2022
Histone Acetyltransferases p300 and CBP Coordinate Distinct Chromatin Remodeling Programs in Vascular Smooth Muscle Plasticity
Chakraborty R, Ostriker AC, Xie Y, Dave JM, Gamez-Mendez A, Chatterjee P, Abu Y, Valentine J, Lezon-Geyda K, Greif DM, Schulz VP, Gallagher PG, Sessa WC, Hwa J, Martin KA. Histone Acetyltransferases p300 and CBP Coordinate Distinct Chromatin Remodeling Programs in Vascular Smooth Muscle Plasticity. Circulation 2022, 145: 1720-1737. PMID: 35502657, DOI: 10.1161/circulationaha.121.057599.Peer-Reviewed Original ResearchConceptsHistone acetylationContractile genesContractile protein expressionPhenotypic switchingHistone acetyl transferase p300Human intimal hyperplasiaPlatelet-derived growth factor treatmentAcetyl transferase p300Key regulatory mechanismSmooth muscle cell phenotypeP300 expressionP300-dependent acetylationSmooth muscle plasticityDistinct functional interactionsMuscle cell phenotypeProtein expressionIntimal hyperplasiaRole of p300Methylcytosine dioxygenase TET2Chromatin modificationsEpigenetic regulationVSMC phenotypic switchingSpecific histoneCardiovascular diseaseMaster regulator
2013
Whole-exome sequencing identifies a novel somatic mutation in MMP8 associated with a t(1;22)-acute megakaryoblastic leukemia
Kim Y, Schulz VP, Satake N, Gruber TA, Teixeira AM, Halene S, Gallagher PG, Krause DS. Whole-exome sequencing identifies a novel somatic mutation in MMP8 associated with a t(1;22)-acute megakaryoblastic leukemia. Leukemia 2013, 28: 945-948. PMID: 24157583, PMCID: PMC3981934, DOI: 10.1038/leu.2013.314.Peer-Reviewed Original Research
2006
Allelic dropout in long QT syndrome genetic testing: A possible mechanism underlying false-negative results
Tester D, Cronk L, Carr J, Schulz V, Salisbury B, Judson R, Ackerman M. Allelic dropout in long QT syndrome genetic testing: A possible mechanism underlying false-negative results. Heart Rhythm 2006, 3: 815-821. PMID: 16818214, DOI: 10.1016/j.hrthm.2006.03.016.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAdultAllelesChildChromatography, High Pressure LiquidDNADNA Mutational AnalysisERG1 Potassium ChannelEther-A-Go-Go Potassium ChannelsExonsFalse Negative ReactionsFemaleGene FrequencyHumansKCNQ1 Potassium ChannelLong QT SyndromeMaleMuscle ProteinsMutationNAV1.5 Voltage-Gated Sodium ChannelPolymerase Chain ReactionPolymorphism, Single NucleotidePotassium Channels, Voltage-GatedRetrospective StudiesSodium ChannelsConceptsLong QT syndromeGenetic testingSingle nucleotide polymorphismsIntronic single nucleotide polymorphismLQTS-causing mutationsCongenital long QT syndromeCommon intronic single nucleotide polymorphismHigh clinical probabilityLong QT syndrome genetic testingLQTS genetic testingCardiac channel genes
2002
Schizosaccharomyces pombe pfh1+Encodes an Essential 5′ to 3′ DNA Helicase That Is a Member of thePIF1 Subfamily of DNA Helicases
Zhou J, Qi H, Schulz V, Mateyak M, Monson E, Zakian V. Schizosaccharomyces pombe pfh1+Encodes an Essential 5′ to 3′ DNA Helicase That Is a Member of thePIF1 Subfamily of DNA Helicases. Molecular Biology Of The Cell 2002, 13: 2180-2191. PMID: 12058079, PMCID: PMC117634, DOI: 10.1091/mbc.02-02-0021.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsDNA HelicasesDNA PrimersDNA, MitochondrialDNA, RibosomalDNA-Binding ProteinsHumansMolecular Sequence DataPolycomb-Group ProteinsProteinsRestriction MappingSaccharomyces cerevisiae ProteinsSchizosaccharomycesSchizosaccharomyces pombe ProteinsTranscription FactorsConceptsS. pombe proteinPombe proteinsDNA helicaseHelicase activityTelomeric DNAS. cerevisiaeATPase/helicase activitySchizosaccharomyces pombe geneSole essential functionDNA helicase activityInvariant lysine residuePombe geneDNA helicasesMitochondrial DNADNA replicationMutant sporesCellular phenotypesHigh identityGenetic analysisEssential functionsSame phenotypePrototype memberHelicaseLysine residuesS phase
2001
Haplotype Variation and Linkage Disequilibrium in 313 Human Genes
Stephens J, Schneider J, Tanguay D, Choi J, Acharya T, Stanley S, Jiang R, Messer C, Chew A, Han J, Duan J, Carr J, Lee M, Koshy B, Kumar A, Zhang G, Newell W, Windemuth A, Xu C, Kalbfleisch T, Shaner S, Arnold K, Schulz V, Drysdale C, Nandabalan K, Judson R, Ruaño G, Vovis G. Haplotype Variation and Linkage Disequilibrium in 313 Human Genes. Science 2001, 293: 489-493. PMID: 11452081, DOI: 10.1126/science.1059431.Peer-Reviewed Original ResearchConceptsSingle nucleotide polymorphismsPairs of SNPsLinkage disequilibriumVariable single nucleotide polymorphismsPatterns of variationIndividual single nucleotide polymorphismsHaplotype variationBiological traitsHuman genesDiverse ancestryDifferent haplotypesGenesNucleotide polymorphismsHuman populationUnrelated individualsHaplotypesRecent expansionPopulation frequencyDisequilibriumTraitsAncestryImportant implicationsInformation contentPolymorphismPopulation
2000
Pif1p Helicase, a Catalytic Inhibitor of Telomerase in Yeast
Zhou J, Monson E, Teng S, Schulz V, Zakian V. Pif1p Helicase, a Catalytic Inhibitor of Telomerase in Yeast. Science 2000, 289: 771-774. PMID: 10926538, DOI: 10.1126/science.289.5480.771.Peer-Reviewed Original ResearchMeSH KeywordsAllelesAmino Acid MotifsAnimalsCatalysisCell LineChromosomes, FungalDNA DamageDNA HelicasesDNA ReplicationDNA, FungalGene ExpressionHumansMutagenesis, Site-DirectedPoint MutationRecombinant ProteinsRecombination, GeneticSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSequence Homology, Amino AcidTelomeraseTelomere
1996
Accelerated loss of telomeric repeats may not explain accelerated replicative decline of Werner syndrome cells
Schulz V, Zakian V, Ogburn C, McKay J, Jarzebowicz A, Martin G, Edland S. Accelerated loss of telomeric repeats may not explain accelerated replicative decline of Werner syndrome cells. Human Genetics 1996, 97: 750-754. PMID: 8641691, DOI: 10.1007/bf02346184.Peer-Reviewed Original ResearchConceptsTRF lengthMean TRF lengthWerner syndromeDiabetes mellitusControl subjectsWS cellsReplicative declineSubset of cellsOcular cataractsGeriatric disordersPremature onsetMean lengthSenescent controlsReplicative capacitySenescent cellsEarly passagesAccelerated lossAccelerated rateChromosomal translocationsNormal somatic cellsWerner syndrome cellsReplicative potentialCellsCell cycle
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