Featured Publications
The Cellular Response to Neuregulins Is Governed by Complex Interactions of the erbB Receptor Family
Riese D, van Raaij T, Plowman G, Andrews G, Stern D. The Cellular Response to Neuregulins Is Governed by Complex Interactions of the erbB Receptor Family. Molecular And Cellular Biology 1995, 15: 5770-5776. PMID: 7565730, PMCID: PMC230829, DOI: 10.1128/mcb.15.10.5770.Peer-Reviewed Original ResearchConceptsReceptor familyEpidermal growth factor receptor tyrosine kinase familyErbB family receptorsErbB receptor familyReceptor tyrosine kinase familyReceptor tyrosine phosphorylationPeptide agonistsFamily receptorsTyrosine kinase familyHuman cancersReceptor interactionEpidermal growth factor homology domainsCell linesCell survivalReceptorsNeuregulinCellular responsesTyrosine phosphorylation
2013
MERTK controls melanoma cell migration and survival and differentially regulates cell behavior relative to AXL
Tworkoski KA, Platt JT, Bacchiocchi A, Bosenberg M, Boggon TJ, Stern DF. MERTK controls melanoma cell migration and survival and differentially regulates cell behavior relative to AXL. Pigment Cell & Melanoma Research 2013, 26: 527-541. PMID: 23617806, PMCID: PMC3918898, DOI: 10.1111/pcmr.12110.Peer-Reviewed Original ResearchMeSH KeywordsAxl Receptor Tyrosine KinaseCdc42 GTP-Binding ProteinCell Line, TumorCell MovementCell ProliferationCell SurvivalC-Mer Tyrosine KinaseCytophotometryGene Expression ProfilingGene Expression Regulation, NeoplasticHEK293 CellsHumansMelanomaNeoplasm MetastasisOligonucleotide Array Sequence AnalysisPhosphorylationProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesSignal TransductionSkin NeoplasmsConceptsCell migrationCell behaviorMelanoma cellsAkt-dependent mannerShRNA-mediated knockdownDifferential cell behaviorDifferent transcriptional signaturesReceptor tyrosine kinase AXLMelanoma cell migrationMelanoma cell proliferationKinase domainTyrosine kinase AXLCell motilityTranscriptional signatureCell survivalColony formationCell proliferationOverexpression of AxlPossible therapeutic targetMelanoma pathogenesisNovel mutationsMerTKAxlTherapeutic targetMutations
2004
A Ddc2-Rad53 Fusion Protein Can Bypass the Requirements for RAD9 and MRC1 in Rad53 Activation
Lee SJ, Duong JK, Stern DF. A Ddc2-Rad53 Fusion Protein Can Bypass the Requirements for RAD9 and MRC1 in Rad53 Activation. Molecular Biology Of The Cell 2004, 15: 5443-5455. PMID: 15456903, PMCID: PMC532024, DOI: 10.1091/mbc.e04-07-0608.Peer-Reviewed Original ResearchConceptsDNA damageDNA damage checkpoint pathwayFusion proteinDamage checkpoint pathwayRad53p activationRad53 activationMethyl methaneCheckpoint pathwaySignaling systemCell survivalMediator requirementMec1pEssential roleProteinCellsActivationExpressionRad53pRad9pDdc2Rad9Mrc1pMinimal requirementsMrc1Oligomerization