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dc.contributor.author김동욱-
dc.date.accessioned2019-06-03T07:48:19Z-
dc.date.available2019-06-03T07:48:19Z-
dc.date.issued2007-01-
dc.identifier.citationNATURE IMMUNOLOGY, v. 8, No. 1, Page. 47-56en_US
dc.identifier.issn1529-2908-
dc.identifier.issn1529-2916-
dc.identifier.urihttps://www.nature.com/articles/ni1423-
dc.identifier.urihttp://repository.hanyang.ac.kr/handle/20.500.11754/106231-
dc.description.abstractPhosphorylation of histone H3 at Ser10 increases chromatin accessibility to transcription factor NF-kappa B on a subset of genes involved in immune responses. Here we report that a bacterial pathogen abrogated phosphorylation of histone H3 to 'shape' the transcriptional responses of infected host cells. We identify the Shigella flexneri protein effector OspF as a dually specific phosphatase that dephosphorylated mitogen-activated protein kinases in the nucleus, thus preventing histone H3 phosphorylation at Ser10 in a gene-specific way. That activity of OspF enabled shigella to block the activation of a subset of NF-kappa B-responsive genes, leading to compromised recruitment of polymorphonuclear leukocytes to infected tissues. S. flexneri has thus evolved the capacity to precisely modulate host cell epigenetic 'information' as a strategy for repressing innate immunity.en_US
dc.description.sponsorshipWe thank R. Weil and S. Memet for critical reading of the manuscript; J. Rohde, C. Rougeot, L. Touqui and A. Garcia for discussions; and B. Regnault and J. Bergounioux for technical assistance. The pGEX 2T plasmid containing human Erk2 was a gift from C. Marshall (Institute of Cancer Research); antibody to histone H3 methylated at Lys9 and phosphorylated at Ser10 was a gift from C. Muchardt (Institut Pasteur); and anti-p50 and anti-p65 were gifts from R. Weil (Institut Pasteur). Supported by the Howard Hughes Medical Institute (P.J.S.).en_US
dc.language.isoen_USen_US
dc.publisherNATURE PUBLISHING GROUPen_US
dc.subjectSHIGELLA-FLEXNERIen_US
dc.subjectMAP KINASEen_US
dc.subjectHISTONE H3en_US
dc.subjectEPITHELIAL-CELLSen_US
dc.subjectACTIVATIONen_US
dc.subjectEXPRESSIONen_US
dc.subjectPHOSPHOACETYLATIONen_US
dc.subjectPHOSPHORYLATIONen_US
dc.subjectRECRUITMENTen_US
dc.subjectSECRETIONen_US
dc.titleAn injected bacterial effector targets chromatin access for transcription factor NF-kappa B to alter transcription of host genes involved in immune responsesen_US
dc.typeArticleen_US
dc.relation.no1-
dc.relation.volume8-
dc.identifier.doi10.1038/ni1423-
dc.relation.page47-56-
dc.relation.journalNATURE IMMUNOLOGY-
dc.contributor.googleauthorArbibe, Laurence-
dc.contributor.googleauthorKim, Dong Wook-
dc.contributor.googleauthorBatsche, Eric-
dc.contributor.googleauthorPedron, Thierry-
dc.contributor.googleauthorMateescu, Bogdan-
dc.contributor.googleauthorMuchardt, Christian-
dc.contributor.googleauthorParsot, Claude-
dc.contributor.googleauthorSansonetti, Philippe J.-
dc.relation.code2007206937-
dc.sector.campusE-
dc.sector.daehakCOLLEGE OF PHARMACY[E]-
dc.sector.departmentDEPARTMENT OF PHARMACY-
dc.identifier.piddongwook-
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COLLEGE OF PHARMACY[E](약학대학) > PHARMACY(약학과) > Articles
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