2024
Growth characteristics of HCT116 xenografts lacking asparagine synthetase vary according to sex
Aladelokun O, Lu L, Zheng J, Yan H, Jain A, Gibson J, Khan S, Johnson C. Growth characteristics of HCT116 xenografts lacking asparagine synthetase vary according to sex. Human Genomics 2024, 18: 67. PMID: 38886847, PMCID: PMC11184737, DOI: 10.1186/s40246-024-00635-3.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAspartate-Ammonia LigaseCarbon-Nitrogen Ligases with Glutamine as Amide-N-DonorCell ProliferationColorectal NeoplasmsFemaleGene Expression Regulation, NeoplasticHCT116 CellsHeterograftsHumansMaleMiceReceptors, EstrogenReceptors, G-Protein-CoupledSex FactorsXenograft Model Antitumor AssaysConceptsFemale tumor-bearing miceFemale CRC patientsTumor-bearing miceCRC patientsTumor growthInferior survivalAssociated with inferior survivalMetabolic reprogrammingG protein-coupled estrogen receptorTriggering metabolic reprogrammingSustained tumor growthSuppressed tumor growthExpression of asparagine synthetaseCancer cell linesBackgroundSex-related differencesSurvival improvementImpact of sexFemale miceEstrogen receptorCancer growthTranslational relevanceRewiring of metabolic pathwaysCancer burdenMetabolic pathwaysAsparagine synthetase
2019
Expression of the type 3 InsP3 receptor is a final common event in the development of hepatocellular carcinoma
Guerra MT, Florentino RM, Franca A, Lima Filho AC, Dos Santos ML, Fonseca RC, Lemos FO, Fonseca MC, Kruglov E, Mennone A, Njei B, Gibson J, Guan F, Cheng YC, Ananthanarayanan M, Gu J, Jiang J, Zhao H, Lima CX, Vidigal PT, Oliveira AG, Nathanson MH, Leite MF. Expression of the type 3 InsP3 receptor is a final common event in the development of hepatocellular carcinoma. Gut 2019, 68: 1676. PMID: 31315892, PMCID: PMC7087395, DOI: 10.1136/gutjnl-2018-317811.Peer-Reviewed Original ResearchMeSH KeywordsAdultAnimalsApoptosisCalcium SignalingCarcinogenesisCarcinoma, HepatocellularCell ProliferationCells, CulturedDNA MethylationFemaleGene Expression Regulation, NeoplasticHepatocytesHumansInositol 1,4,5-Trisphosphate ReceptorsLiverLiver NeoplasmsLiver RegenerationMaleMice, KnockoutMiddle AgedSurvival AnalysisConceptsChronic liver diseaseITPR3 expressionLiver cancer cellsLiver diseaseMouse modelFinal common eventCancer cellsSpecimens of patientsIndependent patient cohortsControl liver specimensHuman HCC cellsType 3 InsP3 receptorHuman liver samplesIncreased expression levelCancer deathPatient cohortCommon molecular eventPoor survivalHepatocellular carcinomaLiver specimensNormal liverHCC cellsAbstractTextHCCType 3 isoform
2016
ABC transporters and NR4A1 identify a quiescent subset of tissue-resident memory T cells
Boddupalli CS, Nair S, Gray SM, Nowyhed HN, Verma R, Gibson JA, Abraham C, Narayan D, Vasquez J, Hedrick CC, Flavell RA, Dhodapkar KM, Kaech SM, Dhodapkar MV. ABC transporters and NR4A1 identify a quiescent subset of tissue-resident memory T cells. Journal Of Clinical Investigation 2016, 126: 3905-3916. PMID: 27617863, PMCID: PMC5096804, DOI: 10.1172/jci85329.Peer-Reviewed Original ResearchConceptsTissue-resident memory T cellsMemory T cellsT cellsTRM cellsCellular therapyAdoptive cellular therapyImmune-deficient micePotential cellular therapySP T cellsSide population cellsHuman T cellsPutative subsetsAdoptive transferDistinct gene expression profilesCell mobilizationImmune surveillanceQuiescent subsetPopulation cellsMiceTherapyQuiescent phenotypeDistinct subsetsMember 1Nuclear receptorsSignature genes
2014
A Humanized Mouse Model of Autoimmune Insulitis
Milam A, Maher SE, Gibson JA, Lebastchi J, Wen L, Ruddle NH, Herold KC, Bothwell AL. A Humanized Mouse Model of Autoimmune Insulitis. Diabetes 2014, 63: 1712-1724. PMID: 24478396, PMCID: PMC3994947, DOI: 10.2337/db13-1141.Peer-Reviewed Original ResearchConceptsT cellsDiabetic donorsInsulin stainingMouse modelAntigen-pulsed cellsAutoantigen-derived peptidesNOD mouse modelHumanized mouse modelType 1 diabetesPancreatic β-cellsT cell linesHuman T cellsIslet infiltrationAutoimmune diabetesNOD-SCIDAutoimmune insulitisHuman diabetesDestructive infiltrationMouse isletsMechanism of inductionΒ-cellsDiabetesDiabetes researchDisease modelsInsulitis
2003
Sp1- and Krüppel-like transcription factors
Kaczynski J, Cook T, Urrutia R. Sp1- and Krüppel-like transcription factors. Genome Biology 2003, 4: 206. PMID: 12620113, PMCID: PMC151296, DOI: 10.1186/gb-2003-4-2-206.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsMeSH KeywordsAmino Acid SequenceAnimalsBinding SitesDNA-Binding ProteinsEvolution, MolecularGene Expression RegulationHumansKruppel-Like Transcription FactorsMolecular Sequence DataPhylogenyRepressor ProteinsSequence Homology, Amino AcidSp1 Transcription FactorTranscription FactorsTranscription, GeneticZinc FingersConceptsKruppel-like factorCellular functionsCell- and promoter-specific mannerSp1-like proteinsGC-rich promoterTranscriptional activation domainCellular transcription machineryZinc-finger proteinPromoter-specific mannerSp1-like factorsTranscription machineryHuman genomeTranscriptional regulationDNA bindingActivation domainAmino terminusGene expressionProteinCell proliferationNeoplastic transformationFamily membersPromoterExpressionGenomeRepressorFundamentals of Transcription Factors and their Impact on Pancreatic Development and Cancer
Fernandez-Zapico M, Bramati P, Zakaria S, Kaczynski J, Urrutia R. Fundamentals of Transcription Factors and their Impact on Pancreatic Development and Cancer. Pancreatology 2003, 3: 276-283. PMID: 12890989, DOI: 10.1159/000071765.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsTranscription factorsEffectors of signaling pathwaysSynthesis of messenger RNARegulate gene expressionPancreatic developmentCellular functionsGene transcriptionTransduce signalsGene expressionTranscriptionSignaling pathwayHuman cellsDevelopment of diseaseBiology of human cellsMessenger RNACell membraneDominant control pointsProteinExpressionCellsGenesRNAApoptosisEffectorPathway
2002
Functional analysis of basic transcription element (BTE)-binding protein (BTEB) 3 and BTEB4, a novel Sp1-like protein, reveals a subfamily of transcriptional repressors for the BTE site of the cytochrome P4501A1 gene promoter
KACZYNSKI J, CONLEY A, ZAPICO M, DELGADO S, ZHANG J, URRUTIA R. Functional analysis of basic transcription element (BTE)-binding protein (BTEB) 3 and BTEB4, a novel Sp1-like protein, reveals a subfamily of transcriptional repressors for the BTE site of the cytochrome P4501A1 gene promoter. Biochemical Journal 2002, 366: 873-882. PMID: 12036432, PMCID: PMC1222816, DOI: 10.1042/bj20020388.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsBlotting, NorthernBlotting, WesternCarcinogensCell Cycle ProteinsCell LineCHO CellsChromatinCricetinaeCytochrome P-450 CYP1A1DNA, ComplementaryDNA-Binding ProteinsDose-Response Relationship, DrugGlutathione TransferaseHumansKruppel-Like Transcription FactorsMolecular Sequence DataPlasmidsPromoter Regions, GeneticProtein BindingProtein Structure, TertiaryRecombinant Fusion ProteinsRepressor ProteinsSequence Homology, Amino AcidSp1 Transcription FactorTrans-ActivatorsTranscription FactorsTranscription, GeneticZinc FingersConceptsGene promoterCYP1A1 gene promoterProtein familyC-terminal zinc-finger motifC-terminal zinc-finger domainBind GC-rich sequencesControl of gene expressionCo-repressor mSin3ASp1-like proteinsZinc-finger motifGC-rich sequencesFamily of proteinsN-terminal regionRepress transcriptionTranscriptional repressionCo-repressorTranscriptional repressorCellular machineryExpressed memberTranscriptional elementsTranscription factorsFunctional characterizationBTEB3Gene expressionTranscriptionSignaling disrupts mSin3A binding to the Mad1‐like Sin3‐interacting domain of TIEG2, an Sp1‐like repressor
Ellenrieder V, Zhang J, Kaczynski J, Urrutia R. Signaling disrupts mSin3A binding to the Mad1‐like Sin3‐interacting domain of TIEG2, an Sp1‐like repressor. The EMBO Journal 2002, 21: 2451-2460. PMID: 12006497, PMCID: PMC126002, DOI: 10.1093/emboj/21.10.2451.Peer-Reviewed Original ResearchMeSH Keywords3T3 CellsAmino Acid SequenceAnimalsBinding SitesCell Cycle ProteinsCHO CellsConsensus SequenceCricetinaeGenes, ReporterKruppel-Like Transcription FactorsMicePhosphorylationProtein BindingRecombinant ProteinsRepressor ProteinsSignal TransductionSin3 Histone Deacetylase and Corepressor ComplexSp1 Transcription FactorTranscription FactorsTransfectionZinc FingersConceptsSin3 interaction domainTranscriptional repressionAnti-proliferative functionMad proteinsRepressor proteinRepression activitySerine/threonine sitesTranscription factorsConstitutive mannerSignaling pathwayRepressionGrowth suppressionFunctional impactTIEG2ProteinRepressorSerine/threonineTIEGTranscriptionPhosphorylationDomainSignalPathwayInteractionBinding
2001
A Conserved α-Helical Motif Mediates the Interaction of Sp1-Like Transcriptional Repressors with the Corepressor mSin3A
Zhang J, Moncrieffe M, Kaczynski J, Ellenrieder V, Prendergast F, Urrutia R. A Conserved α-Helical Motif Mediates the Interaction of Sp1-Like Transcriptional Repressors with the Corepressor mSin3A. Molecular And Cellular Biology 2001, 21: 5041-5049. PMID: 11438660, PMCID: PMC87230, DOI: 10.1128/mcb.21.15.5041-5049.2001.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid MotifsAmino Acid SequenceAnimalsApoptosis Regulatory ProteinsBlotting, WesternCell Cycle ProteinsCell DivisionCHO CellsCircular DichroismCricetinaeGenetic VectorsGlutathione TransferaseLuciferasesMolecular Sequence DataMutationPeptide BiosynthesisPlasmidsPrecipitin TestsProtein BindingProtein BiosynthesisProtein Structure, TertiaryRecombinant Fusion ProteinsRepressor ProteinsSequence Homology, Amino AcidSin3 Histone Deacetylase and Corepressor ComplexSp1 Transcription FactorTranscription, GeneticTransforming Growth Factor betaZinc FingersConceptsSp1-like proteinsRepress transcriptionDeacetylase complexRepression motifTranscriptional repressionSin3 histone deacetylase complexBind GC-rich sequencesMechanism of transcriptional repressionSp1-like transcription factorsMSin3A-histone deacetylase complexGC-rich sequencesMammalian cell homeostasisCorepressor mSin3ARepression domainTranscriptional repressorA-helicesMSin3ATranscription factorsTIEG2Antiproliferative functionCell homeostasisMotifTranscriptionRepressionProteinThe Sp1-like Protein BTEB3 Inhibits Transcription via the Basic Transcription Element Box by Interacting with mSin3A and HDAC-1 Co-repressors and Competing with Sp1*
Kaczynski J, Zhang J, Ellenrieder V, Conley A, Duenes T, Kester H, van der Burg B, Urrutia R. The Sp1-like Protein BTEB3 Inhibits Transcription via the Basic Transcription Element Box by Interacting with mSin3A and HDAC-1 Co-repressors and Competing with Sp1*. Journal Of Biological Chemistry 2001, 276: 36749-36756. PMID: 11477107, DOI: 10.1074/jbc.m105831200.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid MotifsAnimalsBinding, CompetitiveBlotting, WesternCell Cycle ProteinsCHO CellsCricetinaeGenes, ReporterGlutathione TransferaseHistone Deacetylase 1Histone DeacetylasesKineticsKruppel-Like Transcription FactorsMolecular Sequence DataPlasmidsPrecipitin TestsPromoter Regions, GeneticProtein BindingProtein Structure, TertiaryRepressor ProteinsSin3 Histone Deacetylase and Corepressor ComplexSp1 Transcription FactorTrans-ActivatorsTranscription, GeneticZinc FingersConceptsCo-repressorN-terminusHDAC-1Bind GC-rich sequencesC-terminal zinc finger motifsGC-rich DNA elementsCo-repressor mSin3ASp1-like proteinsZinc finger motifsDNA-binding domainGC-rich sequencesSp1-like activityGel shift assaysMammalian cell homeostasisMechanism of repressionChinese hamster ovary cellsFinger motifDNA elementsSp1 familyRepressor domainRepressor proteinBTEB3GAL4 assayTranscriptional repressionTranscriptional repressor