The Autism-Related Protein CHD8 Cooperates with C/EBPβ to Regulate Adipogenesis

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The Autism-Related Protein CHD8 Cooperates with C/EBPβ to Regulate Adipogenesis

Persistent ID (NDL): info:ndljp/pid/11246160

Material type: 博士論文

Author: 喜多, 泰之

Publisher: -

Publication date: 2018-10-31

Material Format: Digital

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Name of awarding university/degree: 九州大学,博士（医学）

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Note (General)：: The gene encoding the chromatin remodeler CHD8 is the most frequently mutated gene in individuals with autism spectrum disorder (ASD). Heterozygous mu...

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Material Type: 博士論文
Title: The Autism-Related Protein CHD8 Cooperates with C/EBPβ to Regulate Adipogenesis
Author/Editor: 喜多, 泰之
Publication Date: 2018-10-31
Publication Date (W3CDTF): 2018-10-31
Alternative Title: 自閉症関連タンパク質CHD8はC/EBPβと協調して脂肪分化を制御する
Contributor: 中島, 欽一
小川, 佳宏
鈴木, 淳史
Degree grantor/type: 九州大学
Date Granted: 2018-10-31
Date Granted (W3CDTF): 2018-10-31
Dissertation Number: 甲第14291号
Degree Type: 博士（医学）
Conferring No. (Dissertation): 甲第14291号
Text Language Code: eng
Note (General): The gene encoding the chromatin remodeler CHD8 is the most frequently mutated gene in individuals with autism spectrum disorder (ASD). Heterozygous mutations in CHD8 give rise to ASD that is often accompanied by macrocephaly, gastrointestinal complaints, and slender habitus. Whereas most phenotypes of CHD8 haploinsufficiency likely result from delayed neurodevelopment, the mechanism underlying slender habitus has remained unknown. Here, we show that CHD8 interacts with CCAAT/enhancer-binding protein β (C/EBPβ) and promotes its transactivation activity during adipocyte differentiation. Adipogenesis was impaired in Chd8-deleted preadipocytes, with the upregulation of C/EBPα and peroxisome-proliferator-activated receptor γ (PPARγ), two master regulators of this process, being attenuated in mutant cells. Furthermore, mice with CHD8 ablation in white preadipocytes had a markedly reduced white adipose tissue mass. Our findings reveal a mode of C/EBPβ regulation by CHD8 during adipogenesis, with CHD8 deficiency resulting in a defect in the development of white adipose tissue.
PubMed番号 : 29768199
DOI: info:doi/10.1016/j.celrep.2018.04.050
https://doi.org/info:doi/10.1016/j.celrep.2018.04.050
Persistent ID (NDL): info:ndljp/pid/11246160
https://dl.ndl.go.jp/pid/11246160
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): 2019-03-03T03:58:25+09:00
Date Created (W3CDTF): 2019-02-12
Format (IMT): application/pdf
Access Restrictions: 国立国会図書館内限定公開
Service for the Digitized Contents Transmission Service: 図書館・個人送信対象外
Availability of remote photoduplication service: 可
Periodical Title (URI): http://hdl.handle.net/2324/2198513
Data Provider (Database): 国立国会図書館 : 国立国会図書館デジタルコレクション
https://dl.ndl.go.jp