{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1361137045801674752.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1128/iai.74.3.1452-1461.2006"}},{"identifier":{"@type":"URI","@value":"https://journals.asm.org/doi/pdf/10.1128/IAI.74.3.1452-1461.2006"}},{"identifier":{"@type":"PMID","@value":"16495515"}}],"dc:title":[{"@value":"<i>Helicobacter pylori</i>Induces IκB Kinase α Nuclear Translocation and Chemokine Production in Gastric Epithelial Cells"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:title>ABSTRACT</jats:title><jats:p>NF-κB is an important transcriptional factor that is involved in multiple cellular responses, such as inflammation and antiapoptosis. IκB kinase α (IKKα) and IKKβ, which are critical regulators of NF-κB activity, possess various mechanisms for NF-κB activation. This variability in NF-κB signaling may be associated with distinct inflammatory responses in specific cell types. The gastric pathogen<jats:italic>Helicobacter pylori</jats:italic>is known to activate NF-κB. However, the role of IKK in<jats:italic>H. pylori</jats:italic>infection remains unclear. In this report, we show that<jats:italic>H. pylori</jats:italic>activates both IKKα and IKKβ in gastric cancer cells and enhances NF-κB signaling in distinct manners. We found that IKKβ acted as an IκBα kinase during<jats:italic>H. pylori</jats:italic>infection, whereas IKKα did not.<jats:italic>H. pylori</jats:italic>induced IKKα nuclear translocation in time-, multiplicity of infection-, and<jats:italic>cag</jats:italic>pathogenicity island-dependent manners. In contrast, p100 processing, which is a known IKKα activity induced by several cytokines, was not induced by<jats:italic>H. pylori</jats:italic>. Both IKKs were responsible for chemokine secretion by infected cells. However, the antiapoptotic effect of<jats:italic>H. pylori</jats:italic>was merely transduced by IKKβ. Microarray analysis and real-time PCR indicated that both IKKs were involved in the transcriptional activation of genes associated with inflammation, antiapoptosis, and signal transduction. Our results indicate that<jats:italic>H. pylori</jats:italic>activates NF-κB via both IKKα and IKKβ using distinct mechanisms. IKKα nuclear translocation induced by<jats:italic>H. pylori</jats:italic>is indispensable for appropriate inflammatory responses but not for antiapoptosis, which suggests a critical role for IKKα in gastritis development.</jats:p>"}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1381137045801674759","@type":"Researcher","foaf:name":[{"@value":"Yoshihiro Hirata"}],"jpcoar:affiliationName":[{"@value":"Department of Gastroenterology, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1381137045801674754","@type":"Researcher","foaf:name":[{"@value":"Shin Maeda"}],"jpcoar:affiliationName":[{"@value":"Department of Gastroenterology, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1381137045801674755","@type":"Researcher","foaf:name":[{"@value":"Tomoya Ohmae"}],"jpcoar:affiliationName":[{"@value":"Department of Gastroenterology, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1381137045801674760","@type":"Researcher","foaf:name":[{"@value":"Wataru Shibata"}],"jpcoar:affiliationName":[{"@value":"Department of Gastroenterology, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1381137045801674758","@type":"Researcher","foaf:name":[{"@value":"Ayako Yanai"}],"jpcoar:affiliationName":[{"@value":"Department of Gastroenterology, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1381137045801674757","@type":"Researcher","foaf:name":[{"@value":"Keiji Ogura"}],"jpcoar:affiliationName":[{"@value":"Department of Gastroenterology, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1381137045801674752","@type":"Researcher","foaf:name":[{"@value":"Haruhiko Yoshida"}],"jpcoar:affiliationName":[{"@value":"Department of Gastroenterology, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1381137045801674753","@type":"Researcher","foaf:name":[{"@value":"Takao Kawabe"}],"jpcoar:affiliationName":[{"@value":"Department of Gastroenterology, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1381137045801674756","@type":"Researcher","foaf:name":[{"@value":"Masao Omata"}],"jpcoar:affiliationName":[{"@value":"Department of Gastroenterology, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan"}]}],"publication":{"publicationIdentifier":[{"@type":"PISSN","@value":"00199567"},{"@type":"EISSN","@value":"10985522"}],"prism:publicationName":[{"@value":"Infection and Immunity"}],"dc:publisher":[{"@value":"American Society for Microbiology"}],"prism:publicationDate":"2006-03","prism:volume":"74","prism:number":"3","prism:startingPage":"1452","prism:endingPage":"1461"},"reviewed":"false","dcterms:accessRights":"http://purl.org/coar/access_right/c_abf2","dc:rights":["https://journals.asm.org/non-commercial-tdm-license"],"url":[{"@id":"https://journals.asm.org/doi/pdf/10.1128/IAI.74.3.1452-1461.2006"}],"createdAt":"2006-02-23","modifiedAt":"2023-05-06","foaf:topic":[{"@id":"https://cir.nii.ac.jp/all?q=Helicobacter%20pylori","dc:title":"Helicobacter pylori"},{"@id":"https://cir.nii.ac.jp/all?q=Stomach","dc:title":"Stomach"},{"@id":"https://cir.nii.ac.jp/all?q=Humans","dc:title":"Humans"},{"@id":"https://cir.nii.ac.jp/all?q=Epithelial%20Cells","dc:title":"Epithelial Cells"},{"@id":"https://cir.nii.ac.jp/all?q=Chemokines","dc:title":"Chemokines"},{"@id":"https://cir.nii.ac.jp/all?q=Microarray%20Analysis","dc:title":"Microarray Analysis"},{"@id":"https://cir.nii.ac.jp/all?q=Helicobacter%20Infections","dc:title":"Helicobacter Infections"},{"@id":"https://cir.nii.ac.jp/all?q=I-kappa%20B%20Kinase","dc:title":"I-kappa B Kinase"}],"relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1360285710950772352","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Role of Interleukin-32 in Helicobacter pylori-Induced Gastric Inflammation"}]},{"@id":"https://cir.nii.ac.jp/crid/1360285710951007872","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Differential Roles of ASK1 and TAK1 in Helicobacter pylori-Induced Cellular Responses"}]},{"@id":"https://cir.nii.ac.jp/crid/1360285714470708096","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Metaplasia in the Stomach—Precursor of Gastric 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