Acetate Recapturing by Nuclear Acetyl-CoA Synthetase 2 Prevents Loss of Histone Acetylation during Oxygen and Serum Limitation

详细信息    查看全文

• 作者：Vinay Bulusu¹ ; ² ; Sergey Tumanov¹ ; ² ; Evdokia Michalopoulou¹ ; ² ; Niels J. van den Broek¹ ; Gillian MacKay¹ ; Colin Nixon¹ ; Sandeep Dhayade¹ ; Zachary T. Schug¹ ; ³ ; Johan Vande Voorde¹ ; Karen Blyth¹ ; Eyal Gottlieb¹ ; Alexei Vazquez¹ ; Jurre J. Kamphorst¹ ; ² ; ⁴ ; ^{jurre.kamphorst@glasgow.ac.uk}
• 关键词：acetate ; acetyl-CoA synthetase 2 ; cancer metabolism ; enzyme localization ; histone acetylation ; histone deacetylation ; hypoxia ; lipogenesis ; metabolite compartmentalization ; stable isotope tracing
• 刊名：Cell Reports
• 出版年：2017
• 出版时间：17 January 2017
• 年：2017
• 卷：18
• 期：3
• 页码：647-658
• 全文大小：3894 K
• 卷排序：18

文摘

Acetyl-CoA synthetase 2 (ACSS2) expression controls acetate uptake and utilization Exogenous acetate is used for fatty acid synthesis rather than histone acetylation The main function of nuclear ACSS2 is to retain acetate released from histones Nuclear and cytosolic acetyl-CoA pools are largely compartmentalized