Cited 113 times in
Zn2+-induced ERK activation mediated by reactive oxygen species causes cell death in differentiated PC12 cells
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 서정택 | - |
dc.date.accessioned | 2018-11-01T16:40:01Z | - |
dc.date.available | 2018-11-01T16:40:01Z | - |
dc.date.issued | 2001 | - |
dc.identifier.issn | 0022-3042 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/164961 | - |
dc.description.abstract | Recent studies have provided evidence that Zn2+ plays a crucial role in ischemia- and seizure-induced neuronal death. However, the intracellular signaling pathways involved in Zn2+-induced cell death are largely unknown. In the present study, we investigated the roles of mitogen-activated protein kinases (MAPKs), such as c-Jun N-terminal kinase (JNK), p38 MAPK and extracellular signal-regulated kinase (ERK), and of reactive oxygen species (ROS) in Zn2+-induced cell death using differentiated PC12 cells. Intracellular accumulation of Zn2+ induced by the combined application of pyrithione (5 microM), a Zn2+ ionophore, and Zn2+ (10 microM) caused cell death and activated JNK and ERK, but not p38 MAPK. Preventing JNK activation by the expression of dominant negative SEK1 (SEKAL) did not attenuate Zn2+-induced cell death, whereas the inhibition of ERK with PD98059 and the expression of dominant negative Ras mutant (RasN17) significantly prevented cell death. Inhibition of protein kinase C (PKC) and phosphatidylinositol-3 kinase had little effect on Zn2+-induced ERK activation. Intracellular Zn2+ accumulation resulted in the generation of ROS, and antioxidants prevented both the ERK activation and the cell death induced by Zn2+. Therefore, we conclude that although Zn2+ activates JNK and ERK, only ERK contributes to Zn2+-induced cell death, and that ERK activation is mediated by ROS via the Ras/Raf/MEK/ERK signaling pathway. | - |
dc.description.statementOfResponsibility | restriction | - |
dc.language | English | - |
dc.publisher | Wiley | - |
dc.relation.isPartOf | JOURNAL OF NEUROCHEMISTRY | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.subject.MESH | Animals | - |
dc.subject.MESH | Antifungal Agents/pharmacology | - |
dc.subject.MESH | Antioxidants/pharmacology | - |
dc.subject.MESH | Apoptosis/drug effects* | - |
dc.subject.MESH | Enzyme Activation | - |
dc.subject.MESH | Enzyme Inhibitors/pharmacology | - |
dc.subject.MESH | Flavonoids/pharmacology | - |
dc.subject.MESH | Immunoblotting | - |
dc.subject.MESH | Indoles/pharmacology | - |
dc.subject.MESH | JNK Mitogen-Activated Protein Kinases | - |
dc.subject.MESH | MAP Kinase Signaling System/physiology | - |
dc.subject.MESH | Maleimides/pharmacology | - |
dc.subject.MESH | Microscopy, Fluorescence | - |
dc.subject.MESH | Mitogen-Activated Protein Kinases/metabolism* | - |
dc.subject.MESH | Neurons/cytology* | - |
dc.subject.MESH | Neurons/drug effects | - |
dc.subject.MESH | Neurons/metabolism PC12 Cells | - |
dc.subject.MESH | Phosphatidylinositol 3-Kinases/antagonists & inhibitors | - |
dc.subject.MESH | Phosphatidylinositol 3-Kinases/metabolism | - |
dc.subject.MESH | Protein Kinase C/antagonists & inhibitors | - |
dc.subject.MESH | Protein Kinase C/metabolism | - |
dc.subject.MESH | Pyridines/pharmacology | - |
dc.subject.MESH | Rats | - |
dc.subject.MESH | Reactive Oxygen Species/metabolism* | - |
dc.subject.MESH | Thiones | - |
dc.subject.MESH | Time Factors | - |
dc.subject.MESH | Transfection | - |
dc.subject.MESH | Zinc/pharmacology* | - |
dc.subject.MESH | p38 Mitogen-Activated Protein Kinases | - |
dc.subject.MESH | ras Proteins/metabolism | - |
dc.title | Zn2+-induced ERK activation mediated by reactive oxygen species causes cell death in differentiated PC12 cells | - |
dc.type | Article | - |
dc.contributor.college | College of Dentistry (치과대학) | - |
dc.contributor.department | Dept. of Oral Biology (구강생물학교실) | - |
dc.contributor.googleauthor | Su Ryeon Seo | - |
dc.contributor.googleauthor | Seon Ah Chong | - |
dc.contributor.googleauthor | Syng‐Ill Lee | - |
dc.contributor.googleauthor | Jee Young Sung | - |
dc.contributor.googleauthor | Young Soo Ahn | - |
dc.contributor.googleauthor | Kwang Chul Chung | - |
dc.contributor.googleauthor | Jeong Taeg Seo | - |
dc.identifier.doi | 10.1046/j.1471-4159.2001.00438.x | - |
dc.contributor.localId | A01905 | - |
dc.relation.journalcode | J01620 | - |
dc.identifier.eissn | 1471-4159 | - |
dc.identifier.pmid | 11483663 | - |
dc.identifier.url | https://onlinelibrary.wiley.com/doi/abs/10.1046/j.1471-4159.2001.00438.x | - |
dc.contributor.alternativeName | Seo, Jeong Taeg | - |
dc.contributor.affiliatedAuthor | 서정택 | - |
dc.citation.volume | 78 | - |
dc.citation.number | 3 | - |
dc.citation.startPage | 600 | - |
dc.citation.endPage | 610 | - |
dc.identifier.bibliographicCitation | JOURNAL OF NEUROCHEMISTRY, Vol.78(3) : 600-610, 2001 | - |
dc.identifier.rimsid | 58284 | - |
dc.type.rims | ART | - |
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