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Article: A dominant function of IKK/NF-κB signaling in global lipopolysaccharide-induced gene expression

TitleA dominant function of IKK/NF-κB signaling in global lipopolysaccharide-induced gene expression
Authors
Issue Date2006
PublisherAmerican Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jbc.org/
Citation
Journal Of Biological Chemistry, 2006, v. 281 n. 41, p. 31142-31151 How to Cite?
AbstractPorphyromonas gingivalis is an etiologic pathogen of periodontitis that is one of the most common inflammatory diseases. Recently, we found that P. gingivalis LPS activated the transcription factor nuclear factor-κB (NF-κB) through the IκB kinase complex (IKK). NF-κB is a transcription factor that controls inflammation and host responses. In this study, we examined the role of IKK/NF-κB in P. gingivalis LPS-induced gene expression on a genome-wide basis using a combination of microarray and biochemical approaches. A total of 88 early response genes were found to be induced by P. gingivalis LPS in a human THP.1 monocytic cell lines. Interestingly, the induction of most of these genes was abolished or attenuated under the inactivation of IKK/NF-κB. Among those IKK/NF-κB-dependent genes, 20 genes were NF-κB-inducible genes reported previously, and 59 genes represented putative novel NF-κB target genes. Using transcription factor binding analysis, we found that most of these putative NF-κB target genes contained one or multiple NF-κB-binding sites. Also, some transcription factor-binding motifs were overrepresented in the promoter of both known and putative NF-κB-dependent genes, indicating that these genes may be regulated in a similar fashion. Furthermore, we found that several transcription factors associated with metabolic and inflammatory responses, including nuclear receptors, activator of protein-1, and early growth responses, were induced by P. gingivalis LPS through IKK/NF-κB, indicating that IKK/NF-κB may utilize these transcription factors to mediate secondary responses. Taken together, our results demonstrate that IKK/NF-κB signaling plays a dominant role in P. gingivalis LPS-induced early response gene expression, suggesting that IKK/NF-κB is a therapeutic target for periodontitis. © 2006 by The American Society for Biochemistry and Molecular Biology, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/154429
ISSN
2014 Impact Factor: 4.573
2014 SCImago Journal Rankings: 2.734
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCarayol, Nen_US
dc.contributor.authorChen, Jen_US
dc.contributor.authorYang, Fen_US
dc.contributor.authorJin, Ten_US
dc.contributor.authorJin, Len_US
dc.contributor.authorStates, Den_US
dc.contributor.authorWang, CYen_US
dc.date.accessioned2012-08-08T08:25:16Z-
dc.date.available2012-08-08T08:25:16Z-
dc.date.issued2006en_US
dc.identifier.citationJournal Of Biological Chemistry, 2006, v. 281 n. 41, p. 31142-31151en_US
dc.identifier.issn0021-9258en_US
dc.identifier.urihttp://hdl.handle.net/10722/154429-
dc.description.abstractPorphyromonas gingivalis is an etiologic pathogen of periodontitis that is one of the most common inflammatory diseases. Recently, we found that P. gingivalis LPS activated the transcription factor nuclear factor-κB (NF-κB) through the IκB kinase complex (IKK). NF-κB is a transcription factor that controls inflammation and host responses. In this study, we examined the role of IKK/NF-κB in P. gingivalis LPS-induced gene expression on a genome-wide basis using a combination of microarray and biochemical approaches. A total of 88 early response genes were found to be induced by P. gingivalis LPS in a human THP.1 monocytic cell lines. Interestingly, the induction of most of these genes was abolished or attenuated under the inactivation of IKK/NF-κB. Among those IKK/NF-κB-dependent genes, 20 genes were NF-κB-inducible genes reported previously, and 59 genes represented putative novel NF-κB target genes. Using transcription factor binding analysis, we found that most of these putative NF-κB target genes contained one or multiple NF-κB-binding sites. Also, some transcription factor-binding motifs were overrepresented in the promoter of both known and putative NF-κB-dependent genes, indicating that these genes may be regulated in a similar fashion. Furthermore, we found that several transcription factors associated with metabolic and inflammatory responses, including nuclear receptors, activator of protein-1, and early growth responses, were induced by P. gingivalis LPS through IKK/NF-κB, indicating that IKK/NF-κB may utilize these transcription factors to mediate secondary responses. Taken together, our results demonstrate that IKK/NF-κB signaling plays a dominant role in P. gingivalis LPS-induced early response gene expression, suggesting that IKK/NF-κB is a therapeutic target for periodontitis. © 2006 by The American Society for Biochemistry and Molecular Biology, Inc.en_US
dc.languageengen_US
dc.publisherAmerican Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jbc.org/en_US
dc.relation.ispartofJournal of Biological Chemistryen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBase Sequenceen_US
dc.subject.meshGene Expression Regulationen_US
dc.subject.meshGenes, Dominanten_US
dc.subject.meshHumansen_US
dc.subject.meshI-Kappa B Kinase - Metabolismen_US
dc.subject.meshLipopolysaccharides - Metabolismen_US
dc.subject.meshMiceen_US
dc.subject.meshMolecular Sequence Dataen_US
dc.subject.meshMonocytes - Microbiologyen_US
dc.subject.meshNf-Kappa B - Metabolismen_US
dc.subject.meshPorphyromonas Gingivalis - Metabolismen_US
dc.subject.meshSignal Transductionen_US
dc.titleA dominant function of IKK/NF-κB signaling in global lipopolysaccharide-induced gene expressionen_US
dc.typeArticleen_US
dc.identifier.emailJin, L:ljjin@hkucc.hku.hken_US
dc.identifier.authorityJin, L=rp00028en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1074/jbc.M603417200en_US
dc.identifier.pmid16914552en_US
dc.identifier.scopuseid_2-s2.0-33750043186en_US
dc.identifier.hkuros124070-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33750043186&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume281en_US
dc.identifier.issue41en_US
dc.identifier.spage31142en_US
dc.identifier.epage31151en_US
dc.identifier.isiWOS:000241075900089-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridCarayol, N=36009813700en_US
dc.identifier.scopusauthoridChen, J=49761227000en_US
dc.identifier.scopusauthoridYang, F=54379471900en_US
dc.identifier.scopusauthoridJin, T=8527982400en_US
dc.identifier.scopusauthoridJin, L=7403328850en_US
dc.identifier.scopusauthoridStates, D=35866621200en_US
dc.identifier.scopusauthoridWang, CY=49762557200en_US
dc.identifier.citeulike11369876-

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