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Modulation of fatty acid synthase by ATR checkpoint kinase Rad3
Shuwan Qiu 1,† , Sheng Liu 1,† , Zannati Ferdous Zaoti1, Xuejuan Wang 1,* , and Gang Cai 1,2,*
1 First Affiliated Hospital of USTC, School of Life Sciences, Hefei National Laboratory for Physical Sciences at Microscale, University of Science and Technology of China, Hefei 230027, China
2 CAS Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, Hefei 230026, China.
These authors contributed equally to this work.
*Correspondence to:Gang Cai, E-mail: gcai@ustc.edu.cn; Xuejuan Wang, E-mail: xuejuan@ustc.edu.cn
J Mol Cell Biol, Volume 11, Issue 12, December 2019, 1098-1100,  https://doi.org/10.1093/jmcb/mjz096

Fatty acid synthase (FAS) is the key enzyme for de novo fatty acid synthesis and exists widely from bacteria to mammalian cells (Schweizer and Hofmann, 2004). It is involved in membrane organization, metabolism regulation, energy storage, and many other processes (Maier et al., 2010). The ataxia telangiectasia-mutated and Rad3-related kinase (ATR) is a master regulator of DNA damage response (DDR) and is highly conserved. ATR is activated by DNA double-strand breaks and various types of DNA replication stresses (Cortez et al., 2001). Recent researches have reported that FAS seems closely related to genome stability (Wu et al., 2016). It has been proved that palmitic acid, the product of FAS, can inhibit ATR phosphorylation and kinase activity in mouse fibroblast (Zeng et al., 2008). These studies suggest that there is a crosstalk between fatty acid metabolism and DDR pathway, but the mechanism remains unknown.