2019
Genomic sites hypersensitive to ultraviolet radiation
Premi S, Han L, Mehta S, Knight J, Zhao D, Palmatier MA, Kornacker K, Brash DE. Genomic sites hypersensitive to ultraviolet radiation. Proceedings Of The National Academy Of Sciences Of The United States Of America 2019, 116: 24196-24205. PMID: 31723047, PMCID: PMC6883822, DOI: 10.1073/pnas.1907860116.Peer-Reviewed Original ResearchMeSH Keywords5' Untranslated RegionsCells, CulturedDNA DamageFibroblastsGene Expression RegulationGenome, HumanHigh-Throughput Nucleotide SequencingHumansMelanocytesMelanomaMutationPromoter Regions, GeneticProtein BiosynthesisPyrimidine DimersPyrimidine NucleotidesSkin NeoplasmsTOR Serine-Threonine KinasesUltraviolet RaysConceptsCyclobutane pyrimidine dimersETS family transcription factorsIndividual gene promotersFamily transcription factorsRNA-binding proteinPrimary human melanocytesSingle-base resolutionEpigenetic marksGenomic averageTranslation regulationGenomic sitesMotif locationsTranscription factorsCell physiologyGene promoterCancer driversGenomeHuman melanocytesCell typesTumor evolutionCell pathwaysRare mutationsUV targetPyrimidine dimersApurinic sites
2018
Inflammasome Priming Mediated via Toll-Like Receptors 2 and 4, Induces Th1-Like Regulatory T Cells in De Novo Autoimmune Hepatitis
Arterbery AS, Yao J, Ling A, Avitzur Y, Martinez M, Lobritto S, Deng Y, Geliang G, Mehta S, Wang G, Knight J, Ekong UD. Inflammasome Priming Mediated via Toll-Like Receptors 2 and 4, Induces Th1-Like Regulatory T Cells in De Novo Autoimmune Hepatitis. Frontiers In Immunology 2018, 9: 1612. PMID: 30072988, PMCID: PMC6060440, DOI: 10.3389/fimmu.2018.01612.Peer-Reviewed Original ResearchToll-like receptor 2Monocytes/macrophagesAutoimmune hepatitisReceptor 2De novo autoimmune hepatitisRegulatory T cell phenotypeTumor necrosis factor αLate allograft dysfunctionLiver transplant subjectsNormal allograft functionNovo autoimmune hepatitisRegulatory T cellsLiver of patientsAdaptive immune mechanismsIFN-γ productionPro-inflammatory cytokinesT-cell phenotypeNecrosis factor αInflammatory signaling pathwaysAllograft dysfunctionAllograft functionDysfunctional TregsSpecific innateTransplant subjectsLiver transplantation
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