About: Mitochondrial dysfunction and oxidative damage in parkin-deficient mice

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scientific journal article

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rdf:type	Item
description	artículu científicu espublizáu en 2004 (ast) vědecký článek publikovaný v roce 2004 (cs) 2004 թվականի ապրիլին հրատարակված գիտական հոդված (hy) 2004 թուականի Ապրիլին հրատարակուած գիտական յօդուած (hyw) наукова стаття, опублікована у квітні 2004 (uk) vedecký článok (publikovaný 2004/04/30) (sk) مقالة علمية (نشرت في 30-4-2004) (ar) wetenschappelijk artikel (gepubliceerd op 2004/04/30) (nl) article publié dans la revue scientifique Journal of Biological Chemistry (fr) im April 2004 veröffentlichter wissenschaftlicher Artikel (de) scientific journal article (en)
publication date	wds:Q28593859-4CD38AF9-D474-4475-99B5-13021CA1CA06
publication date	2004-04-30 00:00:00Z (xsd:dateTime)
language of work or name	wds:Q28593859-9F6015E0-100D-4622-90E6-A71854AFB93F
language of work or name	English
cites work	wds:Q28593859-71480C31-07C8-4F91-8E33-C8600E56B12C
cites work	Mutations in the parkin gene cause autosomal recessive juvenile parkinsonism
author name string	wds:Q28593859-0881D916-DAD4-4A1A-91DF-753E525F045C wds:Q28593859-1B76B180-82FA-4A90-936E-A008A74D9434 wds:Q28593859-4E4BCA09-6667-4195-957A-5121564352B7 wds:Q28593859-4F34F9C9-6C3D-4079-83B6-6A6D4C002B3C wds:Q28593859-76AE8617-9BC5-48F3-B1CF-A47C46F56566 wds:Q28593859-816DD512-B90E-44A0-842E-1D5F107497A6 wds:Q28593859-9A0C0E0D-49CD-4F30-948D-5DF85C89833B wds:Q28593859-DE684C7A-6F64-4992-9D42-8930FE682526
OpenCitations bibliographic resource ID	wds:Q28593859-1125B434-711D-4D64-B79E-68DE79A51425
OpenCitations bibliographic resource ID	https://w3id.org/oc/corpus/br/1265967
author name string	Jie Shen Stefan Krauss Joachim Klose Matthew S. Goldberg Dijana Sagi Maik Wacker Claudia Motz James J. Palacino
OpenCitations bibliographic resource ID	1265967
rdfs:label	Mitochondrial dysfunction and oxidative damage in parkin-deficient mice (en) Mitochondrial dysfunction and oxidative damage in parkin-deficient mice (nl) Mitochondrial dysfunction and oxidative damage in parkin-deficient mice (ast)
skos:prefLabel	Mitochondrial dysfunction and oxidative damage in parkin-deficient mice (en) Mitochondrial dysfunction and oxidative damage in parkin-deficient mice (nl) Mitochondrial dysfunction and oxidative damage in parkin-deficient mice (ast)
name	Mitochondrial dysfunction and oxidative damage in parkin-deficient mice (en) Mitochondrial dysfunction and oxidative damage in parkin-deficient mice (nl) Mitochondrial dysfunction and oxidative damage in parkin-deficient mice (ast)
title	wds:Q28593859-57457AFE-53D8-4C9A-BC5D-1C0571BEF480
title	Mitochondrial dysfunction and oxidative damage in parkin-deficient mice (en)
page(s)	wds:Q28593859-F9E1ABBF-D8A7-4C48-9BEE-68C1BD9F8993
page(s)	18614–18622
instance of	wds:Q28593859-168E7C63-BBBD-4043-B6AB-D6011A10DED3
instance of	scholarly article
main subject	wds:Q28593859-C38DCD17-B21C-47BC-B87F-9309388BC5F8 wds:Q28593859-F033681A-C614-4EC1-820C-01A3833C20E9
main subject	mitochondrion Parkin RBR E3 ubiquitin protein ligase
PubMed ID	wds:Q28593859-97DCDF30-7305-4106-8598-21AACE0F85C7
PubMed ID	http://rdf.ncbi.nlm.nih.gov/pubchem/reference/14985362
PubMed ID	14985362
published in	wds:Q28593859-B314A3D0-822D-4E5A-89DA-29D3F1C7A77E
published in	Journal of Biological Chemistry
issue	wds:Q28593859-2DF77732-6D6F-48CA-A5F7-51A0E728192E
volume	wds:Q28593859-B193B371-99E6-45BC-ACC6-5E8CBA85CECF
issue	18
volume	279
DOI	wds:Q28593859-37424F47-9E37-4C4E-82E5-7AA5B843A299
DOI	http://dx.doi.org/10.1074/JBC.M401135200
DOI	10.1074/JBC.M401135200
ResearchGate publication ID	wds:Q28593859-0285F332-AAE5-44FD-9FAD-2E5DB6B300BC
ResearchGate publication ID	8684140
is about of	https://www.wikidata.org/wiki/Special:EntityData/Q28593859
is cites work of	The role of oxidative stress in Parkinson's disease Parkin interacts with Ambra1 to induce mitophagy Parkin, PINK1, and DJ-1 form a ubiquitin E3 ligase complex promoting unfolded protein degradation Inactivation of Pink1 gene in vivo sensitizes dopamine-producing neurons to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and can be rescued by autosomal recessive Parkinson disease genes, Parkin or DJ-1 Structure and Function of Parkin, PINK1, and DJ-1, the Three Musketeers of Neuroprotection Molecular pathogenesis of Parkinson disease: insights from genetic studies Genetic animal models of Parkinson's disease Oxidative stress in genetic mouse models of Parkinson's disease Genetic mouse models of Parkinson's disease The state of the art. Modelling of Parkinson's disease in mice Convergent mechanisms in etiologically-diverse dystonias Mitochondrial dynamics and Parkinson's disease: focus on parkin C6ORF66 is an assembly factor of mitochondrial complex I Parkin protects against mitochondrial toxins and beta-amyloid accumulation in skeletal muscle cells. PARK2 deletions occur frequently in sporadic colorectal cancer and accelerate adenoma development in Apc mutant mice. Common chromosomal fragile site FRA16D tumor suppressor WWOX gene expression and metabolic reprograming in cells. Value of genetic models in understanding the cause and mechanisms of Parkinson's disease Biochemical aspects of the neuroprotective mechanism of PTEN-induced kinase-1 (PINK1) The parkin protein as a therapeutic target in Parkinson's disease Genetic clues to the pathogenesis of Parkinson's disease The role of free radicals in the aging brain and Parkinson's Disease: convergence and parallelism Parkinson's disease: animal models and dopaminergic cell vulnerability Mitochondrial biology and oxidative stress in Parkinson disease pathogenesis Dopamine quinone modifies and decreases the abundance of the mitochondrial selenoprotein glutathione peroxidase 4. Pathways to Parkinsonism Redux: convergent pathobiological mechanisms in genetics of Parkinson's disease Parkinson's disease mouse models in translational research The parkin mutant phenotype in the fly is largely rescued by metal-responsive transcription factor (MTF-1) Parkin is an E3 ubiquitin-ligase for normal and mutant ataxin-2 and prevents ataxin-2-induced cell death Parkin-dependent degradation of the F-box protein Fbw7β promotes neuronal survival in response to oxidative stress by stabilizing Mcl-1

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