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@ARTICLE{Wesener:292155,
      author       = {M. C. Wesener and S. M. E. Weiler and M. Bissinger and T.
                      F. Klessinger and F. Rose and S. Merker and M. Luzarowski
                      and T. Ruppert and B. Helm$^*$ and U. Klingmüller$^*$ and
                      P. Schirmacher and K. Breuhahn},
      title        = {{CRKL} {E}nhances {YAP} {S}ignaling through {B}inding and
                      {JNK}/{JUN} {P}athway {A}ctivation in {L}iver {C}ancer.},
      journal      = {International journal of molecular sciences},
      volume       = {25},
      number       = {15},
      issn         = {1422-0067},
      address      = {Basel},
      publisher    = {Molecular Diversity Preservation International},
      reportid     = {DKFZ-2024-01643},
      pages        = {8549},
      year         = {2024},
      abstract     = {The Hippo pathway transducers yes-associated protein (YAP)
                      and WW-domain containing transcription regulator 1
                      (WWTR1/TAZ) are key regulators of liver tumorigenesis,
                      promoting tumor formation and progression. Although the
                      first inhibitors are in clinical trials, targeting the
                      relevant upstream regulators of YAP/TAZ activity could prove
                      equally beneficial. To identify regulators of YAP/TAZ
                      activity in hepatocarcinoma (HCC) cells, we carried out a
                      proximity labelling approach (BioID) coupled with mass
                      spectrometry. We verified CRK-like proto-oncogene adaptor
                      protein (CRKL) as a new YAP-exclusive interaction partner.
                      CRKL is highly expressed in HCC patients, and its expression
                      is associated with YAP activity as well as poor survival
                      prognosis. In vitro experiments demonstrated CRKL-dependent
                      cell survival and the loss of YAP binding induced through
                      actin disruption. Moreover, we delineated the activation of
                      the JNK/JUN pathway by CRKL, which promoted YAP
                      transcription. Our data illustrate that CRKL not only
                      promoted YAP activity through its binding but also through
                      the induction of YAP transcription by JNK/JUN activation.
                      This emphasizes the potential use of targeting the JNK/JUN
                      pathway to suppress YAP expression in HCC patients.},
      keywords     = {Humans / Liver Neoplasms: metabolism / Liver Neoplasms:
                      pathology / Liver Neoplasms: genetics / Adaptor Proteins,
                      Signal Transducing: metabolism / Adaptor Proteins, Signal
                      Transducing: genetics / Transcription Factors: metabolism /
                      Transcription Factors: genetics / YAP-Signaling Proteins:
                      metabolism / Carcinoma, Hepatocellular: metabolism /
                      Carcinoma, Hepatocellular: pathology / Carcinoma,
                      Hepatocellular: genetics / Nuclear Proteins: metabolism /
                      Nuclear Proteins: genetics / Proto-Oncogene Mas / Cell Line,
                      Tumor / Protein Binding / MAP Kinase Signaling System / Gene
                      Expression Regulation, Neoplastic / Signal Transduction /
                      AP1 (Other) / BioID (Other) / CRK (Other) / HCC (Other) /
                      Hippo (Other) / MS (Other) / TEAD (Other) / c-Jun (Other) /
                      proteomics (Other) / survival (Other) / Adaptor Proteins,
                      Signal Transducing (NLM Chemicals) / Transcription Factors
                      (NLM Chemicals) / CRKL protein (NLM Chemicals) /
                      YAP-Signaling Proteins (NLM Chemicals) / MAS1 protein, human
                      (NLM Chemicals) / YAP1 protein, human (NLM Chemicals) /
                      Nuclear Proteins (NLM Chemicals) / Proto-Oncogene Mas (NLM
                      Chemicals)},
      cin          = {B200},
      ddc          = {540},
      cid          = {I:(DE-He78)B200-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39126118},
      pmc          = {pmc:PMC11312940},
      doi          = {10.3390/ijms25158549},
      url          = {https://inrepo02.dkfz.de/record/292155},
}