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@ARTICLE{Sachs:614226,
      author       = {Sachs, Wiebke and Blume, Lukas and Loreth, Desiree and
                      Schebsdat, Lisa and Hatje, Favian and Koehler, Sybille and
                      Wedekind, Uta and Sachs, Marlies and Zieliniski, Stephanie
                      and Brand, Johannes and Conze, Christian and Florea, Bogdan
                      I. and Heppner, Frank and Krüger, Elke and Rinschen, Markus
                      M. and Kretz, Oliver and Thünauer, Roland and
                      Meyer-Schwesinger, Catherine},
      title        = {{T}he proteasome modulates endocytosis specifically in
                      glomerular cells to promote kidney filtration},
      journal      = {Nature Communications},
      volume       = {15},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {PUBDB-2024-05766},
      pages        = {1897},
      year         = {2024},
      note         = {DFG Research Infrastructure Portal: $RI_00489$ for
                      excellent technical assistance},
      abstract     = {Kidney filtration is ensured by the interaction of
                      podocytes, endothelial and mesangial cells. Immunoglobulin
                      accumulation at the filtration barrier is pathognomonic for
                      glomerular injury. The mechanisms that regulate filter
                      permeability are unknown. Here, we identify a pivotal role
                      for the proteasome in a specific cell type. Combining
                      genetic and inhibitor-based human, pig, mouse, and
                      Drosophila models we demonstrate that the proteasome
                      maintains filtration barrier integrity, with podocytes
                      requiring the constitutive and glomerular endothelial cells
                      the immunoproteasomal activity. Endothelial immunoproteasome
                      deficiency as well as proteasome inhibition disrupt the
                      filtration barrier in mice, resulting in pathologic
                      immunoglobulin deposition. Mechanistically, we observe
                      reduced endocytic activity, which leads to altered membrane
                      recycling and endocytic receptor turnover. This work expands
                      the concept of the (immuno)proteasome as a control protease
                      orchestrating protein degradation and antigen presentation
                      and endocytosis, providing new therapeutic targets to treat
                      disease-associated glomerular protein accumulations.},
      cin          = {CSSB-CF-ALFM},
      ddc          = {500},
      cid          = {I:(DE-H253)CSSB-CF-ALFM-20210629},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      experiment   = {EXP:(DE-H253)ALFM-20250101},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:38429282},
      UT           = {WOS:001447479900019},
      doi          = {10.1038/s41467-024-46273-0},
      url          = {https://bib-pubdb1.desy.de/record/614226},
}