Journal
CELL METABOLISM
Volume 19, Issue 4, Pages 694-701Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2014.03.009
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Funding
- National Cancer Institute of the National Institutes of Health [T32-CA009120-37]
- UCLA Scholars in Oncologic Molecular Imagining program
- UCLA Tumor Cell Biology Program
- NIH [R25T CA098010, DP2OD008454-01]
- United States Health and Human Services Ruth L. Kirschstein Institutional National Research Service [T32 CA 009056]
- NCI/NIH [P01 CA168585, R21 CA169993]
- American Cancer Society Research Scholar Award [RSG-12-257-01-TBE]
- CalTech-UCLA Joint Center for Translational Medicine
- National Center for Advancing Translational Sciences UCLA CTSI [UL1TR000124]
- Concern Foundation CONquer CanCER Now Award
- Searle Scholars Program
- Caltech/UCLA Nanosystems Biology Cancer Center [NCI U54 CA151819]
- UCLA Broad Stem Cell Research Center-Concern Foundation Research Award
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Virus infections trigger metabolic changes in host cells that support the bioenergetic and biosynthetic demands of viral replication. Although recent studies have characterized virus-induced changes in host cell metabolism (Munger et al., 2008; Terry et al., 2012), the molecular mechanisms by which viruses reprogram cellular metabolism have remained elusive. Here, we show that the gene product of adenovirus E4ORF1 is necessary for adenovirus-induced upregulation of host cell glucose metabolism and sufficient to promote enhanced glycolysis in cultured epithelial cells by activation of MYC. E4ORF1 localizes to the nucleus, binds to MYC, and enhances MYC binding to glycolytic target genes, resulting in elevated expression of specific glycolytic enzymes. E4ORF1 activation of MYC promotes increased nucleotide biosynthesis from glucose intermediates and enables optimal adenovirus replication in primary lung epithelial cells. Our findings show how a viral protein exploits host cell machinery to reprogram cellular metabolism and promote optimal progeny virion generation.
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