{"created":"2023-06-20T14:25:24.355694+00:00","id":533,"links":{},"metadata":{"_buckets":{"deposit":"a1b09141-1b8f-45f4-a33a-6f6821e000c4"},"_deposit":{"created_by":3,"id":"533","owners":[3],"pid":{"revision_id":0,"type":"depid","value":"533"},"status":"published"},"_oai":{"id":"oai:dmu.repo.nii.ac.jp:00000533","sets":["81:41"]},"author_link":["2189"],"item_2_biblio_info_12":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2007-03-01","bibliographicIssueDateType":"Issued"},"bibliographicIssueNumber":"1","bibliographicPageEnd":"T11","bibliographicPageStart":"T1","bibliographicVolumeNumber":"34","bibliographic_titles":[{"bibliographic_title":"Dokkyo journal of medical sciences"}]}]},"item_2_description_10":{"attribute_name":"抄録(日)","attribute_value_mlt":[{"subitem_description":"強皮症の線維化は主に線維芽細胞(FB)のcollagen遺伝子転写の亢進によりおこる. macrolideには様々な薬理作用が知られるが最近,新しいerythromycin誘導体EM703のマウスbleomycin誘導肺線維化を抑制する作用が報告された.今回は正常および強皮症皮膚FBのcollagen遺伝子発現に対する影響を検討した.培養FBのcollagen産生を抗I型collagen抗体で, mRNA量をnorthern blotで,遺伝子の転写をluciferase assayで, collagen上流遺伝子への核蛋白結合をgel shift assayで解析した. EM703は正常FBに対してI型collagen産生, mRNA量を最大30%にまで温度依存性に抑制し, I型collagen遺伝子の転写を30%に抑制した.これは上流遺伝子を下流へ徐々にdeleteしても見られ,わずか-133baseにまでdeleteしても見られた.一方, -100のCCAAT-boxをGCAAGに置換変異すると約90%に抑制されたのみであった.しかしEM703添加で核のCCAAT-binding factor (CBF)の結合活性の低下はなかった.同剤は強皮症FBに対してもI型collagenの発現を抑制した. EM703は正常および強皮症FBのI型collagenの転写を抑制し,それは主にCBFの結合活性の低下なしにCCAAT-boxを介してなされると示唆される.","subitem_description_type":"Other"}]},"item_2_description_8":{"attribute_name":"記事種別(日)","attribute_value_mlt":[{"subitem_description":"学位申請論文","subitem_description_type":"Other"}]},"item_2_description_9":{"attribute_name":"記事種別(英)","attribute_value_mlt":[{"subitem_description":"Doctoral Treatise","subitem_description_type":"Other"}]},"item_2_source_id_1":{"attribute_name":"雑誌書誌ID","attribute_value_mlt":[{"subitem_source_identifier":"AA00629581"}]},"item_2_source_id_19":{"attribute_name":"ISSN","attribute_value_mlt":[{"subitem_source_identifier":"03855023","subitem_source_identifier_type":"ISSN"}]},"item_2_text_6":{"attribute_name":"著者所属(日)","attribute_value_mlt":[{"subitem_text_value":"獨協医科大学皮膚科学"}]},"item_2_title_3":{"attribute_name":"論文名よみ","attribute_value_mlt":[{"subitem_title":"エリスロマイシン ユウドウタイ EM703 ノ セイジョウ オヨビ キョウヒショウ センイガサイボウ ノ Iガタ コラーゲン テンシャ ニ タイスル ヨクセイ コウカ"}]},"item_creator":{"attribute_name":"著者","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"池田, 秀幸"},{"creatorName":"イケダ, ヒデユキ","creatorNameLang":"ja-Kana"}],"nameIdentifiers":[{}]}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2017-05-24"}],"displaytype":"detail","filename":"KJ00005058609.pdf","filesize":[{"value":"1.2 MB"}],"format":"application/pdf","licensetype":"license_note","mimetype":"application/pdf","url":{"label":"KJ00005058609.pdf","url":"https://dmu.repo.nii.ac.jp/record/533/files/KJ00005058609.pdf"},"version_id":"bd21dfcd-a0fb-4b19-9964-5ec8e35516d7"}]},"item_keyword":{"attribute_name":"キーワード","attribute_value_mlt":[{"subitem_subject":"エリスロマイシン誘導体EM703"},{"subitem_subject":"線維芽細胞"},{"subitem_subject":"コラーゲン遺伝子発現"},{"subitem_subject":"転写"},{"subitem_subject":"強皮症"}]},"item_language":{"attribute_name":"言語","attribute_value_mlt":[{"subitem_language":"jpn"}]},"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":"エリスロマイシン誘導体EM703の正常および強皮症線維芽細胞のI型コラーゲン転写に対する抑制効果","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"エリスロマイシン誘導体EM703の正常および強皮症線維芽細胞のI型コラーゲン転写に対する抑制効果"}]},"item_type_id":"2","owner":"3","path":["41"],"pubdate":{"attribute_name":"公開日","attribute_value":"2017-05-24"},"publish_date":"2017-05-24","publish_status":"0","recid":"533","relation_version_is_last":true,"title":["エリスロマイシン誘導体EM703の正常および強皮症線維芽細胞のI型コラーゲン転写に対する抑制効果"],"weko_creator_id":"3","weko_shared_id":3},"updated":"2023-06-20T16:09:30.483624+00:00"}