Parkin protects against mitochondrial toxins and beta-amyloid accumulation in skeletal muscle cells (Q46975934)

27 December 2017

title

Parkin protects against mitochondrial toxins and beta-amyloid accumulation in skeletal muscle cells (English)

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27 December 2017

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Kenneth M Rosen

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27 December 2017

Vimal Veereshwarayya

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27 December 2017

Charbel E-H Moussa

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27 December 2017

Qinghao Fu

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27 December 2017

Matthew S Goldberg

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27 December 2017

Michael G Schlossmacher

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27 December 2017

Jie Shen

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27 December 2017

Henry W Querfurth

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27 December 2017

language of work or name

English

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publication date

3 March 2006

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27 December 2017

Journal of Biological Chemistry

published in

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27 December 2017

volume

281

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27 December 2017

issue

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27 December 2017

page(s)

12809-12816

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27 December 2017

Mutations in the parkin gene cause autosomal recessive juvenile parkinsonism

cites work

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

A wide variety of mutations in the parkin gene are responsible for autosomal recessive parkinsonism in Europe. French Parkinson's Disease Genetics Study Group and the European Consortium on Genetic Susceptibility in Parkinson's Disease

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Familial Parkinson disease gene product, parkin, is a ubiquitin-protein ligase

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

An unfolded putative transmembrane polypeptide, which can lead to endoplasmic reticulum stress, is a substrate of Parkin

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Parkin ubiquitinates the alpha-synuclein-interacting protein, synphilin-1: implications for Lewy-body formation in Parkinson disease

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Ubiquitination of a new form of alpha-synuclein by parkin from human brain: implications for Parkinson's disease

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Parkin functions as an E2-dependent ubiquitin- protein ligase and promotes the degradation of the synaptic vesicle-associated protein, CDCrel-1

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Accumulation of the authentic parkin substrate aminoacyl-tRNA synthetase cofactor, p38/JTV-1, leads to catecholaminergic cell death.

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

CHIP is associated with Parkin, a gene responsible for familial Parkinson's disease, and enhances its ubiquitin ligase activity

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Parkin interacts with the proteasome subunit alpha4

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Parkin localizes to the Lewy bodies of Parkinson disease and dementia with Lewy bodies

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Parkin prevents mitochondrial swelling and cytochrome c release in mitochondria-dependent cell death.

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Genetic and genomic studies of Drosophila parkin mutants implicate oxidative stress and innate immune responses in pathogenesis.

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Drosophila parkin mutants have decreased mass and cell size and increased sensitivity to oxygen radical stress

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Mitochondrial dysfunction and oxidative damage in parkin-deficient mice

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Inclusion-body myositis and myopathies: different etiologies, possibly similar pathogenic mechanisms

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Transfer of beta-amyloid precursor protein gene using adenovirus vector causes mitochondrial abnormalities in cultured normal human muscle

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

βAPP gene transfer into cultured human muscle induces inclusion-body myositis aspects

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Presence of BACE1 and BACE2 in muscle fibres of patients with sporadic inclusion-body myositis

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Association of active extracellular signal-regulated protein kinase with paired helical filaments of inclusion-body myositis muscle suggests its role in inclusion-body myositis tau phosphorylation

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Endoplasmic reticulum stress and unfolded protein response in inclusion body myositis muscle.

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Immunolocalization of ubiquitin in muscle biopsies of patients with inclusion body myositis and oculopharyngeal muscular dystrophy.

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Impaired innervation of cultured human muscle overexpressing betaAPP experimentally and genetically: relevance to inclusion-body myopathies

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Inclusion body myositis-like phenotype induced by transgenic overexpression of beta APP in skeletal muscle

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Amyloid-beta deposition in skeletal muscle of transgenic mice: possible model of inclusion body myopathy

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Parkin-deficient mice exhibit nigrostriatal deficits but not loss of dopaminergic neurons

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Heat shock protein 70 participates in the neuroprotective response to intracellularly expressed beta-amyloid in neurons.

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Germline transmission and tissue-specific expression of transgenes delivered by lentiviral vectors

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Inclusion body myositis, a review

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Lewy body Parkinson's disease in a large pedigree with 77 Parkin mutation carriers

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Mitochondrial pathology and apoptotic muscle degeneration in Drosophila parkin mutants

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Amyloid beta-peptide is produced by cultured cells during normal metabolism

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Oligomerization of endogenous and synthetic amyloid beta-protein at nanomolar levels in cell culture and stabilization of monomer by Congo red.

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Naturally secreted oligomers of amyloid beta protein potently inhibit hippocampal long-term potentiation in vivo

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Targeting of cell-surface beta-amyloid precursor protein to lysosomes: alternative processing into amyloid-bearing fragments.

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Nuclear and cytoplasmic localization of the beta-amyloid peptide (1-43) in transfected 293 cells

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Evidence that neurones accumulating amyloid can undergo lysis to form amyloid plaques in Alzheimer's disease

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Detection of a novel intraneuronal pool of insoluble amyloid beta protein that accumulates with time in culture

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Soluble pool of Abeta amyloid as a determinant of severity of neurodegeneration in Alzheimer's disease

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Parkin-associated Parkinson's disease

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Functional association of the parkin gene promoter with idiopathic Parkinson's disease

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Mitochondrial dysfunction and oxidative damage in Alzheimer's and Parkinson's diseases and coenzyme Q10 as a potential treatment

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Contributions of mitochondrial alterations, resulting from bad genes and a hostile environment, to the pathogenesis of Alzheimer's disease

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Altered metabolism of the amyloid beta precursor protein is associated with mitochondrial dysfunction in Down's syndrome

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Selective increase in cellular A beta 42 is related to apoptosis but not necrosis.

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Dopamine covalently modifies and functionally inactivates parkin

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Inactivation of parkin by oxidative stress and C-terminal truncations: a protective role of molecular chaperones

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

The C-terminal fragment of the Alzheimer's disease amyloid protein precursor is degraded by a proteasome-dependent mechanism distinct from gamma-secretase

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Proteasome-mediated degradation of the C-terminus of the Alzheimer's disease beta-amyloid protein precursor: effect of C-terminal truncation on production of beta-amyloid protein

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

Proteasome inhibition and aggresome formation in sporadic inclusion-body myositis and in amyloid-beta precursor protein-overexpressing cultured human muscle fibers

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

The molecular and cellular pathology of inflammatory muscle diseases

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.M512649200

21 January 2018

Identifiers

DOI

10.1074/JBC.M512649200

1 reference

27 December 2017

1 reference

27 December 2017