DC Field | Value | Language |
---|---|---|
dc.contributor.author | Choi, BH | - |
dc.contributor.author | Hur, EM | - |
dc.contributor.author | Lee, JH | - |
dc.contributor.author | Jun, DJ | - |
dc.contributor.author | Kim, KT | - |
dc.date.accessioned | 2016-04-01T01:57:32Z | - |
dc.date.available | 2016-04-01T01:57:32Z | - |
dc.date.created | 2009-02-28 | - |
dc.date.issued | 2006-04-01 | - |
dc.identifier.issn | 0021-9533 | - |
dc.identifier.other | 2006-OAK-0000005846 | - |
dc.identifier.uri | https://oasis.postech.ac.kr/handle/2014.oak/24091 | - |
dc.description.abstract | Mitogen-activated protein kinase (MAPK) phosphatase-1 (MKP-1) is a dual-specificity phosphatase that is involved in the regulation of cell survival, differentiation and apoptosis through inactivating MAPKs by dephosphorylation. Here, we provide evidence for a role of MKP-1 in the glutamate-induced cell death of HT22 hippocampal cells and primary mouse cortical neurons. We suggest that, during glutamate-induced oxidative stress, protein kinase C (PKC) delta becomes activated and induces sustained activation of extracellular signal-regulated kinase 1/2 (ERK1/2) through a mechanism that involves degradation of MKP-1. Glutamate-induced activation of ERK1/2 was blocked by inhibition of PKC delta, confirming that ERK1/2 is regulated by PKC delta. Prolonged exposure to glutamate caused reduction in the protein level of MKP-1, which correlated with the sustained activation of ERK1/2. Furthermore, knockdown of endogenous MKP-1 by small interfering (si) RNA resulted in pronounced enhancement of ERK1/2 phosphorylation accompanied by increased cytotoxicity under glutamate exposure. In glutamate-treated cells, MKP-1 was polyubiquitylated and proteasome inhibitors markedly blocked the degradation of MKP-1. Moreover, inhibition of glutamate-induced PKC delta activation suppressed the downregulation and ubiquitylation of MKP-1. Taken together, these results demonstrate that activation of PKC delta triggers degradation of MKP-1 through the ubiquitin-proteasome pathway, thereby contributing to persistent activation of ERK1/2 under glutamate-induced oxidative toxicity. | - |
dc.description.statementofresponsibility | X | - |
dc.language | English | - |
dc.publisher | COMPANY OF BIOLOGISTS LTD | - |
dc.relation.isPartOf | JOURNAL OF CELL SCIENCE | - |
dc.subject | glutamate | - |
dc.subject | MKP-1 | - |
dc.subject | immature cortical neuron | - |
dc.subject | neuronal cell death | - |
dc.subject | ubiquitylation | - |
dc.subject | proteasomal degradation | - |
dc.subject | OXIDATIVE STRESS | - |
dc.subject | TYROSINE PHOSPHORYLATION | - |
dc.subject | PROTEOLYTIC ACTIVATION | - |
dc.subject | INDUCED APOPTOSIS | - |
dc.subject | DOPAMINERGIC DEGENERATION | - |
dc.subject | CONDITIONAL EXPRESSION | - |
dc.subject | CEREBRAL-ISCHEMIA | - |
dc.subject | INDUCTION | - |
dc.subject | RECEPTOR | - |
dc.subject | PATHWAY | - |
dc.title | Protein kinase C delta-mediated proteasomal degradation of MAP kinase phosphatase-1 contributes to glutamate-induced neuronal cell death | - |
dc.type | Article | - |
dc.contributor.college | 생명과학과 | - |
dc.identifier.doi | 10.1242/JCS.02837 | - |
dc.author.google | Choi, BH | - |
dc.author.google | Hur, EM | - |
dc.author.google | Lee, JH | - |
dc.author.google | Jun, DJ | - |
dc.author.google | Kim, KT | - |
dc.relation.volume | 119 | - |
dc.relation.issue | 7 | - |
dc.relation.startpage | 1329 | - |
dc.relation.lastpage | 1340 | - |
dc.contributor.id | 10104775 | - |
dc.relation.journal | JOURNAL OF CELL SCIENCE | - |
dc.relation.index | SCI급, SCOPUS 등재논문 | - |
dc.relation.sci | SCI | - |
dc.collections.name | Journal Papers | - |
dc.type.rims | ART | - |
dc.identifier.bibliographicCitation | JOURNAL OF CELL SCIENCE, v.119, no.7, pp.1329 - 1340 | - |
dc.identifier.wosid | 000236763900013 | - |
dc.date.tcdate | 2019-01-01 | - |
dc.citation.endPage | 1340 | - |
dc.citation.number | 7 | - |
dc.citation.startPage | 1329 | - |
dc.citation.title | JOURNAL OF CELL SCIENCE | - |
dc.citation.volume | 119 | - |
dc.contributor.affiliatedAuthor | Kim, KT | - |
dc.identifier.scopusid | 2-s2.0-33646765383 | - |
dc.description.journalClass | 1 | - |
dc.description.journalClass | 1 | - |
dc.description.wostc | 88 | - |
dc.description.scptc | 87 | * |
dc.date.scptcdate | 2018-05-121 | * |
dc.type.docType | Article | - |
dc.subject.keywordPlus | OXIDATIVE STRESS | - |
dc.subject.keywordPlus | TYROSINE PHOSPHORYLATION | - |
dc.subject.keywordPlus | PROTEOLYTIC ACTIVATION | - |
dc.subject.keywordPlus | INDUCED APOPTOSIS | - |
dc.subject.keywordPlus | DOPAMINERGIC DEGENERATION | - |
dc.subject.keywordPlus | CONDITIONAL EXPRESSION | - |
dc.subject.keywordPlus | CEREBRAL-ISCHEMIA | - |
dc.subject.keywordPlus | INDUCTION | - |
dc.subject.keywordPlus | RECEPTOR | - |
dc.subject.keywordPlus | PATHWAY | - |
dc.subject.keywordAuthor | glutamate | - |
dc.subject.keywordAuthor | MKP-1 | - |
dc.subject.keywordAuthor | immature cortical neuron | - |
dc.subject.keywordAuthor | neuronal cell death | - |
dc.subject.keywordAuthor | ubiquitylation | - |
dc.subject.keywordAuthor | proteasomal degradation | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Cell Biology | - |
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