Phosphoproteomic analysis of neuronal cell death by glutamate-induced oxidative stress = 글루타메이트유도 산화적 스트레스에 의한 신경세포의 인산화 단백질체 연구

Cited 32 time in scopus
Metadata Downloads

Full metadata record

DC FieldValueLanguage
dc.contributor.authorT H Kang-
dc.contributor.authorKwang-Hee Bae-
dc.contributor.authorM J Yoo-
dc.contributor.authorWon Kon-Kim-
dc.contributor.authorH R Hwang-
dc.contributor.authorHye-Yun Jung-
dc.contributor.authorPhil Young Lee-
dc.contributor.authorSunghyun Kang-
dc.contributor.authorTae-Sung Yoon-
dc.contributor.authorSung Goo Park-
dc.contributor.authorSeong Eon Ryu-
dc.contributor.authorSang Chul Lee-
dc.date.accessioned2017-04-19T09:07:42Z-
dc.date.available2017-04-19T09:07:42Z-
dc.date.issued2007-
dc.identifier.issn16159853-
dc.identifier.uri10.1002/pmic.200601028ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/7990-
dc.description.abstractOxidative stress is one of the major causes of neuronal cell death in disorders such as perinatal hypoxia and ischemia. Protein phosphorylation is the most significant PTM of proteins and plays an important role in stress-induced signal transduction. Thus, the analysis of alternative protein phosphorylation states which occur during oxidative stress-induced cell death could provide valuable information regarding cell death. In this study, a reference phosphoproteome map of the mouse hippocampal cell line HT22 was constructed based on 125 spots that were identified by MALDI-TOF or LC-ESI-Q-TOF-MS analysis. In addition, proteins of HT22 cells at various stages of oxidative stress-induced cell death were separated by 2-DE and alterations in phosphoproteins were detected by Pro-Q Diamond staining. A total of 17 spots showing significant quantitative changes and seven newly appearing spots were identified after glutamate treatment. Splicing factor 2, peroxiredoxin 2, S100 calcium binding protein A11, and purine nucleoside phosphorylase were identified as up- or down-regulated proteins. CDC25A, caspase-8, and cyp51 protein appeared during oxidative stress-induced cell death. The data in this study from phosphoproteomic analysis provide a valuable resource for the understanding of HT22 cell death mechanisms mediated by oxidative stress.-
dc.publisherWiley-
dc.titlePhosphoproteomic analysis of neuronal cell death by glutamate-induced oxidative stress = 글루타메이트유도 산화적 스트레스에 의한 신경세포의 인산화 단백질체 연구-
dc.title.alternativePhosphoproteomic analysis of neuronal cell death by glutamate-induced oxidative stress-
dc.typeArticle-
dc.citation.titleProteomics-
dc.citation.number15-
dc.citation.endPage2635-
dc.citation.startPage2624-
dc.citation.volume7-
dc.contributor.affiliatedAuthorKwang-Hee Bae-
dc.contributor.affiliatedAuthorWon Kon-Kim-
dc.contributor.affiliatedAuthorSunghyun Kang-
dc.contributor.affiliatedAuthorTae-Sung Yoon-
dc.contributor.affiliatedAuthorSung Goo Park-
dc.contributor.affiliatedAuthorSang Chul Lee-
dc.contributor.alternativeName강태혁-
dc.contributor.alternativeName배광희-
dc.contributor.alternativeName유민정-
dc.contributor.alternativeName김원곤-
dc.contributor.alternativeName황향란-
dc.contributor.alternativeName정혜윤-
dc.contributor.alternativeName이필영-
dc.contributor.alternativeName강성현-
dc.contributor.alternativeName윤태성-
dc.contributor.alternativeName박성구-
dc.contributor.alternativeName류성언-
dc.contributor.alternativeName이상철-
dc.identifier.bibliographicCitationProteomics, vol. 7, no. 15, pp. 2624-2635-
dc.identifier.doi10.1002/pmic.200601028-
dc.subject.keywordApoptosis-
dc.subject.keywordHT22-
dc.subject.keywordOxidative stress-
dc.subject.keywordPhosphoproteome-
dc.subject.keywordROS-
dc.subject.localApoptosis-
dc.subject.localHT22-
dc.subject.localOxidative stress-
dc.subject.localPhosphoproteome-
dc.subject.localROS-
dc.description.journalClassY-
Appears in Collections:
Division of Biomedical Research > Metabolic Regulation Research Center > 1. Journal Articles
Division of Biomedical Research > Disease Target Structure Research Center > 1. Journal Articles
Files in This Item:
  • There are no files associated with this item.


Items in OpenAccess@KRIBB are protected by copyright, with all rights reserved, unless otherwise indicated.