cancer Cell

JF - Cancer Cell

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ER -

Oncogene-Stimulated Congestion at the KEAP1 Stress Signaling Hub Allows Bypass of NRF2 and Induction of NRF2-Target Genes that Promote Tumor Survival

Abstract

ASJC Scopus subject areas

UN SDGs

Access to Document

Other files and links

Fingerprint

Contribution by NRF2 Upregulation to Lung Carcinogenesis and the Possible Therapeutic Value of NRF2 Inhibition by GSK-3 (Joint with Universities of St Andrews, Edinburgh and Pennsylvania)

The Spatiotemporal Regulation of the Keap1/Nrf2 Pathway (Joint with University College London)

Cite this

Oncogene-Stimulated Congestion at the KEAP1 Stress Signaling Hub Allows Bypass of NRF2 and Induction of NRF2-Target Genes that Promote Tumor Survival

Abstract

ASJC Scopus subject areas

UN SDGs

Access to Document

Other files and links

Fingerprint

Projects

Contribution by NRF2 Upregulation to Lung Carcinogenesis and the Possible Therapeutic Value of NRF2 Inhibition by GSK-3 (Joint with Universities of St Andrews, Edinburgh and Pennsylvania)

The Spatiotemporal Regulation of the Keap1/Nrf2 Pathway (Joint with University College London)

Cite this