Inflammatory macrophage dependence on NAD+ salvage is a consequence of reactive oxygen species–mediated DNA damage
Alanna M. Cameron(Max Planck Institute of Immunobiology and Epigenetics), Edward J. Pearce(Bloomberg (United States)), Cameron S. Field(Max Planck Institute of Immunobiology and Epigenetics), Fabian Hässler(Max Planck Institute of Immunobiology and Epigenetics), Ryan Kyle(Max Planck Institute of Immunobiology and Epigenetics), Daniel J. Puleston(Bloomberg (United States)), David E. Sanin(Agency for Science, Technology and Research), Erika L. Pearce(Bloomberg (United States)), Joerg M. Buescher(VIB-KU Leuven Center for Microbiology), Lea J. Flachsmann(University of Freiburg), Ângela Castoldi(Max Planck Institute of Immunobiology and Epigenetics), Annette E. Patterson(Max Planck Institute of Immunobiology and Epigenetics), Beth Kelly(Bloomberg (United States))
Cited by 267
Related Papers
Metabolic reprogramming in macrophages and dendritic cells in innate immunity
|Cell Research|2015|1.8k
Itaconate Links Inhibition of Succinate Dehydrogenase with Macrophage Metabolic Remodeling and Regulation of Inflammation
|Cell Metabolism|2016|1.5k
Toll-like receptor–induced changes in glycolytic metabolism regulate dendritic cell activation
|Blood|2010|1.2k
TLR-driven early glycolytic reprogramming via the kinases TBK1-IKKɛ supports the anabolic demands of dendritic cell activation
|Nature Immunology|2014|1k
A roadmap for interpreting 13C metabolite labeling patterns from cells
|Current Opinion in Biotechnology|2015|652