2018
TRIF deficiency protects non-obese diabetic mice from type 1 diabetes by modulating the gut microbiota and dendritic cells
Gülden E, Chao C, Tai N, Pearson JA, Peng J, Majewska-Szczepanik M, Zhou Z, Wong FS, Wen L. TRIF deficiency protects non-obese diabetic mice from type 1 diabetes by modulating the gut microbiota and dendritic cells. Journal Of Autoimmunity 2018, 93: 57-65. PMID: 29960834, PMCID: PMC6108920, DOI: 10.1016/j.jaut.2018.06.003.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Vesicular TransportAdoptive TransferAnimalsBacteroidetesBurkholderialesCell ProliferationDendritic CellsDiabetes Mellitus, ExperimentalDisease SusceptibilityFemaleFirmicutesGastrointestinal MicrobiomeGene Expression RegulationLymphocyte ActivationMiceMice, Inbred NODMice, KnockoutMyeloid Differentiation Factor 88Signal TransductionT-LymphocytesToll-Like Receptor 3Toll-Like Receptor 4ConceptsWT NOD miceNOD miceType 1 diabetesGut microbiotaDiabetes developmentDendritic cellsCell activationNon-obese diabetic (NOD) mouse modelMyeloid differentiation primary response gene 88Wild-type NOD miceNon-obese diabetic (NOD) miceToll-like receptor signalingDiabetes susceptibilityStrong inflammatory immune responseDevelopment of diabetesInflammatory immune responseDiabetic mouse modelAdapter-inducing interferonImmune cell activationT cell activationTRIF deficiencyAdaptor protein downstreamFurther immunological analysisHuman T1D.T1D development
2009
Cellular and humoral immune responses in the early stages of diabetic nephropathy in NOD mice
Xiao X, Ma B, Dong B, Zhao P, Tai N, Chen L, Wong FS, Wen L. Cellular and humoral immune responses in the early stages of diabetic nephropathy in NOD mice. Journal Of Autoimmunity 2009, 32: 85-93. PMID: 19200691, DOI: 10.1016/j.jaut.2008.12.003.Peer-Reviewed Original ResearchConceptsDiabetic NOD miceNOD miceDiabetic nephropathyDiabetic miceNon-diabetic NOD miceNon-obese diabetic (NOD) miceDuration of diabetesUrinary albumin excretionAdditional therapeutic targetsHumoral immune responseAlbumin excretionAutoimmune diabetesDendritic cellsDiabetes onsetImmune changesKidney weightIgG depositsHumoral immunityT cellsImmune responseNephropathyComplement C3Therapeutic targetB cellsImmune system
2007
Identification of a cis-acting element of human dihydrofolate reductase mRNA
Tai N, Schmitz JC, Chen TM, O’Neill M, Chu E. Identification of a cis-acting element of human dihydrofolate reductase mRNA. Biochemical And Biophysical Research Communications 2007, 369: 795-800. PMID: 18045573, DOI: 10.1016/j.bbrc.2007.09.044.Peer-Reviewed Original Research
2004
Characterization of a cis-acting regulatory element in the protein-coding region of human dihydrofolate reductase mRNA
Ningwen T, SCHMITZ JC, CHEN TM, Edward C. Characterization of a cis-acting regulatory element in the protein-coding region of human dihydrofolate reductase mRNA. Biochemical Journal 2004, 378: 999-1006. PMID: 14664697, PMCID: PMC1224025, DOI: 10.1042/bj20031396.Peer-Reviewed Original Research
2002
Thymidylate synthase as a translational regulator of cellular gene expression
Liu J, Schmitz JC, Lin X, Tai N, Yan W, Farrell M, Bailly M, Chen T, Chu E. Thymidylate synthase as a translational regulator of cellular gene expression. Biochimica Et Biophysica Acta 2002, 1587: 174-182. PMID: 12084459, DOI: 10.1016/s0925-4439(02)00080-7.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic AgentsGene Expression RegulationGenes, p53HumansModels, BiologicalNeoplasmsProtein BiosynthesisRNA-Binding ProteinsRNA, MessengerThymidylate SynthaseConceptsTranslational regulatorCell cycleRNA binding proteinCellular gene expressionProcess of apoptosisTumor suppressor geneFolate-dependent enzymesTranslational repressionCellular mRNAsCognate mRNATranscription factorsMRNA interactionsMyc familyVivo model systemsGene expressionTS proteinCellular resistanceSuppressor geneBinding proteinMolecular elementsP53 tumor suppressor geneFunctional consequencesAbility of TSAutoregulatory controlProtein