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@MISC{Mller:279492,
      author       = {Müller, Stephan A and Lichtenthaler, Stefan},
      title        = {{D}ataset: {P}lasma proteomics of {BACE}1, 2, and double
                      {KO} mice},
      publisher    = {PRoteomics IDEntifications Database},
      reportid     = {DZNE-2025-00819},
      year         = {2024},
      abstract     = {The beta-secretase BACE1 is a central drug target for
                      Alzheimer’s disease. Clinically tested, BACE1-directed
                      inhibitors also block the homologous protease BACE2. Yet,
                      little is known about physiological BACE2 substrates and
                      functions in vivo. Here, we performed glycoprotein
                      enrichment and subsequent discovery proteomics to identify
                      substrates of the protease BACE2 in plasma of mice.
                      Therefore, we analysed plasma from BACE2 KO, BACE1/2 double
                      KO and WT controls, as well as BACE1 KO with a separate WT
                      control. Inactivation of BACE2, but not BACE1, inhibited
                      shedding of VEGFR3/FLT4. Thus, sVEGFR3 represents a
                      pharmacodynamic plasma marker for BACE2 activity in vivo.},
      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/279492},
}