KAT2B Is Required for Pancreatic Beta Cell Adaptation to Metabolic Stress by Controlling the Unfolded Protein Response

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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

•: The expression of UPR markers is altered in diabetic islets
•: Loss of Kat2b contributes to defective insulin secretion and β cell compensation
•: KAT2B regulates an UPR gene program in pancreatic β cells
•: KAT2B expression is reduced in mouse and human diabetic β cells

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