{"@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/1360848660445166208.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1111/febs.12848"}},{"identifier":{"@type":"URI","@value":"https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1111%2Ffebs.12848"}},{"identifier":{"@type":"URI","@value":"https://onlinelibrary.wiley.com/doi/pdf/10.1111/febs.12848"}},{"identifier":{"@type":"URI","@value":"https://onlinelibrary.wiley.com/doi/full-xml/10.1111/febs.12848"}},{"identifier":{"@type":"URI","@value":"https://febs.onlinelibrary.wiley.com/doi/pdf/10.1111/febs.12848"}},{"identifier":{"@type":"PMID","@value":"24835508"}}],"resourceType":"学術雑誌論文(journal article)","dc:title":[{"@value":"Activity of the upstream <scp>TATA</scp>‐less promoter of the <i>p21</i><sup><i>Waf1/Cip1</i></sup> gene depends on transcription factor <scp>IIA</scp> (<scp>TFIIA</scp>) in addition to <scp>TFIIA</scp>‐reactive <scp>TBP</scp>‐like protein"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:sec><jats:label /><jats:p><jats:styled-content style=\"fixed-case\">TATA</jats:styled-content>‐binding protein‐like protein (<jats:styled-content style=\"fixed-case\">TLP</jats:styled-content>) binds to transcription factor <jats:styled-content style=\"fixed-case\">IIA</jats:styled-content> (<jats:styled-content style=\"fixed-case\">TFIIA</jats:styled-content>) with high affinity, although the significance of this binding is poorly understood. In this study, we investigated the role of <jats:styled-content style=\"fixed-case\">TFIIA</jats:styled-content> in transcriptional regulation of the <jats:italic>p21</jats:italic><jats:sup><jats:italic>Waf1/Cip1</jats:italic></jats:sup> (<jats:italic>p21</jats:italic>) gene. It has been shown that <jats:styled-content style=\"fixed-case\">TLP</jats:styled-content> is indispensable for p53‐activated transcription from an upstream <jats:styled-content style=\"fixed-case\">TATA</jats:styled-content>‐less promoter of the <jats:italic>p21</jats:italic> gene. We found that mutant <jats:styled-content style=\"fixed-case\">TLP</jats:styled-content>s having decreased <jats:styled-content style=\"fixed-case\">TFIIA</jats:styled-content>‐binding ability exhibited weakened transcriptional activation function for the upstream promoter. Activity of the upstream promoter was enhanced considerably by an increased amount of <jats:styled-content style=\"fixed-case\">TFIIA</jats:styled-content> in a p53‐dependent manner, whereas activity of the <jats:styled-content style=\"fixed-case\">TATA</jats:styled-content>‐containing downstream promoter was enhanced only slightly. <jats:styled-content style=\"fixed-case\">TFIIA</jats:styled-content> potentiated the upstream promoter additively with <jats:styled-content style=\"fixed-case\">TLP</jats:styled-content>. Although <jats:styled-content style=\"fixed-case\">TFIIA</jats:styled-content> is recruited to both promoters, activity of the upstream promoter was much more dependent on <jats:styled-content style=\"fixed-case\">TFIIA</jats:styled-content>. Recruitment of <jats:styled-content style=\"fixed-case\">TFIIA</jats:styled-content> and <jats:styled-content style=\"fixed-case\">TLP</jats:styled-content> to the upstream promoter was augmented in etoposide‐treated cells, in which the amount of <jats:styled-content style=\"fixed-case\">TFIIA</jats:styled-content>–<jats:styled-content style=\"fixed-case\">TLP</jats:styled-content> complex is increased, and <jats:styled-content style=\"fixed-case\">TFIIA</jats:styled-content>‐reactive <jats:styled-content style=\"fixed-case\">TLP</jats:styled-content> was required for the recruitment of both factors. It was confirmed that etoposide‐stimulated transcription depends on <jats:styled-content style=\"fixed-case\">TLP</jats:styled-content>. We also found that <jats:styled-content style=\"fixed-case\">TFIIA</jats:styled-content>‐reactive <jats:styled-content style=\"fixed-case\">TLP</jats:styled-content> acts to decrease cell growth rate, which can be explained by interaction of the <jats:italic>p21</jats:italic> promoter with the transcription factors that we examined. The results of the present study suggest that the upstream <jats:styled-content style=\"fixed-case\">TATA</jats:styled-content>‐less promoter of <jats:italic>p21</jats:italic> needs <jats:styled-content style=\"fixed-case\">TFIIA</jats:styled-content> and <jats:styled-content style=\"fixed-case\">TFIIA</jats:styled-content>‐reactive <jats:styled-content style=\"fixed-case\">TLP</jats:styled-content> for p53‐dependent transcriptional enhancement.</jats:p></jats:sec><jats:sec><jats:title>Structured digital abstract</jats:title><jats:p>\n<jats:list list-type=\"bullet\">\n\n<jats:list-item><jats:p><jats:ext-link xmlns:xlink=\"http://www.w3.org/1999/xlink\" xlink:href=\"http://www.uniprot.org/uniprot/P62340\">TLP</jats:ext-link> <jats:ext-link xmlns:xlink=\"http://www.w3.org/1999/xlink\" xlink:href=\"http://www.ebi.ac.uk/ontology-lookup/?termId=MI:0914\">physically interacts</jats:ext-link> with <jats:ext-link xmlns:xlink=\"http://www.w3.org/1999/xlink\" xlink:href=\"http://www.uniprot.org/uniprot/P52655\">TFIIA beta</jats:ext-link> and <jats:ext-link xmlns:xlink=\"http://www.w3.org/1999/xlink\" xlink:href=\"http://www.uniprot.org/uniprot/P52655\">TFIIA alpha</jats:ext-link> by <jats:ext-link xmlns:xlink=\"http://www.w3.org/1999/xlink\" xlink:href=\"http://www.ebi.ac.uk/ontology-lookup/?termId=MI:0007\">anti tag coimmunoprecipitation</jats:ext-link> (<jats:ext-link xmlns:xlink=\"http://www.w3.org/1999/xlink\" xlink:href=\"http://www.ebi.ac.uk/intact/interaction/EBI-9524851\">View interaction</jats:ext-link>)</jats:p></jats:list-item>\n\n<jats:list-item><jats:p><jats:ext-link xmlns:xlink=\"http://www.w3.org/1999/xlink\" xlink:href=\"http://www.uniprot.org/uniprot/P52655\">TFIIA alpha/beta</jats:ext-link> <jats:ext-link xmlns:xlink=\"http://www.w3.org/1999/xlink\" xlink:href=\"http://www.ebi.ac.uk/ontology-lookup/?termId=MI:0915\">physically interacts</jats:ext-link> with <jats:ext-link xmlns:xlink=\"http://www.w3.org/1999/xlink\" xl ..."}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1380848660445166212","@type":"Researcher","foaf:name":[{"@value":"Hidefumi Suzuki"}],"jpcoar:affiliationName":[{"@value":"Graduate School of Science Chiba University  Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1380848660445166210","@type":"Researcher","foaf:name":[{"@value":"Ryo Maeda"}],"jpcoar:affiliationName":[{"@value":"Graduate School of Science Chiba University  Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1380848660445166081","@type":"Researcher","foaf:name":[{"@value":"Tomoyoshi Nakadai"}],"jpcoar:affiliationName":[{"@value":"Graduate School of Science Chiba University  Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1380848660445166209","@type":"Researcher","foaf:name":[{"@value":"Taka‐aki Tamura"}],"jpcoar:affiliationName":[{"@value":"Graduate School of Science Chiba University  Japan"}]}],"publication":{"publicationIdentifier":[{"@type":"PISSN","@value":"1742464X"},{"@type":"EISSN","@value":"17424658"}],"prism:publicationName":[{"@value":"The FEBS Journal"}],"dc:publisher":[{"@value":"Wiley"}],"prism:publicationDate":"2014-06-06","prism:volume":"281","prism:number":"14","prism:startingPage":"3126","prism:endingPage":"3137"},"reviewed":"false","dcterms:accessRights":"http://purl.org/coar/access_right/c_abf2","dc:rights":["http://creativecommons.org/licenses/by/3.0/"],"url":[{"@id":"https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1111%2Ffebs.12848"},{"@id":"https://onlinelibrary.wiley.com/doi/pdf/10.1111/febs.12848"},{"@id":"https://onlinelibrary.wiley.com/doi/full-xml/10.1111/febs.12848"},{"@id":"https://febs.onlinelibrary.wiley.com/doi/pdf/10.1111/febs.12848"}],"createdAt":"2014-05-17","modifiedAt":"2023-10-02","foaf:topic":[{"@id":"https://cir.nii.ac.jp/all?q=Cell%20Biology","dc:title":"Cell Biology"},{"@id":"https://cir.nii.ac.jp/all?q=Molecular%20Biology","dc:title":"Molecular Biology"},{"@id":"https://cir.nii.ac.jp/all?q=Biochemistry","dc:title":"Biochemistry"}],"project":[{"@id":"https://cir.nii.ac.jp/crid/1040000782437315072","@type":"Project","projectIdentifier":[{"@type":"KAKEN","@value":"13J04583"},{"@type":"JGN","@value":"JP13J04583"},{"@type":"URI","@value":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-13J04583/"}],"notation":[{"@language":"ja","@value":"細胞傷害応答におけるＴＬＰのｐ５３活性化機構と応答配列認識機構の解明"}]},{"@id":"https://cir.nii.ac.jp/crid/1040282257187436032","@type":"Project","projectIdentifier":[{"@type":"KAKEN","@value":"24570193"},{"@type":"JGN","@value":"JP24570193"},{"@type":"URI","@value":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-24570193/"}],"notation":[{"@language":"ja","@value":"ｐ５３ーｐ２１経路の新規メディエーターであるＴＬＰの作用機序の解明"},{"@language":"en","@value":"Mechanism of TLP as a mediator in p53-p21 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