p62 accumulates and enhances aggregate formation in model systems of familial amyotrophic lateral sclerosis (Q40171781)

18 September 2017

p62 accumulates and enhances aggregate formation in model systems of familial amyotrophic lateral sclerosis (English)

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amyotrophic lateral sclerosis

18 September 2017

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author name string

Jozsef Gal

1

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18 September 2017

Anna-Lena Ström

2

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18 September 2017

Renee Kilty

3

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18 September 2017

Fujian Zhang

4

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18 September 2017

Haining Zhu

5

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18 September 2017

language of work or name

English

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publication date

12 February 2007

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Journal of Biological Chemistry

18 September 2017

10

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based on heuristic

inferred from page(s)

published in

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18 September 2017

282

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18 September 2017

11068-11077

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18 September 2017

15

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Mutations in Cu/Zn superoxide dismutase gene are associated with familial amyotrophic lateral sclerosis

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Transgenic mice carrying a human mutant superoxide dismutase transgene develop neuronal cytoskeletal pathology resembling human amyotrophic lateral sclerosis lesions

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Structural properties and neuronal toxicity of amyotrophic lateral sclerosis-associated Cu/Zn superoxide dismutase 1 aggregates.

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p62, a phosphotyrosine-independent ligand of the SH2 domain of p56lck, belongs to a new class of ubiquitin-binding proteins

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Inhibition of sequestosome 1/p62 up-regulation prevents aggregation of ubiquitinated proteins induced by prostaglandin J2 without reducing its neurotoxicity

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Sequestosome 1/p62 shuttles polyubiquitinated tau for proteasomal degradation

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

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Increased expression of p62 in expanded polyglutamine-expressing cells and its association with polyglutamine inclusions.

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ALS phenotypes with mutations in CHMP2B (charged multivesicular body protein 2B)

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Motor neuron degeneration in mice that express a human Cu,Zn superoxide dismutase mutation

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Neuroblastoma x spinal cord (NSC) hybrid cell lines resemble developing motor neurons

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Mitochondrial proteomic analysis of a cell line model of familial amyotrophic lateral sclerosis

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Intracellular conformational alterations of mutant SOD1 and the implications for fALS-associated SOD1 mutant induced motor neuron cell death

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Aggresomes, inclusion bodies and protein aggregation

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Proteasomal inhibition by misfolded mutant superoxide dismutase 1 induces selective motor neuron death in familial amyotrophic lateral sclerosis

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Focal dysfunction of the proteasome: a pathogenic factor in a mouse model of amyotrophic lateral sclerosis

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Hassles with taking out the garbage: aggravating aggresomes.

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Evidence for p62 aggregate formation: role in cell survival

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

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PB1 domain-mediated heterodimerization in NADPH oxidase and signaling complexes of atypical protein kinase C with Par6 and p62

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Fibrillar inclusions and motor neuron degeneration in transgenic mice expressing superoxide dismutase 1 with a disrupted copper-binding site

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Misfolded CuZnSOD and amyotrophic lateral sclerosis

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Degradation of Amyotrophic Lateral Sclerosis-linked Mutant Cu,Zn-Superoxide Dismutase Proteins by Macroautophagy and the Proteasome

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Structure and functional properties of the ubiquitin binding protein p62

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The atypical protein kinase C-interacting protein p62 is a scaffold for NF-kappaB activation by nerve growth factor

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The p62 scaffold regulates nerve growth factor-induced NF-kappaB activation by influencing TRAF6 polyubiquitination

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TRAF6-mediated ubiquitination regulates nuclear translocation of NRIF, the p75 receptor interactor

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Identifiers

DOI

10.1074/JBC.M608787200

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18 September 2017

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