WEKO3
アイテム
{"_buckets": {"deposit": "739ad2df-e162-4971-a049-7f3091f010b1"}, "_deposit": {"created_by": 1, "id": "47722", "owners": [1], "pid": {"revision_id": 0, "type": "depid", "value": "47722"}, "status": "published"}, "_oai": {"id": "oai:repo.qst.go.jp:00047722", "sets": ["1"]}, "author_link": ["478834", "478835", "478836", "478833", "478837"], "item_8_biblio_info_7": {"attribute_name": "書誌情報", "attribute_value_mlt": [{"bibliographicIssueDates": {"bibliographicIssueDate": "2017-01", "bibliographicIssueDateType": "Issued"}, "bibliographicPageEnd": "17", "bibliographicPageStart": "10", "bibliographicVolumeNumber": "813", "bibliographic_titles": [{"bibliographic_title": "Mutation Research/Genetic Toxicology and Environmental Mutagenesis"}]}]}, "item_8_description_5": {"attribute_name": "抄録", "attribute_value_mlt": [{"subitem_description": "The antioxidative response mediated by transcription factor NRF2 is thought to be a pivotal cellular defense system against various extrinsic stresses. It has been reported that activation of the NRF2 pathway confers cells with resistance to ionizing radiation-induced damage. However, the underlying mechanism remains largely unknown. In the current research, it was found that α-particle radiation has the ability to stimulate NRF2 expression in human osteosarcoma U-2 OS cells. Knockdown of cellular NRF2 level by shRNA-mediated gene silencing decreased the survival rate, increased the micronucleus formation rate and apoptosis rate in irradiated cells. Consistently, knockdown of NRF2 resulted in decreased expression of p65 and Bcl-2, and increased expression of p53 and Bax. Besides, it was observed that increased expression of NRF2 was partially dependent on radiation induced phosphorylation of ERK 1/2. Further results showed that radiation promoted autophagy flux which leads to the enhanced phosphorylation of ERK 1/2, as evidenced by the resultls that knockdown of ATG5 (Autophagy protein 5) gene by shRNA suppressed both radiation induced ERK 1/2 phosphorylation and NRF2 upregulation. Based on these results, it is proposed that attenuation of NRF2 antioxidative pathway can sensitize U-2 OS cells to radiation, where NRF2 antioxidative response is regulated by autophagy mediated activation of ERK 1/2 kinases.", "subitem_description_type": "Abstract"}]}, "item_8_publisher_8": {"attribute_name": "出版者", "attribute_value_mlt": [{"subitem_publisher": "Elsevier"}]}, "item_8_relation_14": {"attribute_name": "DOI", "attribute_value_mlt": [{"subitem_relation_type_id": {"subitem_relation_type_id_text": "10.1016/j.mrgentox.2016.11.006", "subitem_relation_type_select": "DOI"}}]}, "item_8_relation_17": {"attribute_name": "関連サイト", "attribute_value_mlt": [{"subitem_relation_name": [{"subitem_relation_name_text": "http://www.sciencedirect.com/science/article/pii/S1383571816300742"}], "subitem_relation_type_id": {"subitem_relation_type_id_text": "http://www.sciencedirect.com/science/article/pii/S1383571816300742", "subitem_relation_type_select": "URI"}}]}, "item_8_source_id_9": {"attribute_name": "ISSN", "attribute_value_mlt": [{"subitem_source_identifier": "1383-5718", "subitem_source_identifier_type": "ISSN"}]}, "item_access_right": {"attribute_name": "アクセス権", "attribute_value_mlt": [{"subitem_access_right": "metadata only access", "subitem_access_right_uri": "http://purl.org/coar/access_right/c_14cb"}]}, "item_creator": {"attribute_name": "著者", "attribute_type": "creator", "attribute_value_mlt": [{"creatorNames": [{"creatorName": "Chen, Ni"}], "nameIdentifiers": [{"nameIdentifier": "478833", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Zhang, Rui"}], "nameIdentifiers": [{"nameIdentifier": "478834", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Konishi, Teruaki"}], "nameIdentifiers": [{"nameIdentifier": "478835", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Wang, Jun"}], "nameIdentifiers": [{"nameIdentifier": "478836", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "小西 輝昭", "creatorNameLang": "en"}], "nameIdentifiers": [{"nameIdentifier": "478837", "nameIdentifierScheme": "WEKO"}]}]}, "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": "Upregulation of NRF2 through autophagy/ERK 1/2 ameliorates ionizing radiation induced cell death of human osteosarcoma U-2 OS", "item_titles": {"attribute_name": "タイトル", "attribute_value_mlt": [{"subitem_title": "Upregulation of NRF2 through autophagy/ERK 1/2 ameliorates ionizing radiation induced cell death of human osteosarcoma U-2 OS"}]}, "item_type_id": "8", "owner": "1", "path": ["1"], "permalink_uri": "https://repo.qst.go.jp/records/47722", "pubdate": {"attribute_name": "公開日", "attribute_value": "2017-04-19"}, "publish_date": "2017-04-19", "publish_status": "0", "recid": "47722", "relation": {}, "relation_version_is_last": true, "title": ["Upregulation of NRF2 through autophagy/ERK 1/2 ameliorates ionizing radiation induced cell death of human osteosarcoma U-2 OS"], "weko_shared_id": -1}
Upregulation of NRF2 through autophagy/ERK 1/2 ameliorates ionizing radiation induced cell death of human osteosarcoma U-2 OS
https://repo.qst.go.jp/records/47722
https://repo.qst.go.jp/records/47722a40e9c75-6674-4de0-ac1e-afaa98b10dfc
Item type | 学術雑誌論文 / Journal Article(1) | |||||
---|---|---|---|---|---|---|
公開日 | 2017-04-19 | |||||
タイトル | ||||||
タイトル | Upregulation of NRF2 through autophagy/ERK 1/2 ameliorates ionizing radiation induced cell death of human osteosarcoma U-2 OS | |||||
言語 | ||||||
言語 | eng | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | journal article | |||||
アクセス権 | ||||||
アクセス権 | metadata only access | |||||
アクセス権URI | http://purl.org/coar/access_right/c_14cb | |||||
著者 |
Chen, Ni
× Chen, Ni× Zhang, Rui× Konishi, Teruaki× Wang, Jun× 小西 輝昭 |
|||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | The antioxidative response mediated by transcription factor NRF2 is thought to be a pivotal cellular defense system against various extrinsic stresses. It has been reported that activation of the NRF2 pathway confers cells with resistance to ionizing radiation-induced damage. However, the underlying mechanism remains largely unknown. In the current research, it was found that α-particle radiation has the ability to stimulate NRF2 expression in human osteosarcoma U-2 OS cells. Knockdown of cellular NRF2 level by shRNA-mediated gene silencing decreased the survival rate, increased the micronucleus formation rate and apoptosis rate in irradiated cells. Consistently, knockdown of NRF2 resulted in decreased expression of p65 and Bcl-2, and increased expression of p53 and Bax. Besides, it was observed that increased expression of NRF2 was partially dependent on radiation induced phosphorylation of ERK 1/2. Further results showed that radiation promoted autophagy flux which leads to the enhanced phosphorylation of ERK 1/2, as evidenced by the resultls that knockdown of ATG5 (Autophagy protein 5) gene by shRNA suppressed both radiation induced ERK 1/2 phosphorylation and NRF2 upregulation. Based on these results, it is proposed that attenuation of NRF2 antioxidative pathway can sensitize U-2 OS cells to radiation, where NRF2 antioxidative response is regulated by autophagy mediated activation of ERK 1/2 kinases. | |||||
書誌情報 |
Mutation Research/Genetic Toxicology and Environmental Mutagenesis 巻 813, p. 10-17, 発行日 2017-01 |
|||||
出版者 | ||||||
出版者 | Elsevier | |||||
ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 1383-5718 | |||||
DOI | ||||||
識別子タイプ | DOI | |||||
関連識別子 | 10.1016/j.mrgentox.2016.11.006 | |||||
関連サイト | ||||||
識別子タイプ | URI | |||||
関連識別子 | http://www.sciencedirect.com/science/article/pii/S1383571816300742 | |||||
関連名称 | http://www.sciencedirect.com/science/article/pii/S1383571816300742 |