Suppression of RNF213, a susceptibility gene for moyamoya disease, inhibits endoplasmic reticulumstress through SEL1L upregulation

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Suppression of RNF213, a susceptibility gene for moyamoya disease, inhibits endoplasmic reticulumstress through SEL1L upregulation

Persistent ID (NDL): info:ndljp/pid/12769980

Material type: 博士論文

Author: AHMED, SHARIF

Publisher: 三重大学

Publication date: 2022-09-21

Material Format: Digital

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Name of awarding university/degree: 三重大学,博士(医学)

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Note (General)：: application/pdfRNF213, a susceptibility gene for moyamoya disease, is associated with stress responses to various stressors. We previously reported th...

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Material Type: 博士論文
Title: Suppression of RNF213, a susceptibility gene for moyamoya disease, inhibits endoplasmic reticulumstress through SEL1L upregulation
Author/Editor: AHMED, SHARIF
Author Heading: AHMED, SHARIF
Publication, Distribution, etc.: 三重大学
Publication Date: 2022-09-21
Publication Date (W3CDTF): 2022-09-21
Degree grantor/type: 三重大学
Date Granted: 2022-09-21
Date Granted (W3CDTF): 2022-09-21
Dissertation Number: 甲医学第2150号
Degree Type: 博士(医学)
Text Language Code: eng
Alias of Author: アハメド, シャリフ
Subject Heading: RNF213
Endoplasmic reticulum stress
SEL1L
HRD1
Moyamoya disease
Target Audience: 一般
Note (General): application/pdf
RNF213, a susceptibility gene for moyamoya disease, is associated with stress responses to various stressors. We previously reported that Rnf213 knockout (KO) mitigated endoplasmic reticulum (ER) stress-induced diabetes in the Akita mouse model of diabetes. However, the role of RNF213 in ER stress regulation remains unknown. In the present study, RNF213 knockdown significantly inhibited the upregulation of ER stress markers (CHOP and spliced XBP1) by chemical ER stress-inducers in HeLa cells. Levels of SEL1L, a critical molecule in ER-associated degradation (ERAD), were increased by RNF213 knockdown, and SEL1L knockdown prevented the inhibitory effect of RNF213 suppression on ER stress in HeLa cells, indicating SEL1L involvement in this inhibition of ER stress. SEL1L upregulation was also confirmed in pancreatic islets of Rnf213 KO/Akita mice and in Rnf213 KO mouse embryonic fibroblasts. Additionally, RNF213 suppression increased levels of HRD1, which forms a complex with SEL1L to degrade misfolded protein in cells under ER stress. In conclusion, we demonstrate that RNF213 depletion inhibits ER stress possibly through elevation of the SEL1L-HRD1 complex, thereby promoting ERAD in vitro and in vivo.
本文/Department of Environmental and Molecular Medicine, Mie University Graduate School of Medicine, Edobashi 2-174, Tsu, Mie, 514-8507, Japan
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Persistent ID (NDL): info:ndljp/pid/12769980
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Collection: 障害者向け資料
Collection (Materials For Handicapped People:1): テキストデータ
Collection (particular): 国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文
https://dl.ndl.go.jp/collections/A00014
Acquisition Basis: 博士論文（自動収集）
Date Accepted (W3CDTF): 2023-04-07T23:08:43+09:00
Format (IMT): application/pdf
Access Restrictions: 国立国会図書館内限定公開
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Availability of remote photoduplication service: 可
Periodical Title (URI): http://hdl.handle.net/10076/00021051
https://mie-u.repo.nii.ac.jp/records/15434
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