@article{DandekarFieselmannFischeretal.2014,
  author    = {Dandekar, Thomas and Fieselmann, Astrid and Fischer, Eva and Popp, Jasmin and Hensel, Michael and Noster, Janina},
  title     = {Salmonella—how a metabolic generalist adopts an intracellular lifestyle during infection},
  series = {Frontiers in Cellular and Infection Microbiology},
  volume    = {4},
  journal   = {Frontiers in Cellular and Infection Microbiology},
  number    = {191},
  issn      = {2235-2988},
  doi       = {10.3389/fcimb.2014.00191},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-120686},
  year      = {2014},
  abstract  = {The human-pathogenic bacterium Salmonella enterica adjusts and adapts to different environments while attempting colonization. In the course of infection nutrient availabilities change drastically. New techniques, "-omics" data and subsequent integration by systems biology improve our understanding of these changes. We review changes in metabolism focusing on amino acid and carbohydrate metabolism. Furthermore, the adaptation process is associated with the activation of genes of the Salmonella pathogenicity islands (SPIs). Anti-infective strategies have to take these insights into account and include metabolic and other strategies. Salmonella infections will remain a challenge for infection biology.},
  language  = {en}
}
@article{BensaadFavaroLewisetal.2014,
  author    = {Bensaad, Karim and Favaro, Elena and Lewis, Caroline A. and Peck, Barrie and Lord, Simon and Collins, Jennifer M. and Pinnick, Katherine E. and Wigfield, Simon and Buffa, Francesca M. and Li, Ji-Liang and Zhang, Qifeng and Wakelam, Michael J. O. and Karpe, Fredrik and Schulze, Almut and Harris, Adrian L.},
  title     = {Fatty Acid Uptake and Lipid Storage Induced by HIF-1 alpha Contribute to Cell Growth and Survival after Hypoxia-Reoxygenation},
  series = {Cell Reports},
  volume    = {9},
  journal   = {Cell Reports},
  number    = {1},
  issn      = {2211-1247},
  doi       = {10.1016/j.celrep.2014.08.056},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-115162},
  pages     = {349-365},
  year      = {2014},
  abstract  = {An in vivo model of antiangiogenic therapy allowed us to identify genes upregulated by bevacizumab treatment, including Fatty Acid Binding Protein 3 (FABP3) and FABP7, both of which are involved in fatty acid uptake. In vitro, both were induced by hypoxia in a hypoxia-inducible factor-1 alpha (HIF-1 alpha)-dependent manner. There was a significant lipid droplet (LD) accumulation in hypoxia that was time and O-2 concentration dependent. Knockdown of endogenous expression of FABP3, FABP7, or Adipophilin (an essential LD structural component) significantly impaired LD formation under hypoxia. We showed that LD accumulation is due to FABP3/7-dependent fatty acid uptake while de novo fatty acid synthesis is repressed in hypoxia. We also showed that ATP production occurs via beta-oxidation or glycogen degradation in a cell-type-dependent manner in hypoxia-reoxygenation. Finally, inhibition of lipid storage reduced protection against reactive oxygen species toxicity, decreased the survival of cells subjected to hypoxia-reoxygenation in vitro, and strongly impaired tumorigenesis in vivo.},
  language  = {en}
}