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@ARTICLE{Bartl:180667,
      author       = {J. Bartl$^*$ and M. Zanini and F. Bernardi and A. Forget
                      and L. Blümel$^*$ and J. Talbot and D. Picard$^*$ and N.
                      Qin$^*$ and G. Cancila and Q. Gao and S. Nath and I. M.
                      Koumba$^*$ and M. Wolter$^*$ and F. Kuonen and M. Langini
                      and T. Beez and C. Munoz and D. Pauck$^*$ and V.
                      Marquardt$^*$ and H. Yu and J. Souphron and M. Korsch$^*$
                      and C. Mölders$^*$ and D. Berger$^*$ and S. Göbbels$^*$
                      and F.-D. Meyer$^*$ and B. Scheffler$^*$ and B. Rotblat and
                      S. Diederichs$^*$ and V. Ramaswamy and H. Suzuki and A. Oro
                      and K. Stühler and A. Stefanski and U. Fischer$^*$ and G.
                      Leprivier$^*$ and D. Willbold and G. Steger and A. Buell and
                      M. Kool$^*$ and P. Lichter$^*$ and S. Pfister$^*$ and P. A.
                      Northcott and M. D. Taylor and A. Borkhardt$^*$ and G.
                      Reifenberger$^*$ and O. Ayrault and M. Remke$^*$},
      title        = {{T}he {HHIP}-{AS}1 lnc{RNA} promotes tumorigenicity through
                      stabilization of dynein complex 1 in human {SHH}-driven
                      tumors.},
      journal      = {Nature Communications},
      volume       = {13},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DKFZ-2022-01467},
      pages        = {4061},
      year         = {2022},
      abstract     = {Most lncRNAs display species-specific expression patterns
                      suggesting that animal models of cancer may only
                      incompletely recapitulate the regulatory crosstalk between
                      lncRNAs and oncogenic pathways in humans. Among these
                      pathways, Sonic Hedgehog (SHH) signaling is aberrantly
                      activated in several human cancer entities. We unravel that
                      aberrant expression of the primate-specific lncRNA HedgeHog
                      Interacting Protein-AntiSense 1 (HHIP-AS1) is a hallmark of
                      SHH-driven tumors including medulloblastoma and atypical
                      teratoid/rhabdoid tumors. HHIP-AS1 is actively transcribed
                      from a bidirectional promoter shared with SHH regulator
                      HHIP. Knockdown of HHIP-AS1 induces mitotic spindle
                      deregulation impairing tumorigenicity in vitro and in vivo.
                      Mechanistically, HHIP-AS1 binds directly to the mRNA of
                      cytoplasmic dynein 1 intermediate chain 2 (DYNC1I2) and
                      attenuates its degradation by hsa-miR-425-5p. We uncover
                      that neither HHIP-AS1 nor the corresponding regulatory
                      element in DYNC1I2 are evolutionary conserved in mice. Taken
                      together, we discover an lncRNA-mediated mechanism that
                      enables the pro-mitotic effects of SHH pathway activation in
                      human tumors.},
      cin          = {ED01 / FR01 / B150 / B062 / HD01 / B060},
      ddc          = {500},
      cid          = {I:(DE-He78)ED01-20160331 / I:(DE-He78)FR01-20160331 /
                      I:(DE-He78)B150-20160331 / I:(DE-He78)B062-20160331 /
                      I:(DE-He78)HD01-20160331 / I:(DE-He78)B060-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:35831316},
      doi          = {10.1038/s41467-022-31574-z},
      url          = {https://inrepo02.dkfz.de/record/180667},
}