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Deamidation Shunts RelA from Mediating Inflammation to Aerobic Glycolysis

Authors
  • Zhao, Jun1
  • Tian, Mao1
  • Zhang, Shu1
  • Delfarah, Alireza2
  • Gao, Ruoyun1
  • Rao, Youliang1
  • Savas, Ali Can1
  • Lu, Anjie3
  • Bubb, Larissa1
  • Lei, Xiao4
  • Moshirian, Rosa1
  • Zhu, Wenjie5
  • Peng, Cheng3
  • Jiang, Taijiao5, 6
  • Chen, Lin4
  • Graham, Nicholas A.2
  • Feng, Pinghui1, 7
  • 1 Street, Los Angeles, CA 90089, USA
  • 2 Mork Family Department of Chemical Engineering and Materials Science, Norris Comprehensive Cancer Center, 3710 McClintock Avenue, Los Angeles, CA 90089, USA
  • 3 Department of Orthopedic and Plastic Surgery, The Third Xiangya Hospital of Central South University, Changsha, Hunan 410013, China
  • 4 Department of Molecular and Computational Biology, 1050 Childs Way, Los Angeles, CA 90089, USA
  • 5 & Peking Union Medical College, Beijing 100005, China
  • 6 Suzhou Institute of Systems Medicine, Suzhou 215123, China
  • 7 Lead Contact
Type
Published Article
Journal
Cell metabolism
Publication Date
Apr 22, 2020
Volume
31
Issue
5
Pages
937–955
Identifiers
DOI: 10.1016/j.cmet.2020.04.006
PMID: 32325032
PMCID: PMC7257911
Source
PubMed Central
License
Unknown

Abstract

CAD, the rate-limiting enzyme of the de novo pyrimidine synthesis pathway, deamidates RelA to promote aerobic glycolysis and cell proliferation at the expense of NF-κB-dependent gene expression and an inflammatory response.

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