2013
RAC1P29S is a spontaneously activating cancer-associated GTPase
Davis MJ, Ha BH, Holman EC, Halaban R, Schlessinger J, Boggon TJ. RAC1P29S is a spontaneously activating cancer-associated GTPase. Proceedings Of The National Academy Of Sciences Of The United States Of America 2013, 110: 912-917. PMID: 23284172, PMCID: PMC3549122, DOI: 10.1073/pnas.1220895110.Peer-Reviewed Original ResearchAmino Acid SubstitutionAnimalsCell Surface ExtensionsChlorocebus aethiopsCOS CellsCrystallography, X-RayEnzyme ActivationGenetic Association StudiesGuanosine TriphosphateHumansHydrolysisKineticsMelanomaMiceMicroscopy, FluorescenceModels, MolecularMutation, MissenseNIH 3T3 CellsOncogenesRac1 GTP-Binding ProteinRecombinant Fusion ProteinsSignal TransductionStatic Electricity
2000
Endoplasmic reticulum retention is a common defect associated with tyrosinase-negative albinism
Halaban R, Svedine S, Cheng E, Smicun Y, Aron R, Hebert D. Endoplasmic reticulum retention is a common defect associated with tyrosinase-negative albinism. Proceedings Of The National Academy Of Sciences Of The United States Of America 2000, 97: 5889-5894. PMID: 10823941, PMCID: PMC18529, DOI: 10.1073/pnas.97.11.5889.Peer-Reviewed Original ResearchMeSH KeywordsAlbinism, OculocutaneousAmino Acid SubstitutionAnimalsCalcium-Binding ProteinsCalnexinCalreticulinCells, CulturedEndoplasmic ReticulumGolgi ApparatusHumansMelanocytesMelanosomesMiceMice, Mutant StrainsMicroscopy, FluorescenceMonophenol MonooxygenasePoint MutationProtein BindingProtein FoldingRecombinant Fusion ProteinsRibonucleoproteinsTransfection
1998
Release of cell cycle constraints in mouse melanocytes by overexpressed mutant E2F1E132, but not by deletion of p16INK4A or p21WAF1/CIP1
Halaban R, Cheng E, Zhang Y, Mandigo C, Miglarese M. Release of cell cycle constraints in mouse melanocytes by overexpressed mutant E2F1E132, but not by deletion of p16INK4A or p21WAF1/CIP1. Oncogene 1998, 16: 2489-2501. PMID: 9627115, DOI: 10.1038/sj.onc.1201773.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCarrier ProteinsCell CycleCell Cycle ProteinsCell SurvivalCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p21CyclinsDNA-Binding ProteinsE2F Transcription FactorsE2F1 Transcription FactorGene Expression RegulationHumansMelanocytesMiceMice, NudeMutagenesisProtein BiosynthesisRecombinant Fusion ProteinsRetinoblastoma ProteinRetinoblastoma-Binding Protein 1Tetradecanoylphorbol AcetateTranscription Factor DP1Transcription FactorsConceptsP21WAF1/CIP1Cell cycle progressionMouse melanocytesTarget genesCycle progressionRetinoblastoma tumor suppressor proteinE2F-mediated transactivationCell cycle constraintsTumor suppressor proteinRole of E2F1Deletion of p16INK4AFree E2FExpression of RbGene disruptionSuppressor proteinEctopic expressionHallmark of melanomaTetradecanoyl phorbol 13Loss of p16INK4aConstitutive expressionMelanoma cell linesCell deathNormal melanocytesIndependent growthMelanocyte growth
1995
Identification of p90RSK as the probable CREB-Ser133 kinase in human melanocytes.
Böhm M, Moellmann G, Cheng E, Alvarez-Franco M, Wagner S, Sassone-Corsi P, Halaban R. Identification of p90RSK as the probable CREB-Ser133 kinase in human melanocytes. Molecular Cancer Research 1995, 6: 291-302. PMID: 7540859.Peer-Reviewed Original ResearchMeSH KeywordsCell CountCell DivisionCells, CulturedCyclic AMPCyclic AMP Response Element-Binding ProteinDrug SynergismEndothelinsFibroblast Growth Factor 2Growth SubstancesHematopoietic Cell Growth FactorsHepatocyte Growth FactorHumansInfant, NewbornMelanocytesPhosphorylationProtein Serine-Threonine KinasesRecombinant Fusion ProteinsRibosomal Protein S6 KinasesSerineStem Cell FactorTime FactorsTranscription FactorsConceptsSynergistic growth factorsMast/stem cell growth factorHuman melanocytesGrowth factorHepatocyte growth factor/scatter factorActivation of p90RSKGrowth factor/scatter factorStem cell growth factorCAMP-responsive element binding proteinKID domainElement-binding proteinNormal human melanocytesTranscription factor 1Peptide growth factorsSer133 phosphorylationTranscriptional activationCell divisionPhosphorylated stateTranscription factorsInduces phosphorylationRegulatory proteinsSignal transducerFibroblast growth factorBasic fibroblast growth factorBinding protein