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Article: DJ-1 protects the nigrostriatal axis from the neurotoxin MPTP by modulation of the AKT pathway

TitleDJ-1 protects the nigrostriatal axis from the neurotoxin MPTP by modulation of the AKT pathway
Authors
KeywordsNeurodegeneration
Parkinson disease
Reactive oxygen species
Issue Date2010
Citation
Proceedings of the National Academy of Sciences of the United States of America, 2010, v. 107, n. 7, p. 3186-3191 How to Cite?
AbstractLoss-of-function DJ-1 (PARK7) mutations have been linked with a familial form of early onset Parkinson disease. Numerous studies have supported the role of DJ-1 in neuronal survival and function. Our initial studies using DJ-1-deficient neurons indicated that DJ-1 specifically protects the neurons against the damage induced by oxidative injury in multiple neuronal types and degenerative experimental paradigms, both in vitro and in vivo. However, the manner by which oxidative stress-induced death is ameliorated by DJ-1 is not completely clear. We now present data that show the involvement of DJ-1 in modulation of AKT, a major neuronal prosurvival pathway induced upon oxidative stress. We provide evidence that DJ-1 promotes AKT phosphorylation in response to oxidative stress induced by H2O2 in vitro and in vivo following 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment. Moreover,weshow that DJ-1 is necessary for normal AKT-mediated protective effects, which can be bypassed by expression of a constitutively active form of AKT. Taken together, these data suggest that DJ-1 is crucial for full activation of AKT upon oxidative injury, which serves as one explanation for the protective effects of DJ-1.
Persistent Identifierhttp://hdl.handle.net/10722/291946
ISSN
2023 Impact Factor: 9.4
2023 SCImago Journal Rankings: 3.737
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorAleyasin, Hossein-
dc.contributor.authorRousseaux, Maxime W.C.-
dc.contributor.authorMarcogliese, Paul C.-
dc.contributor.authorHewitt, Sarah J.-
dc.contributor.authorIrrcher, Isabella-
dc.contributor.authorJoselin, Alvin P.-
dc.contributor.authorParsanejad, Mohammad-
dc.contributor.authorKim, Raymond H.-
dc.contributor.authorRizzu, Patrizia-
dc.contributor.authorCallaghan, Steve M.-
dc.contributor.authorSlacka, Ruth S.-
dc.contributor.authorMak, Tak W.-
dc.contributor.authorPark, David S.-
dc.date.accessioned2020-11-17T14:55:26Z-
dc.date.available2020-11-17T14:55:26Z-
dc.date.issued2010-
dc.identifier.citationProceedings of the National Academy of Sciences of the United States of America, 2010, v. 107, n. 7, p. 3186-3191-
dc.identifier.issn0027-8424-
dc.identifier.urihttp://hdl.handle.net/10722/291946-
dc.description.abstractLoss-of-function DJ-1 (PARK7) mutations have been linked with a familial form of early onset Parkinson disease. Numerous studies have supported the role of DJ-1 in neuronal survival and function. Our initial studies using DJ-1-deficient neurons indicated that DJ-1 specifically protects the neurons against the damage induced by oxidative injury in multiple neuronal types and degenerative experimental paradigms, both in vitro and in vivo. However, the manner by which oxidative stress-induced death is ameliorated by DJ-1 is not completely clear. We now present data that show the involvement of DJ-1 in modulation of AKT, a major neuronal prosurvival pathway induced upon oxidative stress. We provide evidence that DJ-1 promotes AKT phosphorylation in response to oxidative stress induced by H2O2 in vitro and in vivo following 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment. Moreover,weshow that DJ-1 is necessary for normal AKT-mediated protective effects, which can be bypassed by expression of a constitutively active form of AKT. Taken together, these data suggest that DJ-1 is crucial for full activation of AKT upon oxidative injury, which serves as one explanation for the protective effects of DJ-1.-
dc.languageeng-
dc.relation.ispartofProceedings of the National Academy of Sciences of the United States of America-
dc.subjectNeurodegeneration-
dc.subjectParkinson disease-
dc.subjectReactive oxygen species-
dc.titleDJ-1 protects the nigrostriatal axis from the neurotoxin MPTP by modulation of the AKT pathway-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1073/pnas.0914876107-
dc.identifier.pmid20133695-
dc.identifier.pmcidPMC2840364-
dc.identifier.scopuseid_2-s2.0-77649266193-
dc.identifier.volume107-
dc.identifier.issue7-
dc.identifier.spage3186-
dc.identifier.epage3191-
dc.identifier.eissn1091-6490-
dc.identifier.isiWOS:000274599500086-
dc.identifier.f10001927965-
dc.identifier.issnl0027-8424-

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