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p38 mitogen-activated protein kinase is a key regulator of 5-phenylselenyl- and 5-methylselenyl-methyl-2'-deoxyuridine-induced apoptosis in human HL-60 cells

DC FieldValueLanguage
dc.contributor.author김병모-
dc.date.accessioned2018-05-10T06:36:36Z-
dc.date.available2018-05-10T06:36:36Z-
dc.date.issued2012-
dc.identifier.issn0006-291X-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/158296-
dc.description.abstractTwo novel, modified thymidine nucleosides, 5-phenylselenyl-methyl-2'-deoxyuridine (PhSe-T) and 5-methylselenyl-methyl-2'-deoxyuridine (MeSe-T), trigger reactive oxygen species (ROS) generation and DNA damage and thereby induce caspase-mediated apoptosis in human HL-60 cells; however, the mechanism leading to caspase activation and apoptotic cell death remains unclear. Therefore, we investigated the signaling molecules involved in nucleoside derivative-induced caspase activation and apoptosis in HL-60 cells. PhSe-T/MeSe-T treatment activated two mitogen-activated protein kinases (MAPKs), extracellular-receptor kinase (ERK) and p38, and induced the phosphorylation of two downstream targets of p38, ATF-2 and MAPKAPK2. In addition, the selective p38 inhibitor SB203580 suppressed PhSe-T/MeSe-T-induced apoptosis and activation of caspase-3, -9, -8, and -2, whereas the jun amino-terminal kinase (JNK) inhibitor SP600125 and the ERK inhibitor PD98059 had no effect. SB203580 and an ROS scavenger, tiron, inhibited PhSe-T/MeSe-T-induced histone H2AX phosphorylation, which is a DNA damage marker. Moreover, tiron inhibited PhSe-T/MeSe-T-induced phosphorylation of p38 and enhanced p38 MAP kinase activity, indicating a role for ROS in PhSe-T/MeSe-T-induced p38 activation. Taken together, our results suggest that PhSe-T/MeSe-T-induced apoptosis is mediated by the p38 pathway and that p38 serves as a link between ROS generation and DNA damage/caspase activation in HL-60 cells.-
dc.description.statementOfResponsibilityrestriction-
dc.languageEnglish-
dc.publisherElsevier-
dc.relation.isPartOfBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rightshttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHApoptosis/drug effects*-
dc.subject.MESHCaspase 2/biosynthesis-
dc.subject.MESHCaspase 3/biosynthesis-
dc.subject.MESHCaspase 8/biosynthesis-
dc.subject.MESHDNA Damage-
dc.subject.MESHDeoxyuridine/analogs & derivatives*-
dc.subject.MESHDeoxyuridine/pharmacology-
dc.subject.MESHEnzyme Activation-
dc.subject.MESHEnzyme Inhibitors/pharmacology-
dc.subject.MESHFlavonoids/pharmacology-
dc.subject.MESHHL-60 Cells-
dc.subject.MESHHumans-
dc.subject.MESHImidazoles/pharmacology-
dc.subject.MESHOrganoselenium Compounds/pharmacology*-
dc.subject.MESHPoly(ADP-ribose) Polymerases/metabolism-
dc.subject.MESHPyridines/pharmacology-
dc.subject.MESHReactive Oxygen Species/metabolism-
dc.subject.MESHp38 Mitogen-Activated Protein Kinases/antagonists & inhibitors-
dc.subject.MESHp38 Mitogen-Activated Protein Kinases/metabolism*-
dc.titlep38 mitogen-activated protein kinase is a key regulator of 5-phenylselenyl- and 5-methylselenyl-methyl-2'-deoxyuridine-induced apoptosis in human HL-60 cells-
dc.typeArticle-
dc.contributor.collegeResearch Institutes-
dc.contributor.departmentYonsei Integrative Research Institute for Cerebral & Cardiovascular Disease-
dc.contributor.googleauthorByeong Mo Kim-
dc.contributor.googleauthorKee-Ho Lee-
dc.contributor.googleauthorIn Seok Hong-
dc.contributor.googleauthorSung Hee Hong-
dc.identifier.doi10.1016/j.bbrc.2011.11.092-
dc.contributor.localIdA00497-
dc.relation.journalcodeJ00281-
dc.identifier.eissn1090-2104-
dc.identifier.pmid22142847-
dc.identifier.urlhttps://www.sciencedirect.com/science/article/pii/S0006291X11021139-
dc.contributor.alternativeNameKim, Byeong Mo-
dc.contributor.affiliatedAuthorKim, Byeong Mo-
dc.citation.volume417-
dc.citation.number1-
dc.citation.startPage237-
dc.citation.endPage244-
dc.identifier.bibliographicCitationBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, Vol.417(1) : 237-244, 2012-
Appears in Collections:
5. Research Institutes (연구소) > Yonsei Integrative Research Institute for Cerebral & Cardiovascular Disease (뇌심혈관질환융합연구사업단) > 1. Journal Papers

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