Parkin is ubiquitinated by Nrdp1 and abrogates Nrdp1-induced oxidative stress (Q24320160)

Pathogenic mutations in Parkinson disease

GOA release 2020-03-11

protein ubiquitination

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Furong Yu

1

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Jianhua Zhou

series ordinal

2

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language of work or name

English

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publication date

25 July 2008

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published in

Neuroscience Letters

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volume

440

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issue

1

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page(s)

4-8

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cites work

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Parkin-associated Parkinson's disease

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The Drosophila parkin homologue is required for normal mitochondrial dynamics during spermiogenesis

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Reactive oxygen species production by monocytes and polymorphonuclear leukocytes during dialysis

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Parkin protects against the toxicity associated with mutant alpha-synuclein: proteasome dysfunction selectively affects catecholaminergic neurons

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Nrdp1-mediated degradation of the gigantic IAP, BRUCE, is a novel pathway for triggering apoptosis

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How does parkin ligate ubiquitin to Parkinson's disease?

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Association between early-onset Parkinson's disease and mutations in the parkin gene

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An RBCC protein implicated in maintenance of steady-state neuregulin receptor levels

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Mitochondrial pathology and apoptotic muscle degeneration in Drosophila parkin mutants

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Nrdp1/FLRF is a ubiquitin ligase promoting ubiquitination and degradation of the epidermal growth factor receptor family member, ErbB3

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

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Mitochondrial dysfunction and oxidative damage in parkin-deficient mice

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RING finger ubiquitin-protein isopeptide ligase Nrdp1/FLRF regulates parkin stability and activity

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

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Parkin protects human dopaminergic neuroblastoma cells against dopamine-induced apoptosis

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

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Parkin enhances mitochondrial biogenesis in proliferating cells

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Characterization and use of the Drosophila metallothionein promoter in cultured Drosophila melanogaster cells

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Parkin attenuates manganese-induced dopaminergic cell death

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Parkin counteracts symptoms in a Drosophila model of Parkinson's disease

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A comparison of clinical and pathological features of young- and old-onset Parkinson's disease

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

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

1 reference

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A Drosophila model of mutant human parkin-induced toxicity demonstrates selective loss of dopaminergic neurons and dependence on cellular dopamine.

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10.1016/J.NEULET.2008.05.052

Identifiers

DOI

1 reference

Consolidated OpenCitations Corpus – April 2017

1 reference

Consolidated OpenCitations Corpus – April 2017

PubMed publication ID

18541373

1 reference

Consolidated OpenCitations Corpus – April 2017