{"_buckets": {"deposit": "b9e7a3b2-bc9c-4621-a98f-e0e81a1386e4"}, "_deposit": {"id": "12294", "owners": [], "pid": {"revision_id": 0, "type": "depid", "value": "12294"}, "status": "published"}, "_oai": {"id": "oai:nagoya.repo.nii.ac.jp:00012294"}, "item_9_biblio_info_6": {"attribute_name": "\u66f8\u8a8c\u60c5\u5831", "attribute_value_mlt": [{"bibliographicIssueDates": {"bibliographicIssueDate": "2010-08", "bibliographicIssueDateType": "Issued"}, "bibliographicIssueNumber": "3-4", "bibliographicPageEnd": "144", "bibliographicPageStart": "139", "bibliographicVolumeNumber": "72", "bibliographic_titles": [{"bibliographic_title": "Nagoya Journal of Medical Science"}]}]}, "item_9_description_4": {"attribute_name": "\u6284\u9332", "attribute_value_mlt": [{"subitem_description": "We previously reported that the disruption of cell spreading by v-Crk was dependent on the activation of the MEK/ERK pathway. Here we demonstrate that the activation of that pathway is sufficient to suppress cell spreading. The MEK/ERK pathway regulates the activity of various proteins including AP-1, which is a transcriptional factor composed of heterodimeric proteins. To examine whether AP-1 activity is required for the suppression of cell spreading by the activation of the MEK/ERK pathway, we expressed BATF, which is a negative regulator of AP-1. The expression of BATF clearly restored cell spreading that was suppressed by the activation of MEK/ERK pathway. In addition, a disrupted formation of stress fibers and focal adhesions by such activation was restored by the suppression of AP-1. Our results define an essential role of the MEK/ERK/AP-1 pathway in the disruption of actin cytoskeleton and cell spreading.", "subitem_description_type": "Abstract"}]}, "item_9_identifier_60": {"attribute_name": "URI", "attribute_value_mlt": [{"subitem_identifier_type": "HDL", "subitem_identifier_uri": "http://hdl.handle.net/2237/14175"}]}, "item_9_identifier_registration": {"attribute_name": "ID\u767b\u9332", "attribute_value_mlt": [{"subitem_identifier_reg_text": "10.18999/nagjms.72.3-4.139", "subitem_identifier_reg_type": "JaLC"}]}, "item_9_publisher_32": {"attribute_name": "\u51fa\u7248\u8005", "attribute_value_mlt": [{"subitem_publisher": "Nagoya University School of Medicine"}]}, "item_9_select_15": {"attribute_name": "\u8457\u8005\u7248\u30d5\u30e9\u30b0", "attribute_value_mlt": [{"subitem_select_item": "publisher"}]}, "item_9_source_id_7": {"attribute_name": "ISSN\uff08print\uff09", "attribute_value_mlt": [{"subitem_source_identifier": "0027-7622", "subitem_source_identifier_type": "ISSN"}]}, "item_9_text_14": {"attribute_name": "\u30d5\u30a9\u30fc\u30de\u30c3\u30c8", "attribute_value_mlt": [{"subitem_text_value": "application/pdf"}]}, "item_creator": {"attribute_name": "\u8457\u8005", "attribute_type": "creator", "attribute_value_mlt": [{"creatorNames": [{"creatorName": "Xu, Feng"}], "nameIdentifiers": [{"nameIdentifier": "38858", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Ito, Satoko"}], "nameIdentifiers": [{"nameIdentifier": "38859", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Hamaguchi, Michinari"}], "nameIdentifiers": [{"nameIdentifier": "38860", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Senga, Takeshi"}], "nameIdentifiers": [{"nameIdentifier": "38861", "nameIdentifierScheme": "WEKO"}]}]}, "item_files": {"attribute_name": "\u30d5\u30a1\u30a4\u30eb\u60c5\u5831", "attribute_type": "file", "attribute_value_mlt": [{"accessrole": "open_date", "date": [{"dateType": "Available", "dateValue": "2018-02-20"}], "displaytype": "detail", "download_preview_message": "", "file_order": 0, "filename": "p139-144_Xu.pdf", "filesize": [{"value": "443.2 kB"}], "format": "application/pdf", "future_date_message": "", "is_thumbnail": false, "licensetype": "license_free", "mimetype": "application/pdf", "size": 443200.0, "url": {"label": "p139-144_Xu.pdf", "url": "https://nagoya.repo.nii.ac.jp/record/12294/files/p139-144_Xu.pdf"}, "version_id": "a5934acc-ed40-4a01-9fe4-c69de7a339e6"}]}, "item_keyword": {"attribute_name": "\u30ad\u30fc\u30ef\u30fc\u30c9", "attribute_value_mlt": [{"subitem_subject": "MEK", "subitem_subject_scheme": "Other"}, {"subitem_subject": "ERK", "subitem_subject_scheme": "Other"}, {"subitem_subject": "AP-1", "subitem_subject_scheme": "Other"}, {"subitem_subject": "BATF", "subitem_subject_scheme": "Other"}, {"subitem_subject": "Cell spreading", "subitem_subject_scheme": "Other"}]}, "item_language": {"attribute_name": "\u8a00\u8a9e", "attribute_value_mlt": [{"subitem_language": "eng"}]}, "item_resource_type": {"attribute_name": "\u8cc7\u6e90\u30bf\u30a4\u30d7", "attribute_value_mlt": [{"resourcetype": "departmental bulletin paper", "resourceuri": "http://purl.org/coar/resource_type/c_6501"}]}, "item_title": "Disruption of Cell Spreading by the Activation of MEK/ERK Pathway is Dependent on AP-1 Activity", "item_titles": {"attribute_name": "\u30bf\u30a4\u30c8\u30eb", "attribute_value_mlt": [{"subitem_title": "Disruption of Cell Spreading by the Activation of MEK/ERK Pathway is Dependent on AP-1 Activity"}]}, "item_type_id": "9", "owner": "1", "path": ["499/508/509/1277"], "permalink_uri": "https://doi.org/10.18999/nagjms.72.3-4.139", "pubdate": {"attribute_name": "\u516c\u958b\u65e5", "attribute_value": "2010-09-21"}, "publish_date": "2010-09-21", "publish_status": "0", "recid": "12294", "relation": {}, "relation_version_is_last": true, "title": ["Disruption of Cell Spreading by the Activation of MEK/ERK Pathway is Dependent on AP-1 Activity"], "weko_shared_id": null}