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@ARTICLE{Laise:180984,
      author       = {P. Laise and M. L. Stanifer and G. Bosker and X. Sun and S.
                      Triana and P. Doldan$^*$ and F. La Manna and M. De Menna and
                      R. B. Realubit and S. Pampou and C. Karan and T. Alexandrov
                      and M. Kruithof-de Julio and A. Califano and S. Boulant$^*$
                      and M. J. Alvarez},
      title        = {{A} model for network-based identification and
                      pharmacological targeting of aberrant,
                      replication-permissive transcriptional programs induced by
                      viral infection.},
      journal      = {Communications biology},
      volume       = {5},
      number       = {1},
      issn         = {2399-3642},
      address      = {London},
      publisher    = {Springer Nature},
      reportid     = {DKFZ-2022-01708},
      pages        = {714},
      year         = {2022},
      note         = {Research Group “Cellular Polarity and ViralInfection”,
                      German Cancer Research Center (DKFZ), Heidelberg, Germany.},
      abstract     = {SARS-CoV-2 hijacks the host cell transcriptional machinery
                      to induce a phenotypic state amenable to its replication.
                      Here we show that analysis of Master Regulator proteins
                      representing mechanistic determinants of the gene expression
                      signature induced by SARS-CoV-2 in infected cells revealed
                      coordinated inactivation of Master Regulators enriched in
                      physical interactions with SARS-CoV-2 proteins, suggesting
                      their mechanistic role in maintaining a host cell state
                      refractory to virus replication. To test their functional
                      relevance, we measured SARS-CoV-2 replication in epithelial
                      cells treated with drugs predicted to activate the entire
                      repertoire of repressed Master Regulators, based on their
                      experimentally elucidated, context-specific mechanism of
                      action. Overall, 15 of the 18 drugs predicted to be
                      effective by this methodology induced significant reduction
                      of SARS-CoV-2 replication, without affecting cell viability.
                      This model for host-directed pharmacological therapy is
                      fully generalizable and can be deployed to identify drugs
                      targeting host cell-based Master Regulator signatures
                      induced by virtually any pathogen.},
      keywords     = {COVID-19: drug therapy / Humans / SARS-CoV-2 /
                      Transcriptome / Virus Diseases / Virus Replication},
      cin          = {F140},
      ddc          = {570},
      cid          = {I:(DE-He78)F140-20160331},
      pnm          = {316 - Infektionen, Entzündung und Krebs (POF4-316)},
      pid          = {G:(DE-HGF)POF4-316},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:35854100},
      pmc          = {pmc:PMC9296638},
      doi          = {10.1038/s42003-022-03663-8},
      url          = {https://inrepo02.dkfz.de/record/180984},
}