The selective autophagy substrate p62 activates the stress responsive transcription factor Nrf2 through inactivation of Keap1 (Q24300456)

GOA release 2020-03-11

author

Eiki Kominami

16

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Akira Kobayashi

object named as

Akira Kobayashi

5

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Tohru Natsume

object named as

Tohru Natsume

14

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Masaaki Komatsu

object named as

Masaaki Komatsu

1

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author name string

Hirofumi Kurokawa

2

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Satoshi Waguri

3

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Keiko Taguchi

4

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Yoshinobu Ichimura

6

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Yu-Shin Sou

7

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Izumi Ueno

8

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Ayako Sakamoto

9

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Kit I Tong

10

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Mihee Kim

11

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Yasumasa Nishito

12

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Shun-ichiro Iemura

13

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Takashi Ueno

15

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Hozumi Motohashi

17

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Keiji Tanaka

18

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Masayuki Yamamoto

p62 Is a common component of cytoplasmic inclusions in protein aggregation diseases

19

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language of work or name

English

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publication date

March 2010

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published in

Nature Cell Biology

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volume

12

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page(s)

213-23

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issue

3

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cites work

1 reference

Crossref

https://api.crossref.org/works/10.1038%2FNCB2021

Impairment of starvation-induced and constitutive autophagy in Atg7-deficient mice

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

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Nrf2-Keap1 defines a physiologically important stress response mechanism

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Sequestosome 1/p62--more than just a scaffold

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An Nrf2/small Maf heterodimer mediates the induction of phase II detoxifying enzyme genes through antioxidant response elements

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Ubiquitin-binding protein p62 is present in neuronal and glial inclusions in human tauopathies and synucleinopathies

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p62/SQSTM1 binds directly to Atg8/LC3 to facilitate degradation of ubiquitinated protein aggregates by autophagy

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Keap1 is a redox-regulated substrate adaptor protein for a Cul3-dependent ubiquitin ligase complex

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Unveiling the roles of autophagy in innate and adaptive immunity

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Hepatocyte-specific deletion of the keap1 gene activates Nrf2 and confers potent resistance against acute drug toxicity.

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Peroxisomal dynamics.

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Keap1-null mutation leads to postnatal lethality due to constitutive Nrf2 activation

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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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Protection against electrophile and oxidative stress by induction of phase 2 genes: the quest for the elusive sensor that responds to inducers.

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Homeostatic levels of p62 control cytoplasmic inclusion body formation in autophagy-deficient mice

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Interaction codes within the family of mammalian Phox and Bem1p domain-containing proteins

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Loss of autophagy diminishes pancreatic beta cell mass and function with resultant hyperglycemia

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Identification of Bach2 as a B-cell-specific partner for small maf proteins that negatively regulate the immunoglobulin heavy chain gene 3' enhancer.

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LC3, a mammalian homologue of yeast Apg8p, is localized in autophagosome membranes after processing

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The roles of intracellular protein-degradation pathways in neurodegeneration

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The Keap1 BTB/POZ dimerization function is required to sequester Nrf2 in cytoplasm

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Transcription factor Nrf2 coordinately regulates a group of oxidative stress-inducible genes in macrophages

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Mallory body--a disease-associated type of sequestosome

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Oxidative and electrophilic stresses activate Nrf2 through inhibition of ubiquitination activity of Keap1

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The role of autophagy in cardiomyocytes in the basal state and in response to hemodynamic stress

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p62/SQSTM1 forms protein aggregates degraded by autophagy and has a protective effect on huntingtin-induced cell death

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Role of BNIP3 and NIX in cell death, autophagy, and mitophagy

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Autophagy: molecular machinery for self-eating

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Dimerization of substrate adaptors can facilitate cullin-mediated ubiquitylation of proteins by a "tethering" mechanism: a two-site interaction model for the Nrf2-Keap1 complex.

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Autophagy is important in islet homeostasis and compensatory increase of beta cell mass in response to high-fat diet

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Direct evidence that sulfhydryl groups of Keap1 are the sensors regulating induction of phase 2 enzymes that protect against carcinogens and oxidants

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Autophagy fights disease through cellular self-digestion

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Different Electrostatic Potentials Define ETGE and DLG Motifs as Hinge and Latch in Oxidative Stress Response

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The Keap1-BTB protein is an adaptor that bridges Nrf2 to a Cul3-based E3 ligase: oxidative stress sensing by a Cul3-Keap1 ligase

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Suppression of basal autophagy in neural cells causes neurodegenerative disease in mice

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Protection against electrophile and oxidant stress by induction of the phase 2 response: fate of cysteines of the Keap1 sensor modified by inducers

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Keap1 recruits Neh2 through binding to ETGE and DLG motifs: characterization of the two-site molecular recognition model

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Loss of autophagy in the central nervous system causes neurodegeneration in mice

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Ref(2)P, the Drosophila melanogaster homologue of mammalian p62, is required for the formation of protein aggregates in adult brain

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Structural basis for defects of Keap1 activity provoked by its point mutations in lung cancer

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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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Structural basis for sorting mechanism of p62 in selective autophagy

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Nrf2-Keap1 regulation of cellular defense mechanisms against electrophiles and reactive oxygen species

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Processing of X-ray diffraction data collected in oscillation mode

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Crossref

https://api.crossref.org/works/10.1038%2FNCB2021

7 January 2021

inferred from DOI database lookup

MOLREP: an Automated Program for Molecular Replacement

1 reference

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https://api.crossref.org/works/10.1038%2FNCB2021

7 January 2021