KAT2B Is Required for Pancreatic Beta Cell Adaptation to Metabolic Stress by Controlling the Unfolded Protein Response
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- 作者：Nabil Rabhi1 ; 2 ; 3 ; Pierre-Damien Denechaud4 ; Xavier Gromada1 ; 2 ; 3 ; Sarah Anissa Hannou1 ; 2 ; 3 ; Hongbo Zhang5 ; Talha Rashid1 ; 2 ; 3 ; Elisabet Salas1 ; 2 ; 3 ; Emmanuelle Durand1 ; 2 ; 3 ; Olivier Sand1 ; 2 ; 3 ; Amé ; lie Bonnefond1 ; 2 ; 3 ; Loic Yengo1 ; 2 ; 3 ; Carine Chavey6 ; Caroline Bonner7 ; Julie Kerr-Conte7 ; Amar Abderrahmani1 ; 2 ; 3 ; Johan Auwerx5 ; Lluis Fajas4 ; Philippe Froguel1 ; 2 ; 3 ; 8 ; p.froguel@imperial.ac.uk" class="auth_mail" title="E-mail the corresponding author ; Jean-Sé ; bastien Annicotte1 ; 2 ; 3 ; jean-sebastien.annicotte@inserm.fr" class="auth_mail" title="E-mail the corresponding author
- 刊名：Cell Reports
- 出版年：2016
- 出版时间：3 May 2016
- 年：2016
- 卷：15
- 期：5
- 页码：1051-1061
- 全文大小：3774 K
文摘
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The expression of UPR markers is altered in diabetic islets
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Loss of Kat2b contributes to defective insulin secretion and β cell compensation
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KAT2B regulates an UPR gene program in pancreatic β cells
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KAT2B expression is reduced in mouse and human diabetic β cells