{"created":"2022-02-02T02:04:34.155276+00:00","id":2012284,"links":{},"metadata":{"_buckets":{"deposit":"f4b66bff-9b7a-481f-9885-225247c8bc8a"},"_deposit":{"id":"2012284","owners":[1],"pid":{"revision_id":0,"type":"depid","value":"2012284"},"status":"published"},"_oai":{"id":"oai:u-ryukyu.repo.nii.ac.jp:02012284","sets":["1642838163960:1642838338003","1642838403551:1642838407795"]},"author_link":[],"item_1617186331708":{"attribute_name":"Title","attribute_value_mlt":[{"subitem_1551255647225":"Degradation of p47 by autophagy contributes to CADM1 overexpression in ATLL cells through the activation of NF-κB","subitem_1551255648112":"ja"}]},"item_1617186419668":{"attribute_name":"Creator","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"Sarkar, Bidhan","creatorNameLang":"en"}]},{"creatorNames":[{"creatorName":"Nishikata, Ichiro","creatorNameLang":"en"}]},{"creatorNames":[{"creatorName":"Nakahata, Shingo","creatorNameLang":"en"}]},{"creatorNames":[{"creatorName":"Ichikawa, Tomonaga","creatorNameLang":"en"}]},{"creatorNames":[{"creatorName":"Shiraga, Toshiyuki","creatorNameLang":"en"}]},{"creatorNames":[{"creatorName":"Saha, Hashi Rani","creatorNameLang":"en"}]},{"creatorNames":[{"creatorName":"Tanaka, Yuetsu","creatorNameLang":"en"}]},{"creatorNames":[{"creatorName":"Shimoda, Kazuya","creatorNameLang":"en"}]},{"creatorNames":[{"creatorName":"Morishita, Kazuhiro","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":"Creative Commons Attribution 4.0 International License"},{"subitem_1522650717957":"en","subitem_1522650727486":"http://creativecommons.org/licenses/by/4.0/","subitem_1522651041219":"http://creativecommons.org/licenses/by/4.0/"}]},"item_1617186626617":{"attribute_name":"Description","attribute_value_mlt":[{"subitem_description":"Cell adhesion molecule 1 (CADM1), a member of the immunoglobulin superfamily, is identified as a novel cell surface marker for human T-cell leukemia virus (HTLV-1)-infected T cells. Adult T-cell leukemia/lymphoma (ATLL) is developed in HTLV-1-infected T-cells after a long infection period. To examine the mechanism of CADM1 overexpression in ATLL, we first identified that CADM1 is transcriptionally up-regulated by a transcriptional enhancer element through NF-κB signaling pathway. In HTLV-1-infected T-cells, CADM1 expression is dependent on HTLV-1/Tax through activation of canonical and non-canonical NF-κB; however, in ATLL cells with frequent loss of Tax expression, the activation of canonical NF-κB only enhances the CADM1 expression. Along with active mutations in signaling molecules under T-cell recepor (TCR) signaling, degradation of p47, a negative regulator of NF-κB, was essential for activation of canonical NF-κB through stabilization of NEMO (NF-κB essential modulator). The mechanism of p47 degradation is primarily dependent on activation of lysosomal-autophagy and the autophagy is activated in most of the HTLV-infected and ATLL cells, suggesting that the p47 degradation may be a first key molecular event during HTLV-1 infection to T-cells as a connector of two important signaling pathways, NF-κB and autophagy.","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":"Springer Nature"}]},"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/20.500.12000/45626"}]},"item_1617186920753":{"attribute_name":"Source Identifier","attribute_value_mlt":[{"subitem_1522646500366":"ISSN","subitem_1522646572813":"2045-2322"}]},"item_1617186941041":{"attribute_name":"Source Title","attribute_value_mlt":[{"subitem_1522650068558":"en","subitem_1522650091861":"Scientific Reports"}]},"item_1617187056579":{"attribute_name":"Bibliographic Information","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2019-03-05","bibliographicIssueDateType":"Issued"},"bibliographicIssueNumber":"3491","bibliographicVolumeNumber":"9"}]},"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":"VoR","subitem_1600292170262":"http://purl.org/coar/version/c_970fb48d4fbd8a85"}]},"item_1617353299429":{"attribute_name":"Relation","attribute_value_mlt":[{"subitem_1522306287251":{"subitem_1522306382014":"DOI","subitem_1522306436033":"https://doi.org/10.1038/s41598-019-39424-7"}},{"subitem_1522306287251":{"subitem_1522306382014":"DOI","subitem_1522306436033":"https://doi.org/10.1038/s41598-019-39424-7"}}]},"item_1617605131499":{"attribute_name":"File","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_access","filename":"s41598-019-39424-7.pdf","mimetype":"application/pdf","url":{"objectType":"fulltext","url":"https://u-ryukyu.repo.nii.ac.jp/record/2012284/files/s41598-019-39424-7.pdf"},"version_id":"7d0292d3-dd8d-42cc-a685-9f15443c02ad"}]},"item_title":"Degradation of p47 by autophagy contributes to CADM1 overexpression in ATLL cells through the activation of NF-κB","item_type_id":"15","owner":"1","path":["1642838338003","1642838407795"],"pubdate":{"attribute_name":"PubDate","attribute_value":"2020-04-15"},"publish_date":"2020-04-15","publish_status":"0","recid":"2012284","relation_version_is_last":true,"title":["Degradation of p47 by autophagy contributes to CADM1 overexpression in ATLL cells through the activation of NF-κB"],"weko_creator_id":"1","weko_shared_id":-1},"updated":"2023-08-03T05:31:21.394676+00:00"}