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Cited 10 times in

Apoptosis signal-regulating kinase-1 aggravates ROS-mediated striatal

DC Field Value Language
dc.contributor.author김경환-
dc.contributor.author김현우-
dc.contributor.author이종은-
dc.contributor.author전소영-
dc.contributor.author조경주-
dc.date.accessioned2014-12-18T09:36:30Z-
dc.date.available2014-12-18T09:36:30Z-
dc.date.issued2013-
dc.identifier.issn0006-291X-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/88490-
dc.description.abstractApoptosis signal-regulating kinase-1 (ASK1), an early signaling element in the cell death pathway, has been suggested to participate in the pathology of neurodegenerative diseases, which may be associated with environmental factors that impact the diseases. Although it is not entirely elucidated, 3-nitropropionic acid (3-NP) provokes mitochondrial dysfunction and selectively forms striatal lesions similar to those found in Huntington’s disease. The current study investigated whether ASK1 is involved in striatal pathology following chronic systemic infusion of 3-NP. The results show that ASK1 acts as a primary mediator of there active oxygen species (ROS) cell death signal cascade in the 3-NP-damaged striatal region by disrupting the positive feedback cycle. In 3-NP-infused striatal lesions, ROS increased ASK1. Superoxide dismutase transgenic (SOD-tg) mice reduced ASK1by scavenging ROS, and reduction of ASK1leads to a reduction in cell death. However, ASK1 down-regulation in 3-NP infusion mice also decreased striatal cell death without scavenging ROS. In contrast decreasing cell death by si-ASK1 treatment along with 3-NP in both SOD tg and wild-type mice (wt), cell death rebounded when ASK1 peptide was added to SOD tg mice. The present study suggests that ROS-inducing ASK1 may be an important step in the pathogenesis of 3-NP infused striatal lesions in murine brains.-
dc.description.statementOfResponsibilityopen-
dc.relation.isPartOfBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleApoptosis signal-regulating kinase-1 aggravates ROS-mediated striatal-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Anatomy (해부학)-
dc.contributor.googleauthorKyoung Joo Cho-
dc.contributor.googleauthorHyun Woo Kim-
dc.contributor.googleauthorSo Yeong Cheon-
dc.contributor.googleauthorJong Eun Lee-
dc.contributor.googleauthorGyung Whan Kim-
dc.identifier.doi10.1016/j.bbrc.2013.08.103-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00310-
dc.contributor.localIdA03522-
dc.contributor.localIdA03804-
dc.contributor.localIdA03146-
dc.contributor.localIdA01125-
dc.relation.journalcodeJ00281-
dc.identifier.eissn1090-2104-
dc.identifier.pmidApoptosis signal-regulating kinase 1 ; 3-Nitropropionic acid ; siRNA ; Superoxide dismutase-
dc.identifier.urlhttp://www.sciencedirect.com/science/article/pii/S0006291X13014769-
dc.subject.keywordApoptosis signal-regulating kinase 1-
dc.subject.keyword3-Nitropropionic acid-
dc.subject.keywordsiRNA-
dc.subject.keywordSuperoxide dismutase-
dc.contributor.alternativeNameKim, Gyung Whan-
dc.contributor.alternativeNameKim, Hyun Woo-
dc.contributor.alternativeNameLee, Jong Eun-
dc.contributor.alternativeNameCheon, So Yeong-
dc.contributor.alternativeNameCho, Kyuong Joo-
dc.contributor.affiliatedAuthorKim, Gyung Whan-
dc.contributor.affiliatedAuthorCheon, So Yeong-
dc.contributor.affiliatedAuthorCho, Kyuong Joo-
dc.contributor.affiliatedAuthorLee, Jong Eun-
dc.contributor.affiliatedAuthorKim, Hyun Woo-
dc.rights.accessRightsnot free-
dc.citation.volume441-
dc.citation.number2-
dc.citation.startPage280-
dc.citation.endPage285-
dc.identifier.bibliographicCitationBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, Vol.441(2) : 280-285, 2013-
dc.identifier.rimsid34061-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Research Institute (부설연구소) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Anatomy (해부학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Neurology (신경과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers

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