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000180984 0247_ $$2doi$$a10.1038/s42003-022-03663-8
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000180984 041__ $$aEnglish
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000180984 1001_ $$aLaise, Pasquale$$b0
000180984 245__ $$aA model for network-based identification and pharmacological targeting of aberrant, replication-permissive transcriptional programs induced by viral infection.
000180984 260__ $$aLondon$$bSpringer Nature$$c2022
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000180984 500__ $$aResearch Group “Cellular Polarity and ViralInfection”, German Cancer Research Center (DKFZ), Heidelberg, Germany.
000180984 520__ $$aSARS-CoV-2 hijacks the host cell transcriptional machinery to induce a phenotypic state amenable to its replication. Here we show that analysis of Master Regulator proteins representing mechanistic determinants of the gene expression signature induced by SARS-CoV-2 in infected cells revealed coordinated inactivation of Master Regulators enriched in physical interactions with SARS-CoV-2 proteins, suggesting their mechanistic role in maintaining a host cell state refractory to virus replication. To test their functional relevance, we measured SARS-CoV-2 replication in epithelial cells treated with drugs predicted to activate the entire repertoire of repressed Master Regulators, based on their experimentally elucidated, context-specific mechanism of action. Overall, 15 of the 18 drugs predicted to be effective by this methodology induced significant reduction of SARS-CoV-2 replication, without affecting cell viability. This model for host-directed pharmacological therapy is fully generalizable and can be deployed to identify drugs targeting host cell-based Master Regulator signatures induced by virtually any pathogen.
000180984 536__ $$0G:(DE-HGF)POF4-316$$a316 - Infektionen, Entzündung und Krebs (POF4-316)$$cPOF4-316$$fPOF IV$$x0
000180984 588__ $$aDataset connected to CrossRef, PubMed, , Journals: inrepo02.dkfz.de
000180984 650_2 $$2MeSH$$aCOVID-19: drug therapy
000180984 650_2 $$2MeSH$$aHumans
000180984 650_2 $$2MeSH$$aSARS-CoV-2
000180984 650_2 $$2MeSH$$aTranscriptome
000180984 650_2 $$2MeSH$$aVirus Diseases
000180984 650_2 $$2MeSH$$aVirus Replication
000180984 7001_ $$aStanifer, Megan L$$b1
000180984 7001_ $$aBosker, Gideon$$b2
000180984 7001_ $$aSun, Xiaoyun$$b3
000180984 7001_ $$aTriana, Sergio$$b4
000180984 7001_ $$0P:(DE-He78)51c7e0db09353baf8fff5d9a63da0abb$$aDoldan, Patricio$$b5
000180984 7001_ $$aLa Manna, Federico$$b6
000180984 7001_ $$aDe Menna, Marta$$b7
000180984 7001_ $$aRealubit, Ronald B$$b8
000180984 7001_ $$aPampou, Sergey$$b9
000180984 7001_ $$aKaran, Charles$$b10
000180984 7001_ $$aAlexandrov, Theodore$$b11
000180984 7001_ $$00000-0002-6085-7706$$aKruithof-de Julio, Marianna$$b12
000180984 7001_ $$00000-0003-4742-3679$$aCalifano, Andrea$$b13
000180984 7001_ $$0P:(DE-He78)4658b59d5b4e54b919fc63ab1213c78f$$aBoulant, Steeve$$b14
000180984 7001_ $$00000-0002-7503-2491$$aAlvarez, Mariano J$$b15
000180984 773__ $$0PERI:(DE-600)2919698-X$$a10.1038/s42003-022-03663-8$$gVol. 5, no. 1, p. 714$$n1$$p714$$tCommunications biology$$v5$$x2399-3642$$y2022
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