WEKO3
インデックスリンク
アイテム
{"_buckets": {"deposit": "0f46b19b-795b-4e28-a78b-b922525cb01c"}, "_deposit": {"created_by": 18, "id": "51503", "owners": [18], "pid": {"revision_id": 0, "type": "depid", "value": "51503"}, "status": "published"}, "_oai": {"id": "oai:kanazawa-u.repo.nii.ac.jp:00051503", "sets": ["3929"]}, "author_link": ["2734", "92945"], "item_9_biblio_info_8": {"attribute_name": "書誌情報", "attribute_value_mlt": [{"bibliographicIssueDates": {"bibliographicIssueDate": "2020-05-27", "bibliographicIssueDateType": "Issued"}, "bibliographicPageStart": "4p.", "bibliographicVolumeNumber": "2017-04-01 - 2020-03-31", "bibliographic_titles": [{"bibliographic_title": "令和1(2019)年度 科学研究費補助金 基盤研究(C) 研究成果報告書"}, {"bibliographic_title": "2019 Fiscal Year Final Research Report", "bibliographic_titleLang": "en"}]}]}, "item_9_creator_33": {"attribute_name": "著者別表示", "attribute_type": "creator", "attribute_value_mlt": [{"creatorNames": [{"creatorName": "Ishiyama, Ken"}], "nameIdentifiers": [{"nameIdentifier": "92945", "nameIdentifierScheme": "WEKO"}, {"nameIdentifier": "60377380", "nameIdentifierScheme": "e-Rad", "nameIdentifierURI": "https://kaken.nii.ac.jp/ja/search/?qm=60377380"}]}]}, "item_9_description_21": {"attribute_name": "抄録", "attribute_value_mlt": [{"subitem_description": "自己免疫性造血不全において、13番染色体長腕の部分欠失(del(13q))を持つ造血幹細胞が優先的に活性化されるメカニズムに、この欠失領域に位置するOLFM4の変異が関与しているか否かを明らかにするために、TF-1細胞及びヒトCD34陽性細胞におけるOLFM4 KOまたはノックダウンの影響を検討した。その結果OLFM4は、TGF-βによる造血幹細胞の赤血球分化を抑制しており、その発現低下は、GPIアンカー膜蛋白であるCD109の欠失と同様に、TGF-β存在下での造血幹細胞の赤血球分化を促進させることが明らかになった。", "subitem_description_type": "Abstract"}, {"subitem_description": "To clarify a role of OLFM4, a gene located in the commonly deleted region of 13q, in the preferential commitment of hematopoietic stem cells (HSCs) with del(13q) in patients with autoimmune hematopoietic failure, we examined the effects of OLFM4 knockout or knockdown in a leukemia cell line TF-1 and CD34+ cells derived from iPS cells or from cord blood. The OLFM4 gene downregulation promoted erythroid differentiation of both TF-1 and CD34+ cells induced by TGF-β. Similarly augmented erythroid differentiation was observed in HSCs that underwent the knockout of a GPI-anchored protein CD109. Haploinsufficiency of OLFM4 as a result of del(13q) may thus explain the preferential commitment of HSCs with del(13q) in bone marrow failure patients with paroxysmal nocturnal hemoglobinuria-phenotype cells.", "subitem_description_type": "Abstract"}]}, "item_9_description_22": {"attribute_name": "内容記述", "attribute_value_mlt": [{"subitem_description": "研究課題/領域番号:17K09947, 研究期間(年度):2017-04-01 - 2020-03-31", "subitem_description_type": "Other"}, {"subitem_description": "出典:「自己免疫性造血不全におけるdel(13q)クローン活性化機序の解明」研究成果報告書 課題番号17K09947\n(KAKEN:科学研究費助成事業データベース(国立情報学研究所))\n(https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-17K09947/17K09947seika/)を加工して作成", "subitem_description_type": "Other"}]}, "item_9_description_5": {"attribute_name": "提供者所属", "attribute_value_mlt": [{"subitem_description": "金沢大学附属病院血液内科", "subitem_description_type": "Other"}]}, "item_9_identifier_registration": {"attribute_name": "ID登録", "attribute_value_mlt": [{"subitem_identifier_reg_text": "10.24517/00057806", "subitem_identifier_reg_type": "JaLC"}]}, "item_9_relation_28": {"attribute_name": "関連URI", "attribute_value_mlt": [{"subitem_relation_name": [{"subitem_relation_name_text": "https://kaken.nii.ac.jp/search/?qm=60377380"}], "subitem_relation_type_id": {"subitem_relation_type_id_text": "https://kaken.nii.ac.jp/search/?qm=60377380", "subitem_relation_type_select": "URI"}}, {"subitem_relation_name": [{"subitem_relation_name_text": "https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-17K09947/"}], "subitem_relation_type_id": {"subitem_relation_type_id_text": "https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-17K09947/", "subitem_relation_type_select": "URI"}}, {"subitem_relation_name": [{"subitem_relation_name_text": "https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-17K09947/17K09947seika/"}], "subitem_relation_type_id": {"subitem_relation_type_id_text": "https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-17K09947/17K09947seika/", "subitem_relation_type_select": "URI"}}]}, "item_9_version_type_25": {"attribute_name": "著者版フラグ", "attribute_value_mlt": [{"subitem_version_resource": "http://purl.org/coar/version/c_ab4af688f83e57aa", "subitem_version_type": "AM"}]}, "item_creator": {"attribute_name": "著者", "attribute_type": "creator", "attribute_value_mlt": [{"creatorNames": [{"creatorName": "石山, 謙"}], "nameIdentifiers": [{"nameIdentifier": "2734", "nameIdentifierScheme": "WEKO"}, {"nameIdentifier": "60377380", "nameIdentifierScheme": "e-Rad", "nameIdentifierURI": "https://kaken.nii.ac.jp/ja/search/?qm=60377380"}, {"nameIdentifier": "60377380", "nameIdentifierScheme": "金沢大学研究者情報", "nameIdentifierURI": "http://ridb.kanazawa-u.ac.jp/public/detail.php?kaken=60377380"}, {"nameIdentifier": "60377380", "nameIdentifierScheme": "研究者番号", "nameIdentifierURI": "https://nrid.nii.ac.jp/nrid/1000060377380"}]}]}, "item_files": {"attribute_name": "ファイル情報", "attribute_type": "file", "attribute_value_mlt": [{"accessrole": "open_date", "date": [{"dateType": "Available", "dateValue": "2021-04-22"}], "displaytype": "detail", "download_preview_message": "", "file_order": 0, "filename": "HO-PR-ISHIYAMA-K-kaken 2020-4p.pdf", "filesize": [{"value": "82.7 kB"}], "format": "application/pdf", "future_date_message": "", "is_thumbnail": false, "licensetype": "license_11", "mimetype": "application/pdf", "size": 82700.0, "url": {"label": "HO-PR-ISHIYAMA-K-kaken 2020-4p.pdf", "url": "https://kanazawa-u.repo.nii.ac.jp/record/51503/files/HO-PR-ISHIYAMA-K-kaken 2020-4p.pdf"}, "version_id": "aeb8c16f-f127-4472-8c13-b84fbcb88c01"}]}, "item_keyword": {"attribute_name": "キーワード", "attribute_value_mlt": [{"subitem_subject": "自己免疫性造血不全", "subitem_subject_scheme": "Other"}, {"subitem_subject": "13番染色体長腕の部分欠失(del(13q))", "subitem_subject_scheme": "Other"}, {"subitem_subject": "OLFM4", "subitem_subject_scheme": "Other"}, {"subitem_subject": "TGF-β", "subitem_subject_scheme": "Other"}, {"subitem_subject": "赤血球分化", "subitem_subject_scheme": "Other"}, {"subitem_subject": "CD109", "subitem_subject_scheme": "Other"}, {"subitem_subject": "Hematology", "subitem_subject_language": "en", "subitem_subject_scheme": "Other"}]}, "item_language": {"attribute_name": "言語", "attribute_value_mlt": [{"subitem_language": "jpn"}]}, "item_resource_type": {"attribute_name": "資源タイプ", "attribute_value_mlt": [{"resourcetype": "research report", "resourceuri": "http://purl.org/coar/resource_type/c_18ws"}]}, "item_title": "自己免疫性造血不全におけるdel(13q)クローン活性化機序の解明", "item_titles": {"attribute_name": "タイトル", "attribute_value_mlt": [{"subitem_title": "自己免疫性造血不全におけるdel(13q)クローン活性化機序の解明"}, {"subitem_title": "Analysis of mechanisms underlying preferential commitment of hematopoietic stem cells with del(13q) in patients with autoimmune hematopoietic failure", "subitem_title_language": "en"}]}, "item_type_id": "9", "owner": "18", "path": ["3929"], "permalink_uri": "https://doi.org/10.24517/00057806", "pubdate": {"attribute_name": "公開日", "attribute_value": "2021-04-22"}, "publish_date": "2021-04-22", "publish_status": "0", "recid": "51503", "relation": {}, "relation_version_is_last": true, "title": ["自己免疫性造血不全におけるdel(13q)クローン活性化機序の解明"], "weko_shared_id": -1}
自己免疫性造血不全におけるdel(13q)クローン活性化機序の解明
https://doi.org/10.24517/00057806
https://doi.org/10.24517/0005780640e51c7a-c7d2-40bf-8b36-d8ded58d7451
名前 / ファイル | ライセンス | アクション |
---|---|---|
HO-PR-ISHIYAMA-K-kaken 2020-4p.pdf (82.7 kB)
|
Item type | 報告書 / Research Paper(1) | |||||
---|---|---|---|---|---|---|
公開日 | 2021-04-22 | |||||
タイトル | ||||||
タイトル | 自己免疫性造血不全におけるdel(13q)クローン活性化機序の解明 | |||||
タイトル | ||||||
言語 | en | |||||
タイトル | Analysis of mechanisms underlying preferential commitment of hematopoietic stem cells with del(13q) in patients with autoimmune hematopoietic failure | |||||
言語 | ||||||
言語 | jpn | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_18ws | |||||
資源タイプ | research report | |||||
ID登録 | ||||||
ID登録 | 10.24517/00057806 | |||||
ID登録タイプ | JaLC | |||||
著者 |
石山, 謙
× 石山, 謙 |
|||||
著者別表示 |
Ishiyama, Ken
× Ishiyama, Ken |
|||||
提供者所属 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 金沢大学附属病院血液内科 | |||||
書誌情報 |
令和1(2019)年度 科学研究費補助金 基盤研究(C) 研究成果報告書 en : 2019 Fiscal Year Final Research Report 巻 2017-04-01 - 2020-03-31, p. 4p., 発行日 2020-05-27 |
|||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | 自己免疫性造血不全において、13番染色体長腕の部分欠失(del(13q))を持つ造血幹細胞が優先的に活性化されるメカニズムに、この欠失領域に位置するOLFM4の変異が関与しているか否かを明らかにするために、TF-1細胞及びヒトCD34陽性細胞におけるOLFM4 KOまたはノックダウンの影響を検討した。その結果OLFM4は、TGF-βによる造血幹細胞の赤血球分化を抑制しており、その発現低下は、GPIアンカー膜蛋白であるCD109の欠失と同様に、TGF-β存在下での造血幹細胞の赤血球分化を促進させることが明らかになった。 | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | To clarify a role of OLFM4, a gene located in the commonly deleted region of 13q, in the preferential commitment of hematopoietic stem cells (HSCs) with del(13q) in patients with autoimmune hematopoietic failure, we examined the effects of OLFM4 knockout or knockdown in a leukemia cell line TF-1 and CD34+ cells derived from iPS cells or from cord blood. The OLFM4 gene downregulation promoted erythroid differentiation of both TF-1 and CD34+ cells induced by TGF-β. Similarly augmented erythroid differentiation was observed in HSCs that underwent the knockout of a GPI-anchored protein CD109. Haploinsufficiency of OLFM4 as a result of del(13q) may thus explain the preferential commitment of HSCs with del(13q) in bone marrow failure patients with paroxysmal nocturnal hemoglobinuria-phenotype cells. | |||||
内容記述 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 研究課題/領域番号:17K09947, 研究期間(年度):2017-04-01 - 2020-03-31 | |||||
内容記述 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 出典:「自己免疫性造血不全におけるdel(13q)クローン活性化機序の解明」研究成果報告書 課題番号17K09947 (KAKEN:科学研究費助成事業データベース(国立情報学研究所)) (https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-17K09947/17K09947seika/)を加工して作成 |
|||||
著者版フラグ | ||||||
出版タイプ | AM | |||||
出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||
関連URI | ||||||
識別子タイプ | URI | |||||
関連識別子 | https://kaken.nii.ac.jp/search/?qm=60377380 | |||||
関連名称 | https://kaken.nii.ac.jp/search/?qm=60377380 | |||||
関連URI | ||||||
識別子タイプ | URI | |||||
関連識別子 | https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-17K09947/ | |||||
関連名称 | https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-17K09947/ | |||||
関連URI | ||||||
識別子タイプ | URI | |||||
関連識別子 | https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-17K09947/17K09947seika/ | |||||
関連名称 | https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-17K09947/17K09947seika/ |