2024
CRISPR-based dissection of microRNA-23a ~ 27a ~ 24-2 cluster functionality in hepatocellular carcinoma
Cui M, Liu Z, Wang S, Bae S, Guo H, Zhou J, Liu R, Wang L. CRISPR-based dissection of microRNA-23a ~ 27a ~ 24-2 cluster functionality in hepatocellular carcinoma. Oncogene 2024, 43: 2708-2721. PMID: 39112518, PMCID: PMC11364504, DOI: 10.1038/s41388-024-03115-z.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCarcinoma, HepatocellularCell Line, TumorCell MovementCell ProliferationClustered Regularly Interspaced Short Palindromic RepeatsCRISPR-Cas SystemsEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansLiver NeoplasmsMiceMicroRNAsMultigene FamilyConceptsMiR-23aMiR-27aCRISPR interferenceCRISPR activationHigh-throughput RNA-seqCell migrationCDK1/cyclin B activityReduced cell growth in vitroMiRNA target predictionCell cycle arrestMiRNA clusterHepatocellular carcinoma cellsCell growth in vitroRNA-seqGene networksTarget predictionCRISPR knockoutOncogenic roleGrowth in vitroCycle arrestMature miRNAsMiRNAsG2/M phaseSignaling pathwayOncogenic functionPositive selection CRISPR screens reveal a druggable pocket in an oligosaccharyltransferase required for inflammatory signaling to NF-κB
Lampson B, Ramίrez A, Baro M, He L, Hegde M, Koduri V, Pfaff J, Hanna R, Kowal J, Shirole N, He Y, Doench J, Contessa J, Locher K, Kaelin W. Positive selection CRISPR screens reveal a druggable pocket in an oligosaccharyltransferase required for inflammatory signaling to NF-κB. Cell 2024, 187: 2209-2223.e16. PMID: 38670073, PMCID: PMC11149550, DOI: 10.1016/j.cell.2024.03.022.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCatalytic DomainClustered Regularly Interspaced Short Palindromic RepeatsCRISPR-Cas SystemsCryoelectron MicroscopyGlycosylationHEK293 CellsHexosyltransferasesHumansInflammationLipopolysaccharidesMembrane ProteinsMiceNF-kappa BSignal TransductionToll-Like Receptor 4ConceptsWhole-genome CRISPR-Cas9 screenCRISPR-Cas9 screensCryoelectron microscopy studiesCell surface localizationLipopolysaccharide receptor Toll-like receptor 4OST complexToll-like receptor 4CRISPR screensNF-kBCatalytic subunitN-glycosylationActivate NF-kBBase editorsUncompetitive inhibition mechanismNGI-1Molecular mechanismsCatalytic siteLPS-treated cellsOligosaccharyltransferaseDruggable pocketSTT3AReceptor Toll-like receptor 4Drug mechanism of actionStructural studiesInflammatory signalingTherapeutic targeting Tudor domains in leukemia via CRISPR-Scan Assisted Drug Discovery
Chan A, Han L, Delaney C, Wang X, Mukhaleva E, Li M, Yang L, Pokharel S, Mattson N, Garcia M, Wang B, Xu X, Zhang L, Singh P, Elsayed Z, Chen R, Kuang B, Wang J, Yuan Y, Chen B, Chan L, Rosen S, Horne D, Müschen M, Chen J, Vaidehi N, Armstrong S, Su R, Chen C. Therapeutic targeting Tudor domains in leukemia via CRISPR-Scan Assisted Drug Discovery. Science Advances 2024, 10: eadk3127. PMID: 38394203, PMCID: PMC10889360, DOI: 10.1126/sciadv.adk3127.Peer-Reviewed Original ResearchMeSH KeywordsAcetyltransferasesClustered Regularly Interspaced Short Palindromic RepeatsDrug DiscoveryHumansLeukemiaTudor DomainConceptsTudor domainDrug discoveryRibosomal gene expressionMolecular dynamics simulationsDomain-focused CRISPR screeningDe novo drug discoveryCompound dockingAcetyltransferase complexCRISPR screensGenetic approachesLead inhibitorDynamics simulationsStructural genetics approachGene expressionH3K9 acetylationEpigenetic dysregulationSgf29Tile scansLeukemia progressionMultiple cancersDrug developmentDiscoveryH3K9DockingLeukemia
2022
Double knockout CRISPR screen for cancer resistance to T cell cytotoxicity
Park J, Codina A, Ye L, Lam S, Guo J, Clark P, Zhou X, Peng L, Chen S. Double knockout CRISPR screen for cancer resistance to T cell cytotoxicity. Journal Of Hematology & Oncology 2022, 15: 172. PMID: 36456981, PMCID: PMC9716677, DOI: 10.1186/s13045-022-01389-y.Peer-Reviewed Original ResearchMeSH KeywordsClustered Regularly Interspaced Short Palindromic RepeatsHumansImmunotherapyMutationNeoplasmsT-LymphocytesConceptsT cell cytotoxicityCell cytotoxicityT cell killingTumor suppressorCancer patientsImmune responseAvailable agentsSurvival analysisClinical patientsCancer treatmentCancer cellsCancer resistanceDirect targetingPotential new conceptCancer mutationsPatientsCell killingNormal samplesResistance pathwaysCellular responsesSuch resistanceCytotoxicityResistance genesGenome-wide bidirectional CRISPR screens identify mucins as host factors modulating SARS-CoV-2 infection
Biering SB, Sarnik SA, Wang E, Zengel JR, Leist SR, Schäfer A, Sathyan V, Hawkins P, Okuda K, Tau C, Jangid AR, Duffy CV, Wei J, Gilmore RC, Alfajaro MM, Strine MS, Nguyenla X, Van Dis E, Catamura C, Yamashiro LH, Belk JA, Begeman A, Stark JC, Shon DJ, Fox DM, Ezzatpour S, Huang E, Olegario N, Rustagi A, Volmer AS, Livraghi-Butrico A, Wehri E, Behringer RR, Cheon DJ, Schaletzky J, Aguilar HC, Puschnik AS, Button B, Pinsky BA, Blish CA, Baric RS, O’Neal W, Bertozzi CR, Wilen CB, Boucher RC, Carette JE, Stanley SA, Harris E, Konermann S, Hsu PD. Genome-wide bidirectional CRISPR screens identify mucins as host factors modulating SARS-CoV-2 infection. Nature Genetics 2022, 54: 1078-1089. PMID: 35879412, PMCID: PMC9355872, DOI: 10.1038/s41588-022-01131-x.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsClustered Regularly Interspaced Short Palindromic RepeatsCOVID-19Epigenesis, GeneticHumansMiceMucinsSARS-CoV-2ConceptsSARS-CoV-2 infectionHost factorsSARS-CoV-2 entry factors ACE2SARS-CoV-2-host interactionsSevere acute respiratory syndrome coronavirus 2Acute respiratory syndrome coronavirus 2Respiratory syndrome coronavirus 2Diverse respiratory virusesMild respiratory illnessRespiratory distress syndromeSARS-CoV-2 host factorsHost-directed therapeuticsSyndrome coronavirus 2Coronavirus disease 2019Human lung epithelial cellsRange of symptomsHost defense mechanismsLung epithelial cellsGenome-wide CRISPR knockoutDistress syndromeRespiratory virusesRespiratory illnessCoronavirus 2Cell cycle regulationHigh molecular weight glycoproteinsInhibition of a Chromatin and Transcription Modulator, SLTM, Increases HIV-1 Reactivation Identified by a CRISPR Inhibition Screen
Pedersen SF, Collora JA, Kim RN, Yang K, Razmi A, Catalano AA, Yeh YJ, Mounzer K, Tebas P, Montaner LJ, Ho YC. Inhibition of a Chromatin and Transcription Modulator, SLTM, Increases HIV-1 Reactivation Identified by a CRISPR Inhibition Screen. Journal Of Virology 2022, 96: e00577-22. PMID: 35730977, PMCID: PMC9278143, DOI: 10.1128/jvi.00577-22.Peer-Reviewed Original ResearchMeSH KeywordsAntiretroviral Therapy, Highly ActiveCD4-Positive T-LymphocytesChromatinClustered Regularly Interspaced Short Palindromic RepeatsGene Knockdown TechniquesHIV InfectionsHIV SeropositivityHIV-1HumansJurkat CellsMatrix Attachment Region Binding ProteinsVirus ActivationConceptsHIV-1-infected cellsHIV-1 reactivationT cell clonesHIV-1HIV-1 protein expressionAntiretroviral therapyDrug treatmentProtein expressionInfected cellsInfected individualsHIV-1-infected individualsCell clonesEffective antiretroviral therapyHIV-1 cureLong-term therapyHIV-1 gene expressionHIV-1 persistenceHIV-1 provirusHIV-1 transcriptionImmune cell killingNovel therapeutic targetCell deathLatent reservoirImmune cellsT cellsAn expanded toolkit for Drosophila gene tagging using synthesized homology donor constructs for CRISPR-mediated homologous recombination
Kanca O, Zirin J, Hu Y, Tepe B, Dutta D, Lin W, Ma L, Ge M, Zuo Z, Liu L, Levis R, Perrimon N, Bellen H. An expanded toolkit for Drosophila gene tagging using synthesized homology donor constructs for CRISPR-mediated homologous recombination. ELife 2022, 11: e76077. PMID: 35723254, PMCID: PMC9239680, DOI: 10.7554/elife.76077.Peer-Reviewed Original ResearchAnimalsClustered Regularly Interspaced Short Palindromic RepeatsCRISPR-Cas SystemsDrosophilaExonsHomologous RecombinationPlasmidsCombinatorial GxGxE CRISPR screen identifies SLC25A39 in mitochondrial glutathione transport linking iron homeostasis to OXPHOS
Shi X, Reinstadler B, Shah H, To TL, Byrne K, Summer L, Calvo SE, Goldberger O, Doench JG, Mootha VK, Shen H. Combinatorial GxGxE CRISPR screen identifies SLC25A39 in mitochondrial glutathione transport linking iron homeostasis to OXPHOS. Nature Communications 2022, 13: 2483. PMID: 35513392, PMCID: PMC9072411, DOI: 10.1038/s41467-022-30126-9.Peer-Reviewed Original ResearchMeSH KeywordsClustered Regularly Interspaced Short Palindromic RepeatsGalactoseGlutathioneHomeostasisIronMembrane Transport ProteinsConceptsDe novo purine biosynthesisMitochondrial iron uptakeStructure-guided mutagenesisNovo purine biosynthesisMetabolic stateMitochondrial glutathione transportGlutathione importGenetic interactionsGenetic perturbationsDifferent metabolic environmentsFitness defectsLack of substrateGene interactionsMitochondrial OXPHOSMitochondrial membranePurine biosynthesisCarrier familyTransport assaysKO cellsIron uptakeGlutathione transportTransport activityIron homeostasisGlutathione homeostasisGenesStructural Basis for Reduced Dynamics of Three Engineered HNH Endonuclease Lys-to-Ala Mutants for the Clustered Regularly Interspaced Short Palindromic Repeat (CRISPR)-Associated 9 (CRISPR/Cas9) Enzyme
Wang J, Skeens E, Arantes PR, Maschietto F, Allen B, Kyro GW, Lisi GP, Palermo G, Batista VS. Structural Basis for Reduced Dynamics of Three Engineered HNH Endonuclease Lys-to-Ala Mutants for the Clustered Regularly Interspaced Short Palindromic Repeat (CRISPR)-Associated 9 (CRISPR/Cas9) Enzyme. Biochemistry 2022, 61: 785-794. PMID: 35420793, PMCID: PMC9069930, DOI: 10.1021/acs.biochem.2c00127.Peer-Reviewed Original ResearchMeSH KeywordsClustered Regularly Interspaced Short Palindromic RepeatsCRISPR-Associated Protein 9CRISPR-Cas SystemsDNAEndonucleasesConceptsShort palindromic repeatsSubstrate specificityPalindromic repeatsAla mutantWT enzymeRNA-binding domainAssociated 9 (Cas9) systemForeign DNA sequencesDNA strandsWild-type enzymeDouble-strand breaksEnhanced substrate specificityHNH active siteDynamics of proteinsType II immunityCas9 proteinDNA substratesDNA sequencesStructural basisMutantsAla substitutionDistinct conformationsSingle LysCatalytic siteEnzymeA genome-scale gain-of-function CRISPR screen in CD8 T cells identifies proline metabolism as a means to enhance CAR-T therapy
Ye L, Park JJ, Peng L, Yang Q, Chow RD, Dong MB, Lam SZ, Guo J, Tang E, Zhang Y, Wang G, Dai X, Du Y, Kim HR, Cao H, Errami Y, Clark P, Bersenev A, Montgomery RR, Chen S. A genome-scale gain-of-function CRISPR screen in CD8 T cells identifies proline metabolism as a means to enhance CAR-T therapy. Cell Metabolism 2022, 34: 595-614.e14. PMID: 35276062, PMCID: PMC8986623, DOI: 10.1016/j.cmet.2022.02.009.Peer-Reviewed Original ResearchMeSH KeywordsCD8-Positive T-LymphocytesClustered Regularly Interspaced Short Palindromic RepeatsGain of Function MutationHumansNeoplasmsProlineReceptors, Chimeric AntigenConceptsCAR T cellsT cell-based immunotherapyRight molecular targetCell-based immunotherapyCAR-T therapyChimeric antigen receptorMultiple cancer modelsCAR-T efficacyFunction CRISPR screensCD8 TPrimary CD8Immune functionImmunological diseasesImmune boosterCancer modelAntigen receptorDistinct gene expressionMolecular targetsCRISPR activation screensMetabolic programsImmunological analysisTherapyCancerEfficacyActivation screens
2021
Tumor immunology CRISPR screening: present, past, and future
Dong MB, Tang K, Zhou X, Zhou JJ, Chen S. Tumor immunology CRISPR screening: present, past, and future. Trends In Cancer 2021, 8: 210-225. PMID: 34920978, PMCID: PMC8854335, DOI: 10.1016/j.trecan.2021.11.009.Peer-Reviewed Original ResearchMeSH KeywordsClustered Regularly Interspaced Short Palindromic RepeatsCRISPR-Cas SystemsGene EditingHumansImmunotherapyNeoplasmsEasyCatch, a convenient, sensitive and specific CRISPR detection system for cancer gene mutations
Liu Y, Chen Y, Dang L, Liu Y, Huang S, Wu S, Ma P, Jiang H, Li Y, Pan Y, Wei Y, Ma X, Liu M, Ji Q, Chi T, Huang X, Wang X, Zhou F. EasyCatch, a convenient, sensitive and specific CRISPR detection system for cancer gene mutations. Molecular Cancer 2021, 20: 157. PMID: 34856977, PMCID: PMC8638196, DOI: 10.1186/s12943-021-01456-x.Peer-Reviewed Original ResearchClustered Regularly Interspaced Short Palindromic RepeatsCRISPR-Cas SystemsGenes, NeoplasmGenetic TestingHumansMutationNeoplasmsReproducibility of ResultsSensitivity and SpecificityDirect characterization of cis-regulatory elements and functional dissection of complex genetic associations using HCR–FlowFISH
Reilly SK, Gosai SJ, Gutierrez A, Mackay-Smith A, Ulirsch JC, Kanai M, Mouri K, Berenzy D, Kales S, Butler GM, Gladden-Young A, Bhuiyan RM, Stitzel ML, Finucane HK, Sabeti PC, Tewhey R. Direct characterization of cis-regulatory elements and functional dissection of complex genetic associations using HCR–FlowFISH. Nature Genetics 2021, 53: 1166-1176. PMID: 34326544, PMCID: PMC8925018, DOI: 10.1038/s41588-021-00900-4.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingBayes TheoremClustered Regularly Interspaced Short Palindromic RepeatsDelta-5 Fatty Acid DesaturaseDeoxyribonuclease IFatty Acid DesaturasesFlow CytometryGATA1 Transcription FactorHumansIn Situ Hybridization, FluorescenceK562 CellsLIM Domain ProteinsModels, GeneticPolymorphism, Single NucleotideProto-Oncogene ProteinsQuantitative Trait LociRegulatory Sequences, Nucleic AcidRNA, Guide, CRISPR-Cas SystemsConceptsCis-regulatory elementsGenome-wide association signalsGenome functionEpigenetic mappingComplex genetic associationsFunctional dissectionNearest geneGenetic variationAssociation signalsNative transcriptsTarget genesCausal variantsMultiple genesEndogenous functionsReporter assaysGenesCre activitySitu hybridizationGenetic associationFlow cytometryLociTranscriptsHierarchical Bayesian modelReaction fluorescenceHybridizationPooled CRISPR screening identifies m6A as a positive regulator of macrophage activation
Tong J, Wang X, Liu Y, Ren X, Wang A, Chen Z, Yao J, Mao K, Liu T, Meng FL, Pan W, Zou Q, Liu J, Zhou Y, Xia Q, Flavell RA, Zhu S, Li HB. Pooled CRISPR screening identifies m6A as a positive regulator of macrophage activation. Science Advances 2021, 7: eabd4742. PMID: 33910903, PMCID: PMC8081357, DOI: 10.1126/sciadv.abd4742.Peer-Reviewed Original ResearchMeSH KeywordsAdenosineAnimalsClustered Regularly Interspaced Short Palindromic RepeatsLipopolysaccharidesMacrophage ActivationMethyltransferasesMiceConceptsMacrophage activationPotential cancer immunotherapy targetInnate immune cellsFaster tumor growthTNF-α productionInnate immune responseCancer immunotherapy targetCre miceImmune cellsImmunotherapy targetImmune responseLPS stimulationTumor growthBacterial infectionsTop candidate genesDeficient macrophagesMultiple cellular responsesMETTL3 deficiencyActivationUnknown roleMETTL3Negative regulatorBinding proteinCellular responsesRNA binding proteinCommon Genetic Variation in Humans Impacts In Vitro Susceptibility to SARS-CoV-2 Infection
Dobrindt K, Hoagland DA, Seah C, Kassim B, O'Shea CP, Murphy A, Iskhakova M, Fernando MB, Powell SK, Deans PJM, Javidfar B, Peter C, Møller R, Uhl SA, Garcia MF, Kimura M, Iwasawa K, Crary JF, Kotton DN, Takebe T, Huckins LM, tenOever BR, Akbarian S, Brennand KJ. Common Genetic Variation in Humans Impacts In Vitro Susceptibility to SARS-CoV-2 Infection. Stem Cell Reports 2021, 16: 505-518. PMID: 33636110, PMCID: PMC7881728, DOI: 10.1016/j.stemcr.2021.02.010.Peer-Reviewed Original ResearchMeSH Keywords3' Untranslated RegionsAdolescentAdultAnimalsCell LineChlorocebus aethiopsClustered Regularly Interspaced Short Palindromic RepeatsCOVID-19FemaleFurinGenetic Predisposition to DiseaseHost-Pathogen InteractionsHumansInduced Pluripotent Stem CellsMaleNeuronsPeptide HydrolasesPolymorphism, Single NucleotideSARS-CoV-2Vero CellsConceptsSARS-CoV-2Clinical complicationsSARS-CoV-2 infectionCommon genetic variationHigh-risk individualsHost genetic variantsSignificant interindividual variabilityNeuron infectionUnderlying comorbiditiesViral loadHealthy individualsViral infectionClinical heterogeneityVitro SusceptibilityEtiologic agentHost responseInterindividual variabilityDiscovery of drugsInfectionHost geneticsHuman induced pluripotent stem cellsSingle nucleotide polymorphismsAntibody repertoireMore diseasesComplicationsNoncanonical open reading frames encode functional proteins essential for cancer cell survival
Prensner J, Enache O, Luria V, Krug K, Clauser K, Dempster J, Karger A, Wang L, Stumbraite K, Wang V, Botta G, Lyons N, Goodale A, Kalani Z, Fritchman B, Brown A, Alan D, Green T, Yang X, Jaffe J, Roth J, Piccioni F, Kirschner M, Ji Z, Root D, Golub T. Noncanonical open reading frames encode functional proteins essential for cancer cell survival. Nature Biotechnology 2021, 39: 697-704. PMID: 33510483, PMCID: PMC8195866, DOI: 10.1038/s41587-020-00806-2.Peer-Reviewed Original ResearchMeSH KeywordsCell Line, TumorCell SurvivalClustered Regularly Interspaced Short Palindromic RepeatsHEK293 CellsHumansNeoplasm ProteinsNeoplasmsOpen Reading FramesConceptsCancer cell linesOpen reading framePotential therapeutic targetCell linesGrowth inhibitory effectsCancer cell survivalInduced gene expression changesBreast cancerTherapeutic targetHuman cancer cell linesReading frameProtein expressionActive proteinProtein 1Gene expression changesCell survivalBiological effectsExpression changesViability defectsHuman genomeGenomic analysisCodon mutagenesisEctopic expressionFunctional proteinsKnockoutGenome-wide CRISPR screens reveal a specific ligand for the glycan-binding immune checkpoint receptor Siglec-7
Wisnovsky S, Möckl L, Malaker SA, Pedram K, Hess GT, Riley NM, Gray MA, Smith BAH, Bassik MC, Moerner WE, Bertozzi CR. Genome-wide CRISPR screens reveal a specific ligand for the glycan-binding immune checkpoint receptor Siglec-7. Proceedings Of The National Academy Of Sciences Of The United States Of America 2021, 118: e2015024118. PMID: 33495350, PMCID: PMC7865165, DOI: 10.1073/pnas.2015024118.Peer-Reviewed Original ResearchAmino Acid MotifsAntigens, Differentiation, MyelomonocyticCell Line, TumorCell MembraneClustered Regularly Interspaced Short Palindromic RepeatsGenome, HumanGlycopeptidesHumansImmunological SynapsesKiller Cells, NaturalLectinsLeukosialinLigandsPolysaccharidesProtein Binding
2020
CRISPR-GEMM Pooled Mutagenic Screening Identifies KMT2D as a Major Modulator of Immune Checkpoint Blockade
Wang G, Chow RD, Zhu L, Bai Z, Ye L, Zhang F, Renauer PA, Dong MB, Dai X, Zhang X, Du Y, Cheng Y, Niu L, Chu Z, Kim K, Liao C, Clark P, Errami Y, Chen S. CRISPR-GEMM Pooled Mutagenic Screening Identifies KMT2D as a Major Modulator of Immune Checkpoint Blockade. Cancer Discovery 2020, 10: 1912-1933. PMID: 32887696, PMCID: PMC7710536, DOI: 10.1158/2159-8290.cd-19-1448.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsClustered Regularly Interspaced Short Palindromic RepeatsDNA-Binding ProteinsHumansImmune Checkpoint InhibitorsMiceMutationNeoplasm ProteinsConceptsImmune checkpoint blockadeCheckpoint blockadeCancer typesMajority of patientsRemarkable clinical efficacyFraction of patientsMajor modulatorComplex molecular landscapeMultiple cancer typesClinical efficacyICB responseImmune infiltrationTumor immunogenicityAntigen presentationMutation burdenMouse modelPatient stratificationMutant tumorsTumor microenvironmentIssue featurePatientsTumorsMolecular landscapeBlockadeCancerMassively parallel techniques for cataloguing the regulome of the human brain
Townsley KG, Brennand KJ, Huckins LM. Massively parallel techniques for cataloguing the regulome of the human brain. Nature Neuroscience 2020, 23: 1509-1521. PMID: 33199899, PMCID: PMC8018778, DOI: 10.1038/s41593-020-00740-1.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsMeSH KeywordsBrainClustered Regularly Interspaced Short Palindromic RepeatsGene Expression RegulationGeneticsHigh-Throughput Screening AssaysHumansInduced Pluripotent Stem CellsRegulatory Elements, TranscriptionalConceptsRegulatory elementsTarget genesParallel reporter assaysPutative regulatory elementsNon-coding regionsDisease-associated lociSpecific expression patternsCandidate risk lociPluripotent stem cellsHigh-throughput assaysRelevant molecular pathwaysTranscriptional responseRegulatory architectureRisk lociExpression patternsReporter assaysComplex brain disordersMolecular pathwaysRegulomeStem cellsRisk architectureGenetic riskGenesLociGenetic diagnosisGenome-wide CRISPR Screens Reveal Host Factors Critical for SARS-CoV-2 Infection
Wei J, Alfajaro MM, DeWeirdt PC, Hanna RE, Lu-Culligan WJ, Cai WL, Strine MS, Zhang SM, Graziano VR, Schmitz CO, Chen JS, Mankowski MC, Filler RB, Ravindra NG, Gasque V, de Miguel FJ, Patil A, Chen H, Oguntuyo KY, Abriola L, Surovtseva YV, Orchard RC, Lee B, Lindenbach BD, Politi K, van Dijk D, Kadoch C, Simon MD, Yan Q, Doench JG, Wilen CB. Genome-wide CRISPR Screens Reveal Host Factors Critical for SARS-CoV-2 Infection. Cell 2020, 184: 76-91.e13. PMID: 33147444, PMCID: PMC7574718, DOI: 10.1016/j.cell.2020.10.028.Peer-Reviewed Original ResearchMeSH KeywordsAngiotensin-Converting Enzyme 2AnimalsCell LineChlorocebus aethiopsClustered Regularly Interspaced Short Palindromic RepeatsCoronavirusCoronavirus InfectionsCOVID-19Gene Knockout TechniquesGene Regulatory NetworksGenome-Wide Association StudyHEK293 CellsHMGB1 ProteinHost-Pathogen InteractionsHumansSARS-CoV-2Vero CellsVirus InternalizationConceptsSARS-CoV-2 infectionSARS-CoV-2Vesicular stomatitis virusGenome-wide CRISPR screenSWI/SNF chromatinSARS-CoV-2 host factorsAcute respiratory syndrome coronavirus 2 infectionSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infectionTherapeutic targetHost factorsCoronavirus disease 2019 (COVID-19) pathogenesisSyndrome coronavirus 2 infectionCRISPR screensHost genesGene productsMiddle East respiratory syndrome CoVCoronavirus 2 infectionGenetic hitsHuman cellsSARS-CoV-2 spikeNovel therapeutic targetPotential therapeutic targetVero E6 cellsSARS-CoV-1Small molecule antagonists
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