2025
Sensitive detection of synthetic response to cancer immunotherapy driven by gene paralog pairs
Dong C, Zhang F, He E, Ren P, Verma N, Zhu X, Feng D, Cai J, Zhao H, Chen S. Sensitive detection of synthetic response to cancer immunotherapy driven by gene paralog pairs. Patterns 2025, 6: 101184. PMID: 40182179, PMCID: PMC11963098, DOI: 10.1016/j.patter.2025.101184.Peer-Reviewed Original ResearchParalogous gene pairsParalogous pairsChimeric antigen receptor T cellsResponse to cancer immunotherapyDouble knockoutCancer immunotherapy responseGene pairsCheckpoint blockadeGenome-wide screenImmunotherapy efficacyCancer immunotherapyEnhance immunotherapyImmunotherapy responseImmunotherapy effectT cellsImmunotherapyCancer treatmentIndividual genesCRISPR screensEnrichment analysisParalogsCancerTreatmentCombined targetFunctional significance
2023
Multiple Subthreshold GPCR Signals Combined by the G-Proteins Gαq and Gαs Activate the Caenorhabditis elegans Egg-Laying Muscles
Olson A, Butt A, Christie N, Shelar A, Koelle M. Multiple Subthreshold GPCR Signals Combined by the G-Proteins Gαq and Gαs Activate the Caenorhabditis elegans Egg-Laying Muscles. Journal Of Neuroscience 2023, 43: 3789-3806. PMID: 37055179, PMCID: PMC10219013, DOI: 10.1523/jneurosci.2301-22.2023.Peer-Reviewed Original ResearchConceptsG protein-coupled receptorsMultiple G protein-coupled receptorsMuscle cellsMuscle activitySerotonin G protein-coupled receptorsDesigner G protein-coupled receptorsIntact animalsG proteinsEndogenous G protein-coupled receptorsIndividual G protein-coupled receptorsGPCR signalsCalcium activityEgg-laying musclesSerotoninIndividual neuronsDouble knockoutNeuronsBehavioral outcomesMuscleMost cellsG protein GαqCellsSubthreshold signalEgg-laying systemSER-1
2020
Cyclin-Dependent Kinase 1 Activity Is a Driver of Cyst Growth in Polycystic Kidney Disease
Zhang C, Balbo B, Ma M, Zhao J, Tian X, Kluger Y, Somlo S. Cyclin-Dependent Kinase 1 Activity Is a Driver of Cyst Growth in Polycystic Kidney Disease. Journal Of The American Society Of Nephrology 2020, 32: 41-51. PMID: 33046531, PMCID: PMC7894654, DOI: 10.1681/asn.2020040511.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisCatalytic DomainCDC2 Protein KinaseCell ProliferationCrosses, GeneticDNA ReplicationExome SequencingFemaleGene Expression ProfilingGene Expression RegulationMaleMiceMice, Inbred C57BLMice, KnockoutMutationPhenotypePolycystic Kidney, Autosomal DominantPyruvate Dehydrogenase Acetyl-Transferring KinaseRNA-SeqTranscription, GeneticTRPP Cation ChannelsConceptsAutosomal dominant polycystic kidney diseaseCyst cell proliferationPolycystic kidney diseaseKidney diseaseADPKD progressionCell proliferationModel of ADPKDCyst growthProgression of ADPKDDominant polycystic kidney diseaseDouble knockout miceCandidate pathwaysKidney functionCyst progressionMouse modelUnbiased transcriptional profilingProgressionCellular mechanismsKinase 1 activityCystic phenotypeSelective targetingKidneyConditional inactivationDouble knockoutProliferation
2019
In vivo profiling of metastatic double knockouts through CRISPR–Cpf1 screens
Chow RD, Wang G, Ye L, Codina A, Kim HR, Shen L, Dong MB, Errami Y, Chen S. In vivo profiling of metastatic double knockouts through CRISPR–Cpf1 screens. Nature Methods 2019, 16: 405-408. PMID: 30962622, PMCID: PMC6592845, DOI: 10.1038/s41592-019-0371-5.Peer-Reviewed Original Research
2014
Endothelial PINK1 Mediates the Protective Effects of NLRP3 Deficiency during Lethal Oxidant Injury
Zhang Y, Sauler M, Shinn AS, Gong H, Haslip M, Shan P, Mannam P, Lee PJ. Endothelial PINK1 Mediates the Protective Effects of NLRP3 Deficiency during Lethal Oxidant Injury. The Journal Of Immunology 2014, 192: 5296-5304. PMID: 24778451, PMCID: PMC4047670, DOI: 10.4049/jimmunol.1400653.Peer-Reviewed Original ResearchConceptsAcute respiratory failurePTEN-induced putative kinase 1Respiratory failureWild-type miceNLRP3 deficiencyAutophagy/mitophagySpecific therapyProtective effectProtein NLRP3Oxidant injuryLung endotheliumHigh mortalityHyperoxiaGenetic deletionHigher basalIntermediate susceptibilityMiceOxidant generationPutative kinase 1PINK1 expressionProteasome activationNovel roleDouble knockoutEndotheliumKinase 1
2013
Dynamin triple knockout cells reveal off target effects of commonly used dynamin inhibitors
Park RJ, Shen H, Liu L, Liu X, Ferguson SM, De Camilli P. Dynamin triple knockout cells reveal off target effects of commonly used dynamin inhibitors. Journal Of Cell Science 2013, 126: 5305-5312. PMID: 24046449, PMCID: PMC3828596, DOI: 10.1242/jcs.138578.Peer-Reviewed Original ResearchConceptsDynamin 1Dynamin inhibitorTKO cellsPeripheral membrane rufflingDouble knockoutDynamin 3 geneClathrin-mediated endocytosisTriple-knockout cellsDynamin-dependent processFluid-phase endocytosisDyngo-4aMembrane fissionMembrane rufflingDKO cellsDynamin 2Knockout cellsLow-level expressionCell physiologyDynaminEndocytosisTarget effectsDKO fibroblastsGenesCellsKO fibroblasts
2011
Interleukin-1β (IL-1β) promotes susceptibility of Toll-like receptor 5 (TLR5) deficient mice to colitis
Carvalho FA, Nalbantoglu I, Ortega-Fernandez S, Aitken JD, Su Y, Koren O, Walters WA, Knight R, Ley RE, Vijay-Kumar M, Gewirtz AT. Interleukin-1β (IL-1β) promotes susceptibility of Toll-like receptor 5 (TLR5) deficient mice to colitis. Gut 2011, 61: 373. PMID: 21646247, DOI: 10.1136/gut.2011.240556.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodies, MonoclonalCecumColitis, UlcerativeDisease Models, AnimalDisease SusceptibilityGene Expression ProfilingInterleukin-1betaMaleMetagenomeMiceMice, KnockoutMyeloid Differentiation Factor 88Receptors, Interleukin-10Reverse Transcriptase Polymerase Chain ReactionSignal TransductionToll-Like Receptor 5ConceptsToll-like receptor 4T5KO miceGut microbiotaColitis modelIL-1βAbsence of TLR4Toll-like receptor 5 deficient (T5KO) miceAnti-inflammatory cytokine interleukin-10Endogenous anti-inflammatory pathwayToll-like receptor 5Loss of TLR5Anti-inflammatory pathwayIL-10 receptorCytokine interleukin-10Double knockoutIL-10 signalingIL-1 receptorProinflammatory gene expressionWild-type littermatesColitogenic microbiotaSpontaneous colitisUniform colitisSevere colitisImmune dysregulationIntestinal inflammationFine balance between HIF1 and HIF2 in smooth muscle is crucial for normal development and survival
Lei L, Liu D, Jiang W, Huang Y, Giordano F. Fine balance between HIF1 and HIF2 in smooth muscle is crucial for normal development and survival. The FASEB Journal 2011, 25: 616.10-616.10. DOI: 10.1096/fasebj.25.1_supplement.616.10.Peer-Reviewed Original ResearchSmooth muscle cellsVon Hippel-LindauSmooth muscleDied of heart failureDeletion of von Hippel-LindauDouble knockoutVascular smooth muscle cellsMicro-CT angiographyNormal developmentEmbryonic lethalityApparent etiologyMidline defectsFetal developmentVascular reactivityEctopia cordisE14.5-15.5Heart failureMuscle cellsVascular spasmIntramyocardial hematomaVascular perfusionMiceGastroschisisVascular segmentsMicro-CT
2003
Inactivating E2f1 reverts apoptosis resistance and cancer sensitivity in Trp53-deficient mice
Wikonkal NM, Remenyik E, Knezevic D, Zhang W, Liu M, Zhao H, Berton TR, Johnson DG, Brash DE. Inactivating E2f1 reverts apoptosis resistance and cancer sensitivity in Trp53-deficient mice. Nature Cell Biology 2003, 5: 655-660. PMID: 12833065, DOI: 10.1038/ncb1001.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisCell Cycle ProteinsCell SurvivalCell Transformation, NeoplasticCells, CulturedDNA DamageDNA-Binding ProteinsE2F Transcription FactorsE2F1 Transcription FactorFemaleFibroblastsGene Expression Regulation, NeoplasticGenes, SuppressorKeratinocytesMaleMiceMice, KnockoutMutationSex RatioSkin NeoplasmsTranscription FactorsTumor Suppressor Protein p53Ultraviolet RaysConceptsUVB-induced apoptosisEarly-onset tumorsDouble knockout miceTrp53-deficient miceKnockout miceCancer sensitivityUVB exposureGenetic abnormalitiesMiceKeratinocyte apoptosisProtective mechanismApoptosis defectsApoptosis resistanceApoptosisDouble knockoutApoptosis pathwayE2F1 transcription factorE2F1 functionsPrimary fibroblastsE2F1Trp53S phase
2002
Control of DNA Replication and Chromosome Ploidy by Geminin and Cyclin A
Mihaylov IS, Kondo T, Jones L, Ryzhikov S, Tanaka J, Zheng J, Higa LA, Minamino N, Cooley L, Zhang H. Control of DNA Replication and Chromosome Ploidy by Geminin and Cyclin A. Molecular And Cellular Biology 2002, 22: 1868-1880. PMID: 11865064, PMCID: PMC135598, DOI: 10.1128/mcb.22.6.1868-1880.2002.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell Cycle ProteinsCell LineCell NucleusCheckpoint Kinase 1ChromosomesCyclin ACyclin BDNADNA ReplicationDNA-Binding ProteinsDown-RegulationDrosophilaDrosophila ProteinsFlow CytometryGene SilencingMolecular Sequence DataPloidiesProtein Kinase InhibitorsProtein KinasesRNA, Double-StrandedSequence Homology, Amino AcidConceptsDNA replicationGeminin deficiencyGenome stabilityCyclin ASingle giant nucleusGiant nucleiCell cycle arrestDrosophila homologueDrosophila cellsGenome instabilityCheckpoint controlChromosome ploidyReplication factorsOverreplicationCyclin BGemininDouble knockoutCycle arrestRapid downregulationDNA contentGenomeSilencingEffect of cyclinHomologuesCyclin
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