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Poly (ADP-ribose) in the pathogenesis of Parkinson's disease.

DC Field Value Language
dc.contributor.authorLee, Y-
dc.contributor.authorKang, HC-
dc.contributor.authorLee, BD-
dc.contributor.authorLee, YI-
dc.contributor.authorKim, YP-
dc.contributor.authorShin, JH-
dc.date.accessioned2015-11-15T23:32:57Z-
dc.date.available2015-11-15T23:32:57Z-
dc.date.issued2014-
dc.identifier.issn1976-6696-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/11969-
dc.description.abstractThe defining feature of Parkinson's disease is a progressive and selective demise of dopaminergic neurons. A recent report on Parkinson's disease animal model demonstrates that poly (ADP-ribose) (PAR) dependent cell death, also named parthanatos, is accountable for selective dopaminergic neuronal loss. Parthanatos is a programmed necrotic cell death, characterized by PARP1 activation, apoptosis inducing factor (AIF) nuclear translocation, and large scale DNA fragmentation. Besides cell death regulation via interaction with AIF, PAR molecule mediates diverse cellular processes including genomic stability, cell division, transcription, epigenetic regulation, and stress granule formation. In this review, we will discuss the roles of PARP1 activation and PAR molecules in the pathological processes of Parkinson's disease. Potential interaction between PAR molecule and Parkinson's disease protein interactome are briefly introduced. Finally, we suggest promising points of therapeutic intervention in the pathological PAR signaling cascade to halt progression in Parkinson's disease.-
dc.language.isoen-
dc.subject.MESHApoptosis-
dc.subject.MESHApoptosis Inducing Factor-
dc.subject.MESHDNA Fragmentation-
dc.subject.MESHDopaminergic Neurons-
dc.subject.MESHEnzyme Inhibitors-
dc.subject.MESHHumans-
dc.subject.MESHParkinson Disease-
dc.subject.MESHPoly Adenosine Diphosphate Ribose-
dc.subject.MESHPoly(ADP-ribose) Polymerases-
dc.titlePoly (ADP-ribose) in the pathogenesis of Parkinson's disease.-
dc.typeArticle-
dc.identifier.pmid24874851-
dc.identifier.urlhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4206713/-
dc.contributor.affiliatedAuthor강, 호철-
dc.type.localJournal Papers-
dc.citation.titleBMB reports-
dc.citation.volume47-
dc.citation.number8-
dc.citation.date2014-
dc.citation.startPage424-
dc.citation.endPage432-
dc.identifier.bibliographicCitationBMB reports, 47(8). : 424-432, 2014-
dc.identifier.eissn1976-670X-
dc.relation.journalidJ019766696-
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Physiology
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