2014
The UPF1 RNA surveillance gene is commonly mutated in pancreatic adenosquamous carcinoma
Liu C, Karam R, Zhou Y, Su F, Ji Y, Li G, Xu G, Lu L, Wang C, Song M, Zhu J, Wang Y, Zhao Y, Foo W, Zuo M, Valasek M, Javle M, Wilkinson M, Lu Y. The UPF1 RNA surveillance gene is commonly mutated in pancreatic adenosquamous carcinoma. Nature Medicine 2014, 20: 596-598. PMID: 24859531, PMCID: PMC4048332, DOI: 10.1038/nm.3548.Peer-Reviewed Original ResearchMeSH KeywordsAlternative SplicingBase SequenceCarcinoma, AdenosquamousGene ComponentsHEK293 CellsHumansImmunohistochemistryIn Situ Nick-End LabelingMolecular Sequence DataMutagenesisMutationNonsense Mediated mRNA DecayPancreatic NeoplasmsReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionRNA HelicasesSequence Analysis, DNATrans-Activators
2005
Defective Jak-Stat Activation in Hepatoma Cells Is Associated with Hepatitis C Viral IFN- Resistance
Zhu H, Nelson D, Crawford J, Liu C. Defective Jak-Stat Activation in Hepatoma Cells Is Associated with Hepatitis C Viral IFN- Resistance. Journal Of Interferon & Cytokine Research 2005, 25: 528-539. PMID: 16181053, DOI: 10.1089/jir.2005.25.528.Peer-Reviewed Original ResearchMeSH KeywordsAntiviral AgentsCarcinoma, HepatocellularCell Line, TumorDNA-Binding ProteinsDrug Resistance, ViralHepacivirusHumansInterferon-alphaLiverLiver NeoplasmsMutationProtein-Tyrosine KinasesRepliconRepressor ProteinsSTAT3 Transcription FactorSuppressor of Cytokine Signaling 3 ProteinSuppressor of Cytokine Signaling ProteinsTrans-ActivatorsTranscription FactorsViral Nonstructural ProteinsConceptsIFN resistanceHCV subgenomic replicon cell culture systemViral infectionChronic hepatitis C viral infectionIFN-sensitive cell linesHepatitis C viral infectionIFN stimulationCell linesRibavirin combination therapyMajority of patientsC viral infectionSTAT3 activationResistant cell linesIFN monotherapyIFN therapySuppressor of cytokineCombination therapyIFN sensitivityJAK-STAT activationIFNPotential mechanismsLong-term cultureCell culture systemExhibit alterationsJAK-STATStimulation of Host NKT Cells by Synthetic Glycolipid Regulates Acute Graft-versus-Host Disease by Inducing Th2 Polarization of Donor T Cells
Hashimoto D, Asakura S, Miyake S, Yamamura T, Van Kaer L, Liu C, Tanimoto M, Teshima T. Stimulation of Host NKT Cells by Synthetic Glycolipid Regulates Acute Graft-versus-Host Disease by Inducing Th2 Polarization of Donor T Cells. The Journal Of Immunology 2005, 174: 551-556. PMID: 15611282, DOI: 10.4049/jimmunol.174.1.551.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, CD1Antigens, CD1dBone Marrow TransplantationEnzyme-Linked Immunosorbent AssayFemaleFlow CytometryGalactosylceramidesGlycolipidsGraft vs Host DiseaseMiceMice, KnockoutSTAT6 Transcription FactorTh2 CellsT-Lymphocyte SubsetsT-LymphocytesTrans-ActivatorsTumor Necrosis Factor-alphaConceptsHost NKT cellsDonor T cellsNKT cellsT cellsTh2 polarizationAcute GVHDAcute graftHost diseaseAlpha-GalCerAllogeneic bone marrow transplantationImmunoregulatory T-cell populationsMortality of GVHDTh2 cytokine responsesSerum TNF-alphaNKT cell ligandBone marrow transplantationSTAT6-dependent mechanismT cell populationsNKT ligandCytokine responsesMarrow transplantationIL-4Recipient miceTNF-alphaGVHD
2004
STAT3 induces anti-hepatitis C viral activity in liver cells
Zhu H, Shang X, Terada N, Liu C. STAT3 induces anti-hepatitis C viral activity in liver cells. Biochemical And Biophysical Research Communications 2004, 324: 518-528. PMID: 15474458, DOI: 10.1016/j.bbrc.2004.09.081.Peer-Reviewed Original ResearchMeSH KeywordsAntiviral AgentsBlotting, NorthernBlotting, WesternCarcinoma, HepatocellularCell LineCell Line, TumorCytokinesDNA-Binding ProteinsDose-Response Relationship, DrugEnzyme InhibitorsGenes, DominantHepacivirusHumansInflammationInterferonsInterleukin-6LigandsLiverLiver NeoplasmsLuciferasesPlasmidsProtein Structure, TertiaryReverse Transcriptase Polymerase Chain ReactionRibavirinRNARNA, MessengerSTAT3 Transcription FactorTime FactorsTrans-ActivatorsTransfectionTyrphostinsConceptsAnti-HCV activityInterferon alphaSTAT3 activationHuman hepatoma cellsHepatitis C virus infectionHCV subgenomic RNA replicationMain therapeutic regimenC virus infectionChronic liver diseaseCytokines IL-6Replicon cell linesIntracellular antiviral stateCell linesHepatoma cellsLiver diseaseTherapeutic regimenActivation of STAT3IL-6Virus infectionEstrogen receptorIFN treatmentAntiviral genesAntiviral pathwaysAntiviral activityAntiviral stateStabilized β-catenin promotes hepatocyte proliferation and inhibits TNFα-induced apoptosis
Shang X, Zhu H, Lin K, Tu Z, Chen J, Nelson D, Liu C. Stabilized β-catenin promotes hepatocyte proliferation and inhibits TNFα-induced apoptosis. Laboratory Investigation 2004, 84: 332-341. PMID: 14767485, DOI: 10.1038/labinvest.3700043.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisBeta CateninCarcinoma, HepatocellularCell DivisionCell LineCell Line, TumorCell Transformation, NeoplasticCyclin D1Cytoskeletal ProteinsDrug StabilityGene Expression RegulationGenes, mycHepatocytesHumansLiver NeoplasmsMiceMice, SCIDMutationTrans-ActivatorsTransfectionTumor Necrosis Factor-alphaConceptsHuman hepatocellular carcinomaHepatocyte proliferationCell linesCommon malignant tumorCell proliferationImmune-deficient miceCell survival abilityLiver cell growthMurine hepatocyte cell lineCell growthHepatocyte cell lineAnchorage-independent cell growthMalignant tumorsHepatocellular carcinomaLiver cancerCyclin D1Inhibits TNFαOncogenic transformationCell apoptosisBeta-catenin mutationsAct DΒ-cateninPotential roleC-MycTumors
2003
β-Catenin Is Expressed Aberrantly in Tumors Expressing Shadow Cells
Hassanein A, Glanz S, Kessler H, Eskin T, Liu C. β-Catenin Is Expressed Aberrantly in Tumors Expressing Shadow Cells. American Journal Of Clinical Pathology 2003, 120: 732-736. PMID: 14608900, DOI: 10.1309/ealeg7ld6w7167px.Peer-Reviewed Original ResearchGene expression associated with interferon alfa antiviral activity in an HCV replicon cell line
Zhu H, Zhao H, Collins C, Eckenrode S, Run Q, McIndoe R, Crawford J, Nelson D, She J, Liu C. Gene expression associated with interferon alfa antiviral activity in an HCV replicon cell line. Hepatology 2003, 37: 1180-1188. PMID: 12717400, DOI: 10.1053/jhep.2003.50184.Peer-Reviewed Original ResearchMeSH KeywordsAntiviral AgentsCarcinoma, HepatocellularDNA-Binding ProteinsGene ExpressionHepacivirusHepatitis C, ChronicHepatocytesHumansInterferon-alphaLiver NeoplasmsRNA, ViralSignal TransductionSTAT1 Transcription FactorSTAT3 Transcription FactorTrans-ActivatorsTumor Cells, CulturedViral ProteinsVirus ReplicationConceptsIFN-alpha antiviral activityIFN-alphaAntiviral activityReplicon cellsHCV replicon cell culture systemChronic hepatitis C viral infectionHepatitis C viral infectionHCV subgenomic RNA replicationHCV replicon cell linesC viral infectionOnly therapeutic optionDirect antiviral activityReplicon cell linesAnti-HCV activityHepatoma cellsDifferent gene expression profilesFeasible experimental modelIFN-alpha signalingCDNA microarray analysisGene expression profilesTherapeutic optionsActivation of STAT3Antiviral efficacyViral infectionResponsive genes
2002
Pretreatment of donors with interleukin-18 attenuates acute graft-versus-host disease via STAT6 and preserves graft-versus-leukemia effects
Reddy P, Teshima T, Hildebrandt G, Williams D, Liu C, Cooke K, Ferrara J. Pretreatment of donors with interleukin-18 attenuates acute graft-versus-host disease via STAT6 and preserves graft-versus-leukemia effects. Blood 2002, 101: 2877-2885. PMID: 12433681, DOI: 10.1182/blood-2002-08-2566.Peer-Reviewed Original ResearchMeSH KeywordsAcute DiseaseAnimalsBone Marrow TransplantationFemaleGraft vs Host DiseaseGraft vs Leukemia EffectHumansInterferon-gammaInterleukin-18Leukemia, ExperimentalMiceMice, Inbred BALB CMice, Inbred C57BLSTAT6 Transcription FactorSurvival RateTissue DonorsT-LymphocytesTrans-ActivatorsTransplantation, HomologousConceptsAllogeneic bone marrow transplantationBone marrow transplantationPretreatment of donorsIL-18Acute GVHDAcute graftHost diseaseLeukemia effectTransplant donorsCytotoxic T lymphocyte activityAcute GVHD mortalityIL-18 pretreatmentDonor T cellsT lymphocyte activityBM transplant recipientsIL-4 secretionSTAT6-dependent mechanismIL-18 treatmentGVHD mortalityGVL effectPreserves graftTransplant recipientsInterleukin-18Marrow transplantationBM donors