L166P mutant DJ-1, causative for recessive Parkinson's disease, is degraded through the ubiquitin-proteasome system (Q28185988)

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object named as

David W Miller

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author name string

Rili Ahmad

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Stephen Hague

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Melisa J Baptista

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Rosa Canet-Aviles

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Chris McLendon

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Donald M Carter

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Peng-Peng Zhu

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Julia Stadler

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Jayanth Chandran

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Gary R Klinefelter

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Craig Blackstone

Journal of Biological Chemistry

12

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language of work or name

English

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publication date

19 September 2003

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published in

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volume

278

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issue

38

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page(s)

36588-95

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cites work

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Mutations in the parkin gene cause autosomal recessive juvenile parkinsonism

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Molecular cloning and expression of rat contraception associated protein 1 (CAP1), a protein putatively involved in fertilization

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DJ-1 positively regulates the androgen receptor by impairing the binding of PIASx alpha to the receptor

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DJ-1 is an indicator for endogenous reactive oxygen species elicited by endotoxin

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Oxidized forms of peroxiredoxins and DJ-1 on two-dimensional gels increased in response to sublethal levels of paraquat

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The 1.6-A crystal structure of the class of chaperones represented by Escherichia coli Hsp31 reveals a putative catalytic triad

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The crystal structure of DJ-1, a protein related to male fertility and Parkinson's disease

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Crystal structure of human DJ-1, a protein associated with early onset Parkinson's disease

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Interaction of the deafness-dystonia protein DDP/TIMM8a with the signal transduction adaptor molecule STAM1

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Localization of the sperm protein SP22 and inhibition of fertility in vivo and in vitro

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

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RAD6-dependent DNA repair is linked to modification of PCNA by ubiquitin and SUMO.

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Crystal structure of an intracellular protease from Pyrococcus horikoshii at 2-A resolution

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The ubiquitin-proteasome proteolytic pathway: destruction for the sake of construction

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A principal role for the proteasome in endoplasmic reticulum-associated degradation of misfolded intracellular cystic fibrosis transmembrane conductance regulator

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Mutant products of the NF2 tumor suppressor gene are degraded by the ubiquitin-proteasome pathway

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Limb-girdle muscular dystrophy (LGMD-1C) mutants of caveolin-3 undergo ubiquitination and proteasomal degradation. Treatment with proteasomal inhibitors blocks the dominant negative effect of LGMD-1C mutanta and rescues wild-type caveolin-3.

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Acceleration of oligomerization, not fibrillization, is a shared property of both alpha-synuclein mutations linked to early-onset Parkinson's disease: implications for pathogenesis and therapy

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

21 January 2018

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

21 January 2018

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21 January 2018

Identifiers

DOI

10.1074/JBC.M304272200

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Consolidated OpenCitations Corpus – April 2017

1692113

1692113

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Consolidated OpenCitations Corpus – April 2017

Consolidated OpenCitations Corpus – April 2017

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