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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},
}