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@MISC{Mller:279493,
      author       = {Müller, Stephan A and Lichtenthaler, Stefan},
      title        = {{D}ataset: {P}roteomics of {CLN}3-deficient murine
                      microglia identifies a disease associated phenotype with
                      lysosomal alterations},
      publisher    = {PRoteomics IDEntifications Database},
      reportid     = {DZNE-2025-00820},
      year         = {2024},
      abstract     = {Loss-of-function mutations in CLN3 cause juvenile Batten
                      disease, featuring neurodegeneration and early-stage
                      neuroinflammation. How loss of CLN3 function leads to early
                      neuroinflammation is not yet understood. Here, we have
                      comprehensively studied microglia from Cln3∆ex7/8 mice, a
                      genetically accurate disease model. Loss of CLN3 function in
                      microglia leads to lysosomal storage material accumulation
                      and abnormal morphology of subcellular organelles. We also
                      discovered pathological proteomic signatures consistent with
                      defects in lysosomal function and indicative of abnormal
                      lipid metabolism. CLN3-deficient microglia were unable to
                      efficiently turnover myelin and metabolize the associated
                      lipids, showing defects in lipid droplet formation and
                      cholesterol accumulation.},
      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/279493},
}