Redox-regulated turnover of Nrf2 is determined by at least two separate protein domains, the redox-sensitive Neh2 degron and the redox-insensitive Neh6 degron (Q28261724)

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Language	Label	Description	Also known as
English	Redox-regulated turnover of Nrf2 is determined by at least two separate protein domains, the redox-sensitive Neh2 degron and the redox-insensitive Neh6 degron	scientific article

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scholarly article

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Redox-regulated turnover of Nrf2 is determined by at least two separate protein domains, the redox-sensitive Neh2 degron and the redox-insensitive Neh6 degron (English)

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Michael McMahon

object named as

Michael McMahon

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object named as

John D Hayes

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author name string

Nerys Thomas

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Ken Itoh

3

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Masayuki Yamamoto

4

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language of work or name

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publication date

23 July 2004

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Journal of Biological Chemistry

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279

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30

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31556-67

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Nrf2 is essential for protection against acute pulmonary injury in mice

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Role of NRF2 in protection against hyperoxic lung injury in mice

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Regulatory mechanisms controlling gene expression mediated by the antioxidant response element

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Integration and diversity of the regulatory network composed of Maf and CNC families of transcription factors

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Positive or negative MARE-dependent transcriptional regulation is determined by the abundance of small Maf proteins

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Hemoprotein Bach1 regulates enhancer availability of heme oxygenase-1 gene

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Nrf1 and Nrf2 positively and c-Fos and Fra1 negatively regulate the human antioxidant response element-mediated expression of NAD(P)H:quinone oxidoreductase1 gene

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Enhanced expression of the transcription factor Nrf2 by cancer chemopreventive agents: role of antioxidant response element-like sequences in the nrf2 promoter

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Keap1 regulates both cytoplasmic-nuclear shuttling and degradation of Nrf2 in response to electrophiles

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Keap1-dependent proteasomal degradation of transcription factor Nrf2 contributes to the negative regulation of antioxidant response element-driven gene expression

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Cadmium Induces Nuclear Export of Bach1, a Transcriptional Repressor of Heme Oxygenase-1 Gene

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Keap1 represses nuclear activation of antioxidant responsive elements by Nrf2 through binding to the amino-terminal Neh2 domain

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Identification of the interactive interface and phylogenic conservation of the Nrf2-Keap1 system.

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Degradation of transcription factor Nrf2 via the ubiquitin-proteasome pathway and stabilization by cadmium

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Increased protein stability as a mechanism that enhances Nrf2-mediated transcriptional activation of the antioxidant response element. Degradation of Nrf2 by the 26 S proteasome

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Functional overlap of sequences that activate transcription and signal ubiquitin-mediated proteolysis

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Ubiquitin-dependent c-Jun degradation in vivo is mediated by the delta domain

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Accumulation of p53 in a mutant cell line defective in the ubiquitin pathway

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A proteasome howdunit: the case of the missing signal

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Mdm-2 and ubiquitin-independent p53 proteasomal degradation regulated by NQO1.

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Proteasomal turnover of p21Cip1 does not require p21Cip1 ubiquitination

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Two domains of Nrf2 cooperatively bind CBP, a CREB binding protein, and synergistically activate transcription

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Scaffolding of Keap1 to the actin cytoskeleton controls the function of Nrf2 as key regulator of cytoprotective phase 2 genes

1 reference

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Ubiquitin in chains

1 reference

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Transferring substrates to the 26S proteasome.

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Involvement of the DNA repair protein hHR23 in p53 degradation

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UFD4 lacking the proteasome-binding region catalyses ubiquitination but is impaired in proteolysis

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Cic1, an adaptor protein specifically linking the 26S proteasome to its substrate, the SCF component Cdc4.

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Gankyrin is an ankyrin-repeat oncoprotein that interacts with CDK4 kinase and the S6 ATPase of the 26 S proteasome

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Proteasomal interactors control activities as diverse as the cell cycle and glutaminergic neurotransmission

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The crystal structure of gankyrin, an oncoprotein found in complexes with cyclin-dependent kinase 4, a 19 S proteasomal ATPase regulator, and the tumor suppressors Rb and p53

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A protein-protein interaction map of the Caenorhabditis elegans 26S proteasome

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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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The BTB protein MEL-26 is a substrate-specific adaptor of the CUL-3 ubiquitin-ligase.

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BTB proteins are substrate-specific adaptors in an SCF-like modular ubiquitin ligase containing CUL-3.

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Targeting of protein ubiquitination by BTB–Cullin 3–Roc1 ubiquitin ligases

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Nrf2 Is a Direct PERK Substrate and Effector of PERK-Dependent Cell Survival

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Deficiency of the Nrf1 and Nrf2 transcription factors results in early embryonic lethality and severe oxidative stress

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Identifiers

10.1074/JBC.M403061200

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Consolidated OpenCitations Corpus – April 2017

OpenCitations bibliographic resource ID

OpenCitations bibliographic resource ID

1 reference

Consolidated OpenCitations Corpus – April 2017

OpenCitations bibliographic resource ID

PubMed publication ID

1 reference

Consolidated OpenCitations Corpus – April 2017

OpenCitations bibliographic resource ID

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