{"created":"2022-01-24T13:41:15.524087+00:00","id":2000889,"links":{},"metadata":{"_buckets":{"deposit":"058e555a-7762-4eac-8d73-8a8845c77d2a"},"_deposit":{"id":"2000889","owners":[1],"pid":{"revision_id":0,"type":"depid","value":"2000889"},"status":"published"},"_oai":{"id":"oai:u-ryukyu.repo.nii.ac.jp:02000889","sets":["1642838163960:1642838338003","1642838403551:1642838407795"]},"author_link":[],"item_1617186331708":{"attribute_name":"Title","attribute_value_mlt":[{"subitem_1551255647225":"Inhibition of heat shock protein-90 modulates multiple functions required for survival of human T-cell leukemia virus type I-infected T-cell lines and adult T-cell leukemia cells","subitem_1551255648112":"en"}]},"item_1617186419668":{"attribute_name":"Creator","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"Kawakami, Hirochika","creatorNameLang":"en"}]},{"creatorNames":[{"creatorName":"Tomita, Mariko","creatorNameLang":"en"}]},{"creatorNames":[{"creatorName":"Okudaira, Taeko","creatorNameLang":"en"}]},{"creatorNames":[{"creatorName":"Chie, Ishikawa","creatorNameLang":"en"}]},{"creatorNames":[{"creatorName":"Matsuda, Takehiro","creatorNameLang":"en"}]},{"creatorNames":[{"creatorName":"Tanaka, Yuetsu","creatorNameLang":"en"}]},{"creatorNames":[{"creatorName":"Nakazato, Tetsuro","creatorNameLang":"en"}]},{"creatorNames":[{"creatorName":"Taira, Naoya","creatorNameLang":"en"}]},{"creatorNames":[{"creatorName":"Ohshiro, Kazuiku","creatorNameLang":"en"}]},{"creatorNames":[{"creatorName":"Mori, Naoki","creatorNameLang":"en"}]}]},"item_1617186476635":{"attribute_name":"Access Rights","attribute_value_mlt":[{"subitem_1522299639480":"open access","subitem_1600958577026":"http://purl.org/coar/access_right/c_abf2"}]},"item_1617186499011":{"attribute_name":"Rights","attribute_value_mlt":[{"subitem_1522650717957":"en","subitem_1522651041219":"Copyright (c) 2007 Wiley-Liss, Inc"}]},"item_1617186609386":{"attribute_name":"Subject","attribute_value_mlt":[{"subitem_1522299896455":"en","subitem_1522300014469":"Other","subitem_1523261968819":"ATL"},{"subitem_1522299896455":"en","subitem_1522300014469":"Other","subitem_1523261968819":"HTLV-I"},{"subitem_1522299896455":"en","subitem_1522300014469":"Other","subitem_1523261968819":"17-AAG"},{"subitem_1522299896455":"en","subitem_1522300014469":"Other","subitem_1523261968819":"Hsp90"},{"subitem_1522299896455":"en","subitem_1522300014469":"Other","subitem_1523261968819":"client protein"}]},"item_1617186626617":{"attribute_name":"Description","attribute_value_mlt":[{"subitem_description":"The molecular chaperone Hsp90 is involved in the stabilization and conformational maturation of many signaling proteins that are deregulated in cancers. The geldanamycin derivative 17-AAG is currently tested in clinical trials and known to inhibit the function of Hsp90 and promote the proteasomal degradation of its misfolded client proteins. ATL is a fatal malignancy of T lymphocytes caused by HTLV-I infection and remains incurable. Since Hsp90 is overexpressed in HTLV-I-infected T-cell lines and primary ATL cells, we analyzed the effects of 17-AAG on cell survival, apoptosis and expression of signal transduction proteins. HTLV-I-infected T-cell lines and primary ATL cells were significantly more sensitive to 17-AAG in cell survival assays than normal PBMCs. 17-AAG induced the inhibition of cell cycle and apoptosis. These effects could be mediated by inactivation of NF-B, AP-1 and PI3K/Akt pathways, as well as reduction of expression of proteins involved in the G1-S cell cycle transition and apoptosis. Proteasome inhibition interfered with 17-AAG-mediated signaling proteins depletion. Collectively, our results indicate that 17-AAG suppresses ATL cell survival through, at least in part, destabilization of several client proteins and suggest that 17-AAG is a potentially useful chemotherapeutic agent for ATL.","subitem_description_type":"Other"},{"subitem_description":"論文","subitem_description_type":"Other"}]},"item_1617186643794":{"attribute_name":"Publisher","attribute_value_mlt":[{"subitem_1522300295150":"en","subitem_1522300316516":"Wiley-Liss, Inc."}]},"item_1617186702042":{"attribute_name":"Language","attribute_value_mlt":[{"subitem_1551255818386":"eng"}]},"item_1617186783814":{"attribute_name":"Identifier","attribute_value_mlt":[{"subitem_identifier_type":"HDL","subitem_identifier_uri":"http://hdl.handle.net/20.500.12000/271"}]},"item_1617186920753":{"attribute_name":"Source Identifier","attribute_value_mlt":[{"subitem_1522646500366":"ISSN","subitem_1522646572813":"00207136"},{"subitem_1522646500366":"NCID","subitem_1522646572813":"AA00680002"}]},"item_1617186941041":{"attribute_name":"Source Title","attribute_value_mlt":[{"subitem_1522650068558":"en","subitem_1522650091861":"International Journal of Cancer"}]},"item_1617187056579":{"attribute_name":"Bibliographic Information","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2007-01","bibliographicIssueDateType":"Issued"},"bibliographicIssueNumber":"8","bibliographicPageEnd":"1820","bibliographicPageStart":"1811","bibliographicVolumeNumber":"120"}]},"item_1617258105262":{"attribute_name":"Resource Type","attribute_value_mlt":[{"resourcetype":"journal article","resourceuri":"http://purl.org/coar/resource_type/c_6501"}]},"item_1617265215918":{"attribute_name":"Version Type","attribute_value_mlt":[{"subitem_1522305645492":"AM","subitem_1600292170262":"http://purl.org/coar/version/c_ab4af688f83e57aa"}]},"item_1617353299429":{"attribute_name":"Relation","attribute_value_mlt":[{"subitem_1522306287251":{"subitem_1522306382014":"DOI","subitem_1522306436033":"10.1002/ijc.22403"}}]},"item_1617605131499":{"attribute_name":"File","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_access","filename":"IJC_v120n8p1811_fig.pdf","mimetype":"application/pdf","url":{"objectType":"fulltext","url":"https://u-ryukyu.repo.nii.ac.jp/record/2000889/files/IJC_v120n8p1811_fig.pdf"},"version_id":"99a9fd02-7b95-4f31-9034-62c0003f4315"},{"accessrole":"open_access","filename":"IJC_v120n8p1811.pdf","mimetype":"application/pdf","url":{"objectType":"fulltext","url":"https://u-ryukyu.repo.nii.ac.jp/record/2000889/files/IJC_v120n8p1811.pdf"},"version_id":"1bcfd429-844a-4b72-adf8-cb1deed5ccba"}]},"item_title":"Inhibition of heat shock protein-90 modulates multiple functions required for survival of human T-cell leukemia virus type I-infected T-cell lines and adult T-cell leukemia cells","item_type_id":"15","owner":"1","path":["1642838338003","1642838407795"],"pubdate":{"attribute_name":"PubDate","attribute_value":"2007-03-08"},"publish_date":"2007-03-08","publish_status":"0","recid":"2000889","relation_version_is_last":true,"title":["Inhibition of heat shock protein-90 modulates multiple functions required for survival of human T-cell leukemia virus type I-infected T-cell lines and adult T-cell leukemia cells"],"weko_creator_id":"1","weko_shared_id":-1},"updated":"2023-08-03T05:33:02.418974+00:00"}