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
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
2002
Signaling 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