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@MISC{Mller:279499,
      author       = {Müller, Stephan A and Lichtenthaler, Stefan},
      title        = {{D}ataset: {E}ndogenous retroviruses promote prion-like
                      spreading of proteopathic seeds},
      publisher    = {PRoteomics IDEntifications Database},
      reportid     = {DZNE-2025-00826},
      year         = {2023},
      abstract     = {Prion-like spreading of protein misfolding is
                      characteristic for neurodegenerative diseases, but the exact
                      mechanisms of intercellular protein aggregate dissemination
                      remain unresolved. Evidence accumulates that endogenous
                      retroviruses, remnants of viral germline infections that are
                      normally epigenetically silenced, become upregulated in
                      neurodegenerative diseases such as amyotrophic lateral
                      sclerosis and tauopathies. Here we uncover that activation
                      of endogenous retroviruses affects prion-like spreading of
                      proteopathic seeds. To identify changes in the proteome of
                      donor cells that might contribute to protein aggregate
                      spreading, we performed mass spectrometry analyses of total
                      cell lysates and donor EV fractions using N2a cells
                      expressing HA epitope-tagged Sup35 NM prion protein at early
                      (P07) and late passages (P16) post cryopreservation. Among
                      the proteins increased in donor cells and EVs upon prolonged
                      culture, we identified mouse endogenous MLV retrovirus
                      proteins to be highly increased.},
      cin          = {AG Lichtenthaler},
      cid          = {I:(DE-2719)1110006},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)32},
      url          = {https://pub.dzne.de/record/279499},
}