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@ARTICLE{Wagner:294321,
      author       = {R. Wagner$^*$ and L. Arnetzl$^*$ and T. Britto-Borges and
                      A. Heit-Mondrzyk$^*$ and A. Bakr$^*$ and E. Sollier$^*$ and
                      N. A. Gkatza and J. Panten$^*$ and S. Delaunay$^*$ and D.
                      Sohn$^*$ and P. Schmezer$^*$ and D. T. Odom$^*$ and K.
                      Müller-Decker and C. Plass$^*$ and C. Dieterich and P.
                      Lutsik$^*$ and S. Bornelöv and M. Frye$^*$},
      title        = {{SRSF}2 safeguards efficient transcription of {DNA} damage
                      and repair genes.},
      journal      = {Cell reports},
      volume       = {43},
      number       = {11},
      issn         = {2211-1247},
      address      = {[New York, NY]},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2024-02154},
      pages        = {114869},
      year         = {2024},
      note         = {#EA:A350#LA:A350#},
      abstract     = {The serine-/arginine-rich splicing factor 2 (SRSF2) plays
                      pivotal roles in pre-mRNA processing and gene transcription.
                      Recurrent mutations, particularly a proline-to-histidine
                      substitution at position 95 (P95H), are common in neoplastic
                      diseases. Here, we assess SRSF2's diverse functions in
                      squamous cell carcinoma. We show that SRSF2 deletion or
                      homozygous P95H mutation both cause extensive DNA damage
                      leading to cell-cycle arrest. Mechanistically, SRSF2
                      regulates efficient bi-directional transcription of DNA
                      replication and repair genes, independent from its function
                      in splicing. Further, SRSF2 haploinsufficiency induces DNA
                      damage without halting the cell cycle. Exposing mouse skin
                      to tumor-promoting carcinogens enhances the clonal expansion
                      of heterozygous Srsf2 P95H epidermal cells but unexpectedly
                      inhibits tumor formation. To survive carcinogen treatment,
                      Srsf2 P95H+/- cells undergo substantial transcriptional
                      rewiring and restore bi-directional gene expression. Thus,
                      our study underscores SRSF2's importance in regulating
                      transcription to orchestrate the cell cycle and the DNA
                      damage response.},
      keywords     = {CP: Cancer (Other) / CP: Molecular biology (Other) / DNA
                      damage (Other) / DNA repair (Other) / DNA replication
                      (Other) / Transcription (Other) / bi-directional promoters
                      (Other) / epithelia (Other) / skin (Other)},
      cin          = {A350 / B370 / B270},
      ddc          = {610},
      cid          = {I:(DE-He78)A350-20160331 / I:(DE-He78)B370-20160331 /
                      I:(DE-He78)B270-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39446588},
      doi          = {10.1016/j.celrep.2024.114869},
      url          = {https://inrepo02.dkfz.de/record/294321},
}