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The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.

Targeting Metabolic Reprogramming by Influenza Infection for Therapeutic Intervention

Smallwood, Heather S., Duan, Susu, Morfouace, Marie, Rezinciuc, Svetlana, Shulkin, Barry L., Shelat, Anang, Zink, Erika E., Milasta, Sandra, Bajracharya, Resha, Oluwaseum, Ajayi J., Roussel, Martine F., Green, Douglas R., Pasa-Tolic, Ljiljana, Thomas, Paul G.·2017·Cell Reports
DOI 10.1016/j.celrep.2017.04.039PMC PMC5599215
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  • In previous preclinical studies, inhibition of mTOR or a target downstream of mTOR protected mice from viral RTIs and upregulated IFN-induced antiviral immune responses.

    “In previous preclinical studies, inhibition of mechanistic target of rapamycin (mTOR) or a target downstream of mTOR protected mice from viral RTIs and upregulated IFN-induced antiviral immune responses.8, 9”

    From Targeting the biology of ageing with mTOR inhibitors to improve immune function in older adults: phase 2b and phase 3 randomised trials (2021) · cites this paper as [9]

    The Results section ('BEZ235 rescues mice from lethal influenza infection'; page unavailable) reports improved survival and reduced viral titers in influenza-infected mice treated with the PI3K/mTOR inhibitor BEZ235. The paper does not report that treatment upregulated IFN-induced antiviral responses or that inhibiting a target downstream of mTOR protected mice. (LLM, conf=0.88)

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Research works printed but not linked: 34

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  4. Csibi, 2014, The mTORC1/S6K1 pathway regulates glutamine metabolism through the eIF4B-dependent control of c-Myc translation, Curr. Biol., 24, 2274, 10.1016/j.cub.2014.08.007 · DOI
  5. Dang, 1999, c-Myc target genes involved in cell growth, apoptosis, and metabolism, Mol. Cell. Biol., 19, 1, 10.1128/MCB.19.1.1 · DOI
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  7. Duffy, 2014, GSK3 inhibitors regulate MYCN mRNA levels and reduce neuroblastoma cell viability through multiple mechanisms, including p53 and Wnt signaling, Mol. Cancer Ther., 13, 454, 10.1158/1535-7163.MCT-13-0560-T · DOI
  8. Hammoudeh, 2009, Multiple independent binding sites for small-molecule inhibitors on the oncoprotein c-Myc, J. Am. Chem. Soc., 131, 7390, 10.1021/ja900616b · DOI
  9. Hirata, 2014, Inhibition of Akt kinase activity suppresses entry and replication of influenza virus, Biochem. Biophys. Res. Commun., 450, 891, 10.1016/j.bbrc.2014.06.077 · DOI
  10. Hue, 2002, Insulin and ischemia stimulate glycolysis by acting on the same targets through different and opposing signaling pathways, J. Mol. Cell. Cardiol., 34, 1091, 10.1006/jmcc.2002.2063 · DOI
  11. Isler, 2005, Production of infectious human cytomegalovirus virions is inhibited by drugs that disrupt calcium homeostasis in the endoplasmic reticulum, J. Virol., 79, 15388, 10.1128/JVI.79.24.15388-15397.2005 · DOI
  12. Jonges, 2010, Influenza virus inactivation for studies of antigenicity and phenotypic neuraminidase inhibitor resistance profiling, J. Clin. Microbiol., 48, 928, 10.1128/JCM.02045-09 · DOI
  13. Julander, 2011, Use of plethysmography in assessing the efficacy of antivirals in a mouse model of pandemic influenza A virus, Antiviral Res., 92, 228, 10.1016/j.antiviral.2011.08.011 · DOI
  14. Legge, 2003, Accelerated migration of respiratory dendritic cells to the regional lymph nodes is limited to the early phase of pulmonary infection, Immunity, 18, 265, 10.1016/S1074-7613(03)00023-2 · DOI
  15. Li, 2015, Clinical implications of antiviral resistance in influenza, Viruses, 7, 4929, 10.3390/v7092850 · DOI
  16. Lin, 2009, Gene regulation and epigenetic remodeling in murine embryonic stem cells by c-Myc, PLoS ONE, 4, e7839, 10.1371/journal.pone.0007839 · DOI
  17. Marsin, 2002, The stimulation of glycolysis by hypoxia in activated monocytes is mediated by AMP-activated protein kinase and inducible 6-phosphofructo-2-kinase, J. Biol. Chem., 277, 30778, 10.1074/jbc.M205213200 · DOI
  18. Monroe, 2008, MASIC: a software program for fast quantitation and flexible visualization of chromatographic profiles from detected LC-MS(/MS) features, Comput. Biol. Chem., 32, 215, 10.1016/j.compbiolchem.2008.02.006 · DOI
  19. Munger, 2008, Systems-level metabolic flux profiling identifies fatty acid synthesis as a target for antiviral therapy, Nat. Biotechnol., 26, 1179, 10.1038/nbt.1500 · DOI
  20. Murray, 2012, Inhibition of influenza A virus replication by antagonism of a PI3K-AKT-mTOR pathway member identified by gene-trap insertional mutagenesis, Antivir. Chem. Chemother., 22, 205, 10.3851/IMP2080 · DOI
  21. Newsholme, 1985, The role of high rates of glycolysis and glutamine utilization in rapidly dividing cells, Biosci. Rep., 5, 393, 10.1007/BF01116556 · DOI
  22. Oshansky, 2012, The human side of influenza, J. Leukoc. Biol., 92, 83, 10.1189/jlb.1011506 · DOI
  23. Rahl, 2010, c-Myc regulates transcriptional pause release, Cell, 141, 432, 10.1016/j.cell.2010.03.030 · DOI · Paper page
  24. Ritter, 2010, Metabolic effects of influenza virus infection in cultured animal cells: Intra- and extracellular metabolite profiling, BMC Syst. Biol., 4, 61, 10.1186/1752-0509-4-61 · DOI
  25. Sanders, 2013, Compromised respiratory function in lethal influenza infection is characterized by the depletion of type I alveolar epithelial cells beyond threshold levels, Am. J. Physiol. Lung Cell. Mol. Physiol., 304, L481, 10.1152/ajplung.00343.2012 · DOI
  26. Shaneyfelt, 2006, Natural products that reduce rotavirus infectivity identified by a cell-based moderate-throughput screening assay, Virol. J., 3, 68, 10.1186/1743-422X-3-68 · DOI
  27. Shin, 2007, Effect of the phosphatidylinositol 3-kinase/Akt pathway on influenza A virus propagation, J. Gen. Virol., 88, 942, 10.1099/vir.0.82483-0 · DOI
  28. Smith, 2012, Effects of acutely inhibiting PI3K isoforms and mTOR on regulation of glucose metabolism in vivo, Biochem. J., 442, 161, 10.1042/BJ20111913 · DOI
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  31. Wang, 2015, Structurally diverse c-Myc inhibitors share a common mechanism of action involving ATP depletion, Oncotarget, 6, 15857, 10.18632/oncotarget.4327 · DOI
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  33. Yu, 2011, Viral effects on metabolism: changes in glucose and glutamine utilization during human cytomegalovirus infection, Trends Microbiol., 19, 360, 10.1016/j.tim.2011.04.002 · DOI
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Metadata

Authors
Smallwood, H. S., Duan, S., Morfouace, M., Rezinciuc, S., Shulkin, B. L., Shelat, A., Zink, E. E., Milasta, S., Bajracharya, R., Oluwaseum, A. J., Roussel, M. F., Green, D. R., Pasa-Tolic, L., & Thomas, P. G.
Venue
Cell Reports
Publisher
Elsevier BV
Published
2017-05
Volume
19
Issue
8
Pages
1640-1653
ISSN
2211-1247
DOI
10.1016/j.celrep.2017.04.039
PMC
PMC5599215
Cited by
171
References
3
Language
en
Licence
Funders
  • National Institute for Allergy and Infectious Diseases (AI091938, HHSN266200700005C, HHSN272201400006C)
  • V Foundation Grant and Cancer Center grant (CA-21765)
  • American Lebanese Syrian Associated Charities
  • NIH National Center for Research Resources (RR018522)
  • Department of Energy’s W.R. Wiley Environmental Molecular Science Laboratory at the Pacific Northwest National Laboratory (DE-AC05-76RL0 1830)

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