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We investigated the role of a core autophagy factor, Atg5, in the development of dextran sodium sulfate (DSS)-induced colitis. Intestinal epithelial cell (IEC)-specific Atg5 gene deficient mice (Atg5ΔIEC mice) were generated by cross of Atg5-floxed mice (Atg5fl/fl) with transgenic mice expressing Cre-recombinase driven by the villin promotor. Mice were given three cycles of 1.5% DSS in drinking water for 5 days and regular water for 14 days over a 60-day period. The dysfunction of autophagy characterized by a marked accumulation of p62 protein, a substrate for autophagy degradation, was detected in epithelial cells in the non-inflamed and inflamed mucosa of inflammatory bowel disease patients. DSS-colitis was exacerbated in Atg5ΔIEC mice compared to control Atg5fl/fl mice. Phosphorylation of inositol-requiring transmembrane kinase/endonuclease1α (IRE1α), a sensor for endoplasmic reticulum stress, and c-Jun N-terminal kinase, a downstream target of IRE1α, were significantly enhanced in IECs in DSS-treated Atg5ΔIEC mice. Accumulation of phosphorylated IRE1α was enhanced by the treatment with chloroquine, an autophagy inhibitor. Apoptotic IECs were more abundant in DSS-treated Atg5ΔIEC mice. These findings suggest that Atg5 suppresses endoplasmic reticulum stress-induced apoptosis of IECs via the degradation of excess p-IRE1α.", "subitem_description_type": "Abstract"}]}, "item_4_description_42": {"attribute_name": "資源タイプ", "attribute_value_mlt": [{"subitem_description": "Journal Article", "subitem_description_type": "Other"}]}, "item_4_publisher_32": {"attribute_name": "出版者", "attribute_value_mlt": [{"subitem_publisher": "一般社団法人　日本酸化ストレス学会"}]}, "item_4_publisher_34": {"attribute_name": "別言語の出版者", "attribute_value_mlt": [{"subitem_publisher": "SOCIETY FOR FREE RADICAL RESEARCH JAPAN"}]}, "item_4_relation_11": {"attribute_name": "DOI", "attribute_value_mlt": [{"subitem_relation_name": [{"subitem_relation_name_text": "10.3164/jcbn.20-90"}], "subitem_relation_type": "isIdenticalTo", "subitem_relation_type_id": {"subitem_relation_type_id_text": "https://doi.org/10.3164/jcbn.20-90", "subitem_relation_type_select": "DOI"}}]}, "item_4_relation_28": {"attribute_name": "論文ID（NAID）", 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{"creatorNames": [{"creatorName": "KUME, Shinji"}], "nameIdentifiers": [{"nameIdentifier": "1869", "nameIdentifierScheme": "WEKO"}, {"nameIdentifier": "00452235", "nameIdentifierScheme": "e-Rad", "nameIdentifierURI": "https://kaken.nii.ac.jp/ja/search/?qm=00452235"}, {"nameIdentifier": "0000-0001-6937-9715", "nameIdentifierScheme": "ORCID", "nameIdentifierURI": "https://orcid.org/0000-0001-6937-9715"}]}, {"creatorNames": [{"creatorName": "KAWAHARA, Masahiro"}], "nameIdentifiers": [{"nameIdentifier": "7509", "nameIdentifierScheme": "WEKO"}, {"nameIdentifier": "80617449", "nameIdentifierScheme": "e-Rad", "nameIdentifierURI": "https://kaken.nii.ac.jp/ja/search/?qm=80617449"}, {"nameIdentifier": "0000-0002-2721-7571", "nameIdentifierScheme": "ORCID", "nameIdentifierURI": "https://orcid.org/0000-0002-2721-7571"}]}, {"creatorNames": [{"creatorName": "MAEGAWA, Hiroshi"}], "nameIdentifiers": [{"nameIdentifier": "538", "nameIdentifierScheme": "WEKO"}, {"nameIdentifier": "00209363", 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