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@ARTICLE{Yildiz:1019800,
      author       = {Yildiz, Can Bora and Kundu, Tathagata and Gehrmann, Julia
                      and Koesling, Jannis and Ravaei, Amin and Wolff, Philip and
                      Kraft, Florian and Maié, Tiago and Jakovcevski, Mira and
                      Pensold, Daniel and Zimmermann, Olav and Rossetti, Giulia
                      and Costa, Ivan G. and Zimmer-Bensch, Geraldine},
      title        = {{E}phrin{A}5 regulates cell motility by modulating
                      {S}nhg15/{DNA} triplex-dependent targeting of {DNMT}1 to the
                      {N}cam1 promoter},
      journal      = {Epigenetics $\&$ chromatin},
      volume       = {16},
      number       = {1},
      issn         = {1756-8935},
      address      = {London},
      publisher    = {BioMed Central},
      reportid     = {FZJ-2023-05631},
      pages        = {42},
      year         = {2023},
      abstract     = {Cell–cell communication is mediated by membrane receptors
                      and their ligands, such as the Eph/ephrin system,
                      orchestrating cell migration during development and in
                      diverse cancer types. Epigenetic mechanisms are key for
                      integrating external “signals”, e.g., from neighboring
                      cells, into the transcriptome in health and disease.
                      Previously, we reported ephrinA5 to trigger transcriptional
                      changes of lncRNAs and protein-coding genes in cerebellar
                      granule cells, a cell model for medulloblastoma. LncRNAs
                      represent important adaptors for epigenetic writers through
                      which they regulate gene expression. Here, we investigate a
                      lncRNA-mediated targeting of DNMT1 to specific gene loci by
                      the combined power of in silico modeling of RNA/DNA
                      interactions and wet lab approaches, in the context of the
                      clinically relevant use case of ephrinA5-dependent
                      regulation of cellular motility of cerebellar granule cells.
                      We provide evidence that Snhg15, a cancer-related lncRNA,
                      recruits DNMT1 to the Ncam1 promoter through RNA/DNA triplex
                      structure formation and the interaction with DNMT1. This
                      mediates DNA methylation-dependent silencing of Ncam1, being
                      abolished by ephrinA5 stimulation-triggered reduction of
                      Snhg15 expression. Hence, we here propose a triple helix
                      recognition mechanism, underlying cell motility regulation
                      via lncRNA-targeted DNA methylation in a clinically relevant
                      context.},
      cin          = {JSC / IAS-5 / INM-9},
      ddc          = {540},
      cid          = {I:(DE-Juel1)JSC-20090406 / I:(DE-Juel1)IAS-5-20120330 /
                      I:(DE-Juel1)INM-9-20140121},
      pnm          = {5111 - Domain-Specific Simulation $\&$ Data Life Cycle Labs
                      (SDLs) and Research Groups (POF4-511) / 5241 - Molecular
                      Information Processing in Cellular Systems (POF4-524) / GRK
                      2416 - GRK 2416: MultiSenses-MultiScales: Neue Ansätze zur
                      Aufklärung neuronaler multisensorischer Integration
                      (368482240) / OPSF678 - Establishing pipelines for machine
                      learning and molecular simulation-based prediction of
                      lncRNA-DNA-protein interactions (EXS-SF-OPSF678)},
      pid          = {G:(DE-HGF)POF4-5111 / G:(DE-HGF)POF4-5241 /
                      G:(GEPRIS)368482240 / G:(DE-82)EXS-SF-OPSF678},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {37880732},
      UT           = {WOS:001091019900001},
      doi          = {10.1186/s13072-023-00516-4},
      url          = {https://juser.fz-juelich.de/record/1019800},
}