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@ARTICLE{Liu:288814,
      author       = {K. Liu and L. Wehling and S. Wan and S. M. E. Weiler and M.
                      Tóth and D. Ibberson and S. Marhenke and A. Ali$^*$ and M.
                      Lam$^*$ and T. Guo and F. Pinna and F. Pedrini and A.
                      Damle-Vartak and A. Dropmann and F. Rose and S. Colucci and
                      W. Cheng and M. Bissinger and J. Schmitt and P. Birner and
                      T. Poth and P. Angel$^*$ and S. Dooley and M. U.
                      Muckenthaler and T. Longerich and A. Vogel and M.
                      Heikenwälder$^*$ and P. Schirmacher and K. Breuhahn},
      title        = {{D}ynamic {YAP} expression in the non-parenchymal liver
                      cell compartment controls heterologous cell communication.},
      journal      = {Cellular and molecular life sciences},
      volume       = {81},
      number       = {1},
      issn         = {1420-682X},
      address      = {Cham (ZG)},
      publisher    = {Springer International Publishing AG},
      reportid     = {DKFZ-2024-00485},
      pages        = {115},
      year         = {2024},
      abstract     = {The Hippo pathway and its transcriptional effectors
                      yes-associated protein (YAP) and transcriptional coactivator
                      with PDZ-binding motif (TAZ) are targets for cancer therapy.
                      It is important to determine if the activation of one factor
                      compensates for the inhibition of the other. Moreover, it is
                      unknown if YAP/TAZ-directed perturbation affects cell-cell
                      communication of non-malignant liver cells.To investigate
                      liver-specific phenotypes caused by YAP and TAZ
                      inactivation, we generated mice with hepatocyte (HC) and
                      biliary epithelial cell (BEC)-specific deletions for both
                      factors (YAPKO, TAZKO and double knock-out (DKO)).
                      Immunohistochemistry, single-cell sequencing, and proteomics
                      were used to analyze liver tissues and serum.The loss of
                      BECs, liver fibrosis, and necrosis characterized livers from
                      YAPKO and DKO mice. This phenotype was weakened in DKO
                      tissues compared to specimens from YAPKO animals. After
                      depletion of YAP in HCs and BECs, YAP expression was induced
                      in non-parenchymal cells (NPCs) in a cholestasis-independent
                      manner. YAP positivity was detected in subgroups of Kupffer
                      cells (KCs) and endothelial cells (ECs). The secretion of
                      pro-inflammatory chemokines and cytokines such as C-X-C
                      motif chemokine ligand 11 (CXCL11), fms-related receptor
                      tyrosine kinase 3 ligand (FLT3L), and soluble intercellular
                      adhesion molecule-1 (ICAM1) was increased in the serum of
                      YAPKO animals. YAP activation in NPCs could contribute to
                      inflammation via TEA domain transcription factor
                      (TEAD)-dependent transcriptional regulation of secreted
                      factors.YAP inactivation in HCs and BECs causes liver
                      damage, and concomitant TAZ deletion does not enhance but
                      reduces this phenotype. Additionally, we present a new
                      mechanism by which YAP contributes to cell-cell
                      communication originating from NPCs.},
      keywords     = {Animals / Mice / Endothelial Cells / Ligands / Liver /
                      Hepatocytes / Cell Communication / Cholangiocyte (Other) /
                      Endothelial cell (Other) / Hepatocyte (Other) / Hippo
                      pathway (Other) / Kupffer cell (Other) / Liver damage
                      (Other) / Proteomics (Other) / Single-cell analysis (Other)
                      / TAZ (Other) / Ligands (NLM Chemicals)},
      cin          = {F180 / D440 / A100},
      ddc          = {610},
      cid          = {I:(DE-He78)F180-20160331 / I:(DE-He78)D440-20160331 /
                      I:(DE-He78)A100-20160331},
      pnm          = {314 - Immunologie und Krebs (POF4-314)},
      pid          = {G:(DE-HGF)POF4-314},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:38436764},
      pmc          = {pmc:PMC10912141},
      doi          = {10.1007/s00018-024-05126-1},
      url          = {https://inrepo02.dkfz.de/record/288814},
}