{"created":"2023-06-19T07:00:47.185621+00:00","id":2226,"links":{},"metadata":{"_buckets":{"deposit":"fe848764-6878-4423-b0c8-c13440b3181c"},"_deposit":{"created_by":3,"id":"2226","owners":[3],"pid":{"revision_id":0,"type":"depid","value":"2226"},"status":"published"},"_oai":{"id":"oai:rakuno.repo.nii.ac.jp:00002226","sets":["9:27:28:29"]},"author_link":["5871","5872","5876","5874","5875","5877","5873","4860"],"item_2_biblio_info_9":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2015-10","bibliographicIssueDateType":"Issued"},"bibliographicIssueNumber":"5","bibliographicPageEnd":"330","bibliographicPageStart":"323","bibliographicVolumeNumber":"36","bibliographic_titles":[{"bibliographic_title":"Biomedical Research"}]}]},"item_2_description_43":{"attribute_name":"資源タイプ","attribute_value_mlt":[{"subitem_description":"Article","subitem_description_type":"Other"}]},"item_2_description_6":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"Tensin2 (Tns2) is thought to be a component of the cytoskeletal structures linking actin filaments with focal adhesions and is known to play a role as an intracellular signal transduction mediator through integrin in podocytes, although the mechanism by which it functions remains unclear. A Tns2-null mutation (nph) leads to massive albuminuria following podocyte foot process effacement in the ICGN mice, the origin of the mutation, and the DBA/2J (D2) mice, but not in the C57BL/6J (B6) mice or 129^<+Ter>/SvJcl (129T) mice. Elucidating the reasons for these differences in diverse genetic backgrounds could help in unraveling Tns2 function in podocytes. We produced congenic mice in which Tns2^<nph> was introgressed into a FVB/NJ background (FVB-Tns2^<nph>), and evaluated the progression of kidney disease. FVB-Tns2^<nph> mice developed albuminuria, renal fibrosis and renal anemia as seen in ICGN mice. The FVB-Tns2nph mice demonstrated podocyte foot process alteration under an electron microscope by as early as 4 weeks of age. This revealed that FVB strain is susceptible to Tns2-deficiency.","subitem_description_type":"Abstract"}]},"item_2_publisher_36":{"attribute_name":"出版者","attribute_value_mlt":[{"subitem_publisher":"Biomedical Research"}]},"item_2_relation_14":{"attribute_name":"DOI","attribute_value_mlt":[{"subitem_relation_type":"isIdenticalTo","subitem_relation_type_id":{"subitem_relation_type_id_text":"10.2220/biomedres.36.323","subitem_relation_type_select":"DOI"}}]},"item_2_source_id_10":{"attribute_name":"ISSN","attribute_value_mlt":[{"subitem_source_identifier":"1880-313X","subitem_source_identifier_type":"ISSN"}]},"item_2_version_type_19":{"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":"SASAKI, Hayato"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"MARUSUGI, Kiyoma"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"KIMURA, Junpei"}],"nameIdentifiers":[{}]},{"creatorAffiliations":[{"affiliationNameIdentifiers":[{"affiliationNameIdentifier":""}],"affiliationNames":[{"affiliationName":""}]}],"creatorNames":[{"creatorName":"KITAMURA, Hiroshi","creatorNameLang":"en"},{"creatorName":"北村, 浩","creatorNameLang":"ja"}],"familyNames":[{},{}],"givenNames":[{},{}],"nameIdentifiers":[{},{}]},{"creatorNames":[{"creatorName":"NAGASAKI, Ken-Ichi"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"TORIGOE, Daisuke"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"AGUI, Takashi"}],"nameIdentifiers":[{}]},{"creatorNames":[{"creatorName":"SASAKI, Nobuya"}],"nameIdentifiers":[{}]}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2017-09-15"}],"displaytype":"detail","filename":"S-2016-148_kitamura.pdf","filesize":[{"value":"2.8 MB"}],"format":"application/pdf","licensetype":"license_note","mimetype":"application/pdf","url":{"label":"S-2016-148_kitamura.pdf","url":"https://rakuno.repo.nii.ac.jp/record/2226/files/S-2016-148_kitamura.pdf"},"version_id":"4ef8294f-f916-42e2-9852-699ea40fdf5a"}]},"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":"Genetic background-dependent diversity in renal failure caused by the tensin2 gene deficiency in the mouse","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"Genetic background-dependent diversity in renal failure caused by the tensin2 gene deficiency in the mouse"}]},"item_type_id":"2","owner":"3","path":["29"],"pubdate":{"attribute_name":"公開日","attribute_value":"2017-06-09"},"publish_date":"2017-06-09","publish_status":"0","recid":"2226","relation_version_is_last":true,"title":["Genetic background-dependent diversity in renal failure caused by the tensin2 gene deficiency in the mouse"],"weko_creator_id":"3","weko_shared_id":-1},"updated":"2023-08-31T01:35:35.069998+00:00"}