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@ARTICLE{Jiang:292544,
      author       = {X. Jiang$^*$ and A. H. Baig$^*$ and G. Palazzo$^*$ and R.
                      Del Pizzo$^*$ and T. Bortecen$^*$ and S. Groessl$^*$ and E.
                      A. Zaal and C. C. Amaya Ramirez$^*$ and A. Kowar$^*$ and D.
                      Aviles-Huerta$^*$ and C. R. Berkers and W. Palm$^*$ and D.
                      Tschaharganeh$^*$ and J. Krijgsveld$^*$ and F.
                      Loayza-Puch$^*$},
      title        = {{P}53-dependent hypusination of e{IF}5{A} affects
                      mitochondrial translation and senescence immune
                      surveillance.},
      journal      = {Nature Communications},
      volume       = {15},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DKFZ-2024-01787},
      pages        = {7458},
      year         = {2024},
      note         = {#EA:B250#LA:B250#LA:B230#},
      abstract     = {Cellular senescence is characterized by a permanent growth
                      arrest and is associated with tissue aging and cancer.
                      Senescent cells secrete a number of different cytokines
                      referred to as the senescence-associated secretory phenotype
                      (SASP), which impacts the surrounding tissue and immune
                      response. Here, we find that senescent cells exhibit higher
                      rates of protein synthesis compared to proliferating cells
                      and identify eIF5A as a crucial regulator of this process.
                      Polyamine metabolism and hypusination of eIF5A play a
                      pivotal role in sustaining elevated levels of protein
                      synthesis in senescent cells. Mechanistically, we identify a
                      p53-dependent program in senescent cells that maintains
                      hypusination levels of eIF5A. Finally, we demonstrate that
                      functional eIF5A is required for synthesizing mitochondrial
                      ribosomal proteins and monitoring the immune clearance of
                      premalignant senescent cells in vivo. Our findings establish
                      an important role of protein synthesis during cellular
                      senescence and suggest a link between eIF5A, polyamine
                      metabolism, and senescence immune surveillance.},
      keywords     = {Peptide Initiation Factors: metabolism / Peptide Initiation
                      Factors: genetics / Eukaryotic Translation Initiation Factor
                      5A / Cellular Senescence / Tumor Suppressor Protein p53:
                      metabolism / RNA-Binding Proteins: metabolism / RNA-Binding
                      Proteins: genetics / Humans / Protein Biosynthesis /
                      Mitochondria: metabolism / Animals / Mice / Immunologic
                      Surveillance / Polyamines: metabolism / Ribosomal Proteins:
                      metabolism / Ribosomal Proteins: genetics / Lysine:
                      metabolism / Lysine: analogs $\&$ derivatives / Peptide
                      Initiation Factors (NLM Chemicals) / Eukaryotic Translation
                      Initiation Factor 5A (NLM Chemicals) / Tumor Suppressor
                      Protein p53 (NLM Chemicals) / RNA-Binding Proteins (NLM
                      Chemicals) / Polyamines (NLM Chemicals) / Ribosomal Proteins
                      (NLM Chemicals) / hypusine (NLM Chemicals) / Lysine (NLM
                      Chemicals)},
      cin          = {B250 / B230 / A330 / F190},
      ddc          = {500},
      cid          = {I:(DE-He78)B250-20160331 / I:(DE-He78)B230-20160331 /
                      I:(DE-He78)A330-20160331 / I:(DE-He78)F190-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39198484},
      pmc          = {pmc:PMC11358140},
      doi          = {10.1038/s41467-024-51901-w},
      url          = {https://inrepo02.dkfz.de/record/292544},
}