2023
Chemiexcitation and melanin in photoreceptor disc turnover and prevention of macular degeneration
Lyu Y, Tschulakow A, Wang K, Brash D, Schraermeyer U. Chemiexcitation and melanin in photoreceptor disc turnover and prevention of macular degeneration. Proceedings Of The National Academy Of Sciences Of The United States Of America 2023, 120: e2216935120. PMID: 37155898, PMCID: PMC10194005, DOI: 10.1073/pnas.2216935120.Peer-Reviewed Original ResearchConceptsRetinal pigment epitheliumIntravitreal injectionMacular degenerationMelanolipofuscin granulesLipofuscin accumulationAge-related macular degenerationAlbino micePigmented miceMouse modelStargardt diseasePigment epitheliumRetinal pathologyRetinal degenerationNitric oxideDegenerationMiceLipofuscinPigment lipofuscinPhotoreceptor disksAlbinoAccelerated accumulationInjectionDiseasePathologyChemiexcited Neurotransmitters and Hormones Create DNA Photoproducts in the Dark
Gonçalves L, Angelé-Martínez C, Premi S, Palmatier M, Prado F, Di Mascio P, Bastos E, Brash D. Chemiexcited Neurotransmitters and Hormones Create DNA Photoproducts in the Dark. ACS Chemical Biology 2023, 18: 484-493. PMID: 36775999, PMCID: PMC10276651, DOI: 10.1021/acschembio.2c00787.Peer-Reviewed Original ResearchConceptsSinglet molecular oxygenOxidation of serotoninMolecular oxygenElectron excitationTriplet stateAdjacent pyrimidine basesAbsence of lightEnergy transferDark processPyrimidine basesSkin pigment melaninBiochemical reactionsMoleculesEnergy levelsCatecholamine neurotransmittersBiomoleculesCycloadditionUltravioletMammalian metabolismCyclobutane pyrimidine dimersOxidationAminesPigment melaninRadicalsPeroxynitriteChemiexcitation: Mammalian Photochemistry in the Dark†
Brash D, Goncalves L. Chemiexcitation: Mammalian Photochemistry in the Dark†. Photochemistry And Photobiology 2023, 99: 251-276. PMID: 36681894, PMCID: PMC10065968, DOI: 10.1111/php.13781.Peer-Reviewed Original ResearchConceptsExcited statesMammalian cellsCyclobutane pyrimidine dimersEvolutionary selectionBond rearrangementUnoccupied orbitalsGround stateReaction productsPyrimidine dimersChemiexcitationRecent findingsBiologyPathogenic eventsRadicalsUltraviolet lightMoleculesDrug-induced deafnessPotential pathogenesisCellsMelaninAchilles heelMammalsBiomoleculesPhotochemistryDNA
2001
Escaping the stem cell compartment: Sustained UVB exposure allows p53-mutant keratinocytes to colonize adjacent epidermal proliferating units without incurring additional mutations
Zhang W, Remenyik E, Zelterman D, Brash D, Wikonkal N. Escaping the stem cell compartment: Sustained UVB exposure allows p53-mutant keratinocytes to colonize adjacent epidermal proliferating units without incurring additional mutations. Proceedings Of The National Academy Of Sciences Of The United States Of America 2001, 98: 13948-13953. PMID: 11707578, PMCID: PMC61147, DOI: 10.1073/pnas.241353198.Peer-Reviewed Original ResearchThe DNA Damage Signal for Mdm2 Regulation, Trp53 Induction, and Sunburn Cell Formation In Vivo Originates from Actively Transcribed Genes
Brash D, Wikonkal N, Remenyik E, van der Horst G, Friedberg E, Cheo D, van Steeg H, Westerman A, van Kranen H. The DNA Damage Signal for Mdm2 Regulation, Trp53 Induction, and Sunburn Cell Formation In Vivo Originates from Actively Transcribed Genes. Journal Of Investigative Dermatology 2001, 117: 1234-1240. PMID: 11710938, DOI: 10.1046/j.0022-202x.2001.01554.x.Peer-Reviewed Original ResearchConceptsDNA photoproductsDNA damage signalsUnrepaired DNA lesionsCell formationSpecific genome regionsTumor suppressor proteinCsb-/- miceUltraviolet-induced apoptosisNucleotide excision repair genesApoptosis signal pathwayExcision repair genesActive genesMutant cellsGenome regionsDNA repairSuppressor proteinDamage signalsMDM2 regulationWild typeDNA lesionsPrevents cellsHomozygous inactivationGenesRepair genesDNA signalsTransgenic expression of survivin in keratinocytes counteracts UVB-induced apoptosis and cooperates with loss of p53
Grossman D, Kim P, Blanc-Brude O, Brash D, Tognin S, Marchisio P, Altieri D. Transgenic expression of survivin in keratinocytes counteracts UVB-induced apoptosis and cooperates with loss of p53. Journal Of Clinical Investigation 2001, 108: 991-999. PMID: 11581300, PMCID: PMC200956, DOI: 10.1172/jci13345.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisChromosomal Proteins, Non-HistoneGene ExpressionHumansInhibitor of Apoptosis ProteinsKeratin-14KeratinocytesKeratinsMiceMice, KnockoutMice, TransgenicMicrotubule-Associated ProteinsNeoplasm ProteinsPhenotypePromoter Regions, GeneticSkinSurvivinTumor Suppressor Protein p53Ultraviolet Rays
2000
Regulation of TNFα production and release in human and mouse keratinocytes and mouse skin after UV‐B irradiation
Yarosh D, Both D, Kibitel J, Anderson C, Elmets C, Brash D, Brown D. Regulation of TNFα production and release in human and mouse keratinocytes and mouse skin after UV‐B irradiation. Photodermatology Photoimmunology & Photomedicine 2000, 16: 263-270. PMID: 11132130, DOI: 10.1034/j.1600-0781.2000.160606.x.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsCell LineCell MembraneEnzyme-Linked Immunosorbent AssayGene Expression RegulationGenes, fosGenes, p53HomozygoteHumansInterleukin-1KeratinocytesMaleMiceMice, Inbred C57BLMice, KnockoutProtein Serine-Threonine KinasesRadiation DosageReceptors, Tumor Necrosis FactorReverse Transcriptase Polymerase Chain ReactionSignal TransductionSirolimusSkinTranscription Factor AP-1Tumor Necrosis Factor-alphaUltraviolet RaysConceptsP53 knockout miceKnockout miceMembrane-bound TNFalphaHomozygous p53 knockout miceC-Fos signalingWild-type miceGene knockout miceRelease of TNFalphaTNFalpha gene expressionAP-1Cultured human keratinocytesImmunosuppressive responseCell culture supernatantsAP-1 transcription factorCultured epidermal cellsIL-1alphaCytokine TNFalphaTNFα productionType micePrimary cytokineTNFalpha inductionTNFalphaBasal levelsMouse skinMice
1999
Induction of cyclin-dependent kinase inhibitors and G1 prolongation by the chemopreventive agent N-acetylcysteine
Liu M, Wikonkal N, Brash D. Induction of cyclin-dependent kinase inhibitors and G1 prolongation by the chemopreventive agent N-acetylcysteine. Carcinogenesis 1999, 20: 1869-1872. PMID: 10469636, DOI: 10.1093/carcin/20.9.1869.Peer-Reviewed Original ResearchMeSH KeywordsAcetylcysteineAnimalsAnticarcinogenic AgentsAntioxidantsCell CycleCell LineChromansCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p21CyclinsFibroblastsFree Radical ScavengersG1 PhaseGene Expression RegulationGene Expression Regulation, NeoplasticGenes, p16GlutathioneHumansKeratinocytesMiceModels, BiologicalNeoplasm ProteinsPapillomaSkin NeoplasmsTumor Cells, CulturedTumor Suppressor Protein p53ConceptsCyclin-dependent kinase inhibitorNovel molecular basisCell cycle transitionKinase inhibitorsDNA replicationDNA repairCellular differentiationMolecular basisG1 prolongationGene expressionAntioxidant N-acetylcysteineN-acetylcysteineIntracellular glutathione levelsArrestAgent N-acetylcysteineInductionInhibitorsGlutathione levelsCyclinChemopreventive agentsChemopreventive activityDifferentiationUsual mechanismP53Replication
1996
The role of the human homologue of Drosophila patched in sporadic basal cell carcinomas
Gailani M, Ståhle-Bäckdahl M, Leffell D, Glyn M, Zaphiropoulos P, Undén A, Dean M, Brash D, Bale A, Toftgård R. The role of the human homologue of Drosophila patched in sporadic basal cell carcinomas. Nature Genetics 1996, 14: 78-81. PMID: 8782823, DOI: 10.1038/ng0996-78.Peer-Reviewed Original ResearchConceptsSporadic basal cell carcinomasSingle-strand conformational polymorphismTumor suppressorDrosophila segment polarity geneSegment polarity genesHedgehog target genesPolarity genesDrosophila mutantsStrong homologyHuman homologueTarget genesMutational inactivationMutant transcriptsStrand conformational polymorphismNorthern blotSSCP variantsGenesNegative feedback mechanismSitu hybridizationConformational polymorphismNevoid basal cell carcinoma syndromeSuppressorAllelic lossInactivationMutationsCellular proofreading
Brash D. Cellular proofreading. Nature Medicine 1996, 2: 525-526. PMID: 8616708, DOI: 10.1038/nm0596-525.Commentaries, Editorials and Letters
1994
Sunburn and p53 in the onset of skin cancer
Ziegler A, Jonason A, Leffellt D, Simon J, Sharma H, Kimmelman J, Remington L, Jacks T, Brash D. Sunburn and p53 in the onset of skin cancer. Nature 1994, 372: 773-776. PMID: 7997263, DOI: 10.1038/372773a0.Peer-Reviewed Original ResearchConceptsActinic keratosisP53 mutationsSquamous cell carcinomaP53 tumor suppressor geneP53-mutated cellsCell carcinomaApoptotic keratinocytesSkin cancerTumor initiatorTumor suppressor geneMouse skinClonal expansionPrecancerous cellsTumor promoterCarcinomaSkinTissue responseP53SunburnCell differentiationDNA damageAberrant cell differentiationCellsResponseKeratosis
1984
Longevity-dependent organ-specific accumulation of DNA damage in two closely related murine species
Su C, Brash D, Turturro A, Hart R. Longevity-dependent organ-specific accumulation of DNA damage in two closely related murine species. Mechanisms Of Ageing And Development 1984, 27: 239-247. PMID: 6492898, DOI: 10.1016/0047-6374(84)90049-6.Peer-Reviewed Original Research
1982
Determination of DNA superhelicity and extremely low levels of DNA strand breaks in low numbers of nonradiolabeled cells by DNA-4′,6-diamidino-2-phenylindole fluorescence in nucleoid gradients
Lipetz P, Brash D, Joseph L, Jewett H, Lisle D, Lantry L, Hart R, Stephens R. Determination of DNA superhelicity and extremely low levels of DNA strand breaks in low numbers of nonradiolabeled cells by DNA-4′,6-diamidino-2-phenylindole fluorescence in nucleoid gradients. Analytical Biochemistry 1982, 121: 339-348. PMID: 7103066, DOI: 10.1016/0003-2697(82)90491-2.Peer-Reviewed Original Research