{"created":"2023-07-27T06:30:23.122081+00:00","id":15386,"links":{},"metadata":{"_buckets":{"deposit":"c569b07d-c590-4536-b778-e96ac997dfaf"},"_deposit":{"created_by":3,"id":"15386","owners":[3],"pid":{"revision_id":0,"type":"depid","value":"15386"},"status":"published"},"_oai":{"id":"oai:kanazawa-u.repo.nii.ac.jp:00015386","sets":["1132:1133:1135"]},"author_link":["27973","27972","27966","27970","27971","27975","27974","53","313","27967","27968","27969"],"item_4_biblio_info_8":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2007-03-01","bibliographicIssueDateType":"Issued"},"bibliographicIssueNumber":"6","bibliographicPageEnd":"1112","bibliographicPageStart":"1104","bibliographicVolumeNumber":"120","bibliographic_titles":[{"bibliographic_title":"Journal of Cell Science"}]}]},"item_4_description_21":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"Human histone H2AX is rapidly phosphorylated on serine 139 in response to DNA double-strand breaks and plays a crucial role in tethering the factors involved in DNA repair and damage signaling. Replication stress caused by hydroxyurea or UV also initiates H2AX phosphorylation in S-phase cells, although UV induced H2AX phosphorylation in non-cycling cells has recently been observed. Here we study the UV induced H2AX phosphorylation in human primary fibroblasts under growth-arrested conditions. This reaction absolutely depends on nucleotide excision repair (NER) and is mechanistically distinct from the replication stress-induced phosphorylation. The treatment of cytosine-β-D-arabinofuranoside strikingly enhances the NER-dependent H2AX phosphorylation and induces the accumulation of replication protein A (RPA) and ATR-interacting protein (ATRIP) at locally UV-damaged subnuclear regions. Consistently, the phosphorylation appears to be mainly mediated by ataxia-telangiectasia mutated and Rad3-related (ATR), although Chk1 (Ser345) is not phosphorylated by the activated ATR. The cellular levels of DNA polymerases δ and ε and proliferating cell nuclear antigen are markedly reduced in quiescent cells. We propose a model that perturbed gap-filling synthesis following dual incision in NER generates single-strand DNA gaps and hence initiates H2AX phosphorylation by ATR with the aid of RPA and ATRIP.","subitem_description_type":"Abstract"}]},"item_4_publisher_17":{"attribute_name":"出版者","attribute_value_mlt":[{"subitem_publisher":"Company of Biologists"}]},"item_4_relation_12":{"attribute_name":"DOI","attribute_value_mlt":[{"subitem_relation_type":"isIdenticalTo","subitem_relation_type_id":{"subitem_relation_type_id_text":"10.1242/jcs.03391","subitem_relation_type_select":"DOI"}}]},"item_4_relation_28":{"attribute_name":"関連URI","attribute_value_mlt":[{"subitem_relation_type_id":{"subitem_relation_type_id_text":"http://jcs.biologists.org/content/120/6/1104","subitem_relation_type_select":"URI"}}]},"item_4_rights_23":{"attribute_name":"権利","attribute_value_mlt":[{"subitem_rights":"Copyright © The Company of Biologists Limited 2007"}]},"item_4_source_id_11":{"attribute_name":"NCID","attribute_value_mlt":[{"subitem_source_identifier":"AA00694823","subitem_source_identifier_type":"NCID"}]},"item_4_source_id_9":{"attribute_name":"ISSN","attribute_value_mlt":[{"subitem_source_identifier":"0021-9533","subitem_source_identifier_type":"ISSN"}]},"item_4_version_type_25":{"attribute_name":"著者版フラグ","attribute_value_mlt":[{"subitem_version_resource":"http://purl.org/coar/version/c_970fb48d4fbd8a85","subitem_version_type":"VoR"}]},"item_creator":{"attribute_name":"著者","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"Matsumoto, Megumi"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"Yaginuma, Kie"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"Igarashi, Ai"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"Imura, Mayumi"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"Hasegawa, Mizuho"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"Iwabuchi, Kuniyoshi"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"Date, Takayasu"}],"nameIdentifiers":[{},{}]},{"creatorNames":[{"creatorName":"Mori, Toshio"}],"nameIdentifiers":[{},{}]},{"creatorNames":[{"creatorName":"Ishizaki, Kanji"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"Yamashita, Katsumi"}],"nameIdentifiers":[{},{},{}]},{"creatorNames":[{"creatorName":"Inobe, Manabu"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"Matsunaga, Tsukasa"}],"nameIdentifiers":[{},{},{},{}]}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2017-10-04"}],"displaytype":"detail","filename":"PH-PR-MATSUNAGA-T-1104.pdf","filesize":[{"value":"2.7 MB"}],"format":"application/pdf","licensetype":"license_note","mimetype":"application/pdf","url":{"label":"PH-PR-MATSUNAGA-T-1104.pdf","url":"https://kanazawa-u.repo.nii.ac.jp/record/15386/files/PH-PR-MATSUNAGA-T-1104.pdf"},"version_id":"17335b9d-b4d4-4a9d-aa2c-44beb3a2b618"}]},"item_language":{"attribute_name":"言語","attribute_value_mlt":[{"subitem_language":"eng"}]},"item_resource_type":{"attribute_name":"資源タイプ","attribute_value_mlt":[{"resourcetype":"journal article","resourceuri":"http://purl.org/coar/resource_type/c_6501"}]},"item_title":"Perturbed gap-filling synthesis in nucleotide excision repair causes histone H2AX phosphorylation in human quiescent cells","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"Perturbed gap-filling synthesis in nucleotide excision repair causes histone H2AX phosphorylation in human quiescent cells"}]},"item_type_id":"4","owner":"3","path":["1135"],"pubdate":{"attribute_name":"公開日","attribute_value":"2017-10-04"},"publish_date":"2017-10-04","publish_status":"0","recid":"15386","relation_version_is_last":true,"title":["Perturbed gap-filling synthesis in nucleotide excision repair causes histone H2AX phosphorylation in human quiescent cells"],"weko_creator_id":"3","weko_shared_id":-1},"updated":"2023-07-28T00:33:20.566014+00:00"}