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@ARTICLE{Rack:126086,
      author       = {P. G. Rack and J. Ni and A. Y. Payumo and V. Nguyen and J.
                      A. Crapster and V. Hovestadt$^*$ and M. Kool$^*$ and D.
                      Jones$^*$ and J. K. Mich and A. J. Firestone and S.
                      Pfister$^*$ and Y.-J. Cho and J. K. Chen},
      title        = {{A}rhgap36-dependent activation of {G}li transcription
                      factors.},
      journal      = {Proceedings of the National Academy of Sciences of the
                      United States of America},
      volume       = {111},
      number       = {30},
      issn         = {1091-6490},
      address      = {Washington, DC},
      publisher    = {National Acad. of Sciences},
      reportid     = {DKFZ-2017-02201},
      pages        = {11061 - 11066},
      year         = {2014},
      abstract     = {Hedgehog (Hh) pathway activation and Gli-dependent
                      transcription play critical roles in embryonic patterning,
                      tissue homeostasis, and tumorigenesis. By conducting a
                      genome-scale cDNA overexpression screen, we have identified
                      the Rho GAP family member Arhgap36 as a positive regulator
                      of the Hh pathway in vitro and in vivo. Arhgap36 acts in a
                      Smoothened (Smo)-independent manner to inhibit Gli repressor
                      formation and to promote the activation of full-length Gli
                      proteins. Arhgap36 concurrently induces the accumulation of
                      Gli proteins in the primary cilium, and its ability to
                      induce Gli-dependent transcription requires kinesin family
                      member 3a and intraflagellar transport protein 88, proteins
                      that are essential for ciliogenesis. Arhgap36 also
                      functionally and biochemically interacts with Suppressor of
                      Fused. Transcriptional profiling further reveals that
                      Arhgap36 is overexpressed in murine medulloblastomas that
                      acquire resistance to chemical Smo inhibitors and that
                      ARHGAP36 isoforms capable of Gli activation are up-regulated
                      in a subset of human medulloblastomas. Our findings reveal a
                      new mechanism of Gli transcription factor activation and
                      implicate ARHGAP36 dysregulation in the onset and/or
                      progression of GLI-dependent cancers.},
      keywords     = {GLI1 protein, human (NLM Chemicals) / GTPase-Activating
                      Proteins (NLM Chemicals) / Gli protein, mouse (NLM
                      Chemicals) / Hedgehog Proteins (NLM Chemicals) /
                      Kruppel-Like Transcription Factors (NLM Chemicals) / Nuclear
                      Proteins (NLM Chemicals) / Receptors, G-Protein-Coupled (NLM
                      Chemicals) / SMO protein, human (NLM Chemicals) / Smo
                      protein, mouse (NLM Chemicals) / Smoothened Receptor (NLM
                      Chemicals) / Transcription Factors (NLM Chemicals) /
                      Zebrafish Proteins (NLM Chemicals) / Zinc Finger Protein
                      GLI1 (NLM Chemicals)},
      cin          = {B060 / B062},
      ddc          = {000},
      cid          = {I:(DE-He78)B060-20160331 / I:(DE-He78)B062-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:25024229},
      pmc          = {pmc:PMC4121843},
      doi          = {10.1073/pnas.1322362111},
      url          = {https://inrepo02.dkfz.de/record/126086},
}