Cited 61 times in
Signal Pathway of Hypoxia-Inducible Factor-1α Phosphorylation and its Interaction with von Hippel-Lindau Tumor Suppressor Protein During Ischemia in MiaPaCa-2 Pancreatic Cancer Cells
DC Field | Value | Language |
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dc.contributor.author | 송재진 | - |
dc.date.accessioned | 2015-08-26T16:43:00Z | - |
dc.date.available | 2015-08-26T16:43:00Z | - |
dc.date.issued | 2005 | - |
dc.identifier.issn | 1078-0432 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/114960 | - |
dc.description.abstract | PURPOSE AND EXPERIMENTAL DESIGN: Previously, we observed that the activation of p38 mitogen-activated protein kinase (MAPK) and c-Jun NH(2)-terminal kinase (JNK1) is mediated through the activation of apoptosis signal-regulating kinase 1 (ASK1) as a result of the reactive oxygen species-mediated dissociation of glutaredoxin and thioredoxin from ASK1. In this study, we examined whether p38 MAPK and JNK1 are involved in the accumulation of hypoxia-inducible factor-1alpha (HIF-1alpha) during ischemia. Human pancreatic cancer MiaPaCa-2 cells were exposed to low glucose (0.1 mmol/L) with hypoxia (0.1% O(2)). RESULTS AND CONCLUSIONS: During ischemia, p38 MAPK and JNK1 were activated in MiaPaCa-2 pancreatic cancer cells. The activated p38 MAPK, but not JNK1, phosphorylated HIF-1alpha. Data from in vivo binding assay of von Hippel-Lindau tumor suppressor protein with HIF-1alpha suggests that the p38-mediated phosphorylation of HIF-1alpha contributed to the inhibition of HIF-1alpha and von Hippel-Lindau tumor suppressor protein interaction during ischemia. SB203580, a specific inhibitor of p38 MAPK, inhibited HIF-1alpha accumulation during ischemia, probably resulting from the ubiquitination and degradation of HIF-1alpha. | - |
dc.description.statementOfResponsibility | open | - |
dc.format.extent | 7607~7613 | - |
dc.relation.isPartOf | CLINICAL CANCER RESEARCH | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.subject.MESH | Adenoviridae/genetics | - |
dc.subject.MESH | Apoptosis | - |
dc.subject.MESH | Blotting, Western | - |
dc.subject.MESH | Catalase/metabolism | - |
dc.subject.MESH | Cell Line, Tumor | - |
dc.subject.MESH | Dose-Response Relationship, Drug | - |
dc.subject.MESH | Electrophoresis, Polyacrylamide Gel | - |
dc.subject.MESH | Enzyme Activation | - |
dc.subject.MESH | Enzyme Inhibitors/pharmacology | - |
dc.subject.MESH | Glucose/metabolism | - |
dc.subject.MESH | Glutaredoxins | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | Hypoxia/metabolism | - |
dc.subject.MESH | Hypoxia-Inducible Factor 1, alpha Subunit/biosynthesis* | - |
dc.subject.MESH | Imidazoles/pharmacology | - |
dc.subject.MESH | Ischemia | - |
dc.subject.MESH | MAP Kinase Kinase Kinase 5/metabolism | - |
dc.subject.MESH | Mitogen-Activated Protein Kinase 8/metabolism | - |
dc.subject.MESH | Models, Biological | - |
dc.subject.MESH | Oxidoreductases/metabolism | - |
dc.subject.MESH | Pancreatic Neoplasms/metabolism* | - |
dc.subject.MESH | Phosphorylation | - |
dc.subject.MESH | Plasmids/metabolism | - |
dc.subject.MESH | Protein Binding | - |
dc.subject.MESH | Pyridines/pharmacology | - |
dc.subject.MESH | Reactive Oxygen Species | - |
dc.subject.MESH | Signal Transduction* | - |
dc.subject.MESH | Thioredoxins/metabolism | - |
dc.subject.MESH | Von Hippel-Lindau Tumor Suppressor Protein/metabolism | - |
dc.subject.MESH | p38 Mitogen-Activated Protein Kinases/metabolism | - |
dc.title | Signal Pathway of Hypoxia-Inducible Factor-1α Phosphorylation and its Interaction with von Hippel-Lindau Tumor Suppressor Protein During Ischemia in MiaPaCa-2 Pancreatic Cancer Cells | - |
dc.type | Article | - |
dc.contributor.college | Researcher Institutes (부설 연구소) | - |
dc.contributor.department | Institute for Cancer Research (암연구소) | - |
dc.contributor.googleauthor | Seok J. Kwon | - |
dc.contributor.googleauthor | Jae J. Song | - |
dc.contributor.googleauthor | Yong J. Lee | - |
dc.identifier.doi | 10.1158/1078-0432.CCR-05-0981 | - |
dc.admin.author | false | - |
dc.admin.mapping | false | - |
dc.contributor.localId | A02056 | - |
dc.relation.journalcode | J00564 | - |
dc.identifier.pmid | 16278378 | - |
dc.subject.keyword | 16278378 | - |
dc.contributor.alternativeName | Song, Jae Jin | - |
dc.contributor.affiliatedAuthor | Song, Jae Jin | - |
dc.rights.accessRights | free | - |
dc.citation.volume | 11 | - |
dc.citation.number | 21 | - |
dc.citation.startPage | 7607 | - |
dc.citation.endPage | 7613 | - |
dc.identifier.bibliographicCitation | CLINICAL CANCER RESEARCH, Vol.11(21) : 7607-7613, 2005 | - |
dc.identifier.rimsid | 39340 | - |
dc.type.rims | ART | - |
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