2019
DNAJB1-PRKACA fusions occur in oncocytic pancreatic and biliary neoplasms and are not specific for fibrolamellar hepatocellular carcinoma
Vyas M, Hechtman J, Zhang Y, Benayed R, Yavas A, Askan G, Shia J, Klimstra D, Basturk O. DNAJB1-PRKACA fusions occur in oncocytic pancreatic and biliary neoplasms and are not specific for fibrolamellar hepatocellular carcinoma. Modern Pathology 2019, 33: 648-656. PMID: 31676785, PMCID: PMC7125037, DOI: 10.1038/s41379-019-0398-2.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedBiliary Tract NeoplasmsBiomarkers, TumorCarcinoma, HepatocellularCyclic AMP-Dependent Protein Kinase Catalytic SubunitsFemaleGene FusionGenetic Predisposition to DiseaseHSP40 Heat-Shock ProteinsHumansLiver NeoplasmsMaleMiddle AgedOxyphil CellsPancreatic NeoplasmsPhenotypePrognosisSodium-Potassium-Exchanging ATPaseConceptsDNAJB1-PRKACA fusionProtein kinase activityKinase activityAnchored multiplex PCR technologyIdentification of sequence mutationsMultiplex PCR technologyFibrolamellar hepatocellular carcinomaDetect gene fusionsCopy number alterationsNext-generation sequencingNext-generation sequencing assayHybridization capture-based next-generation sequencing assaySequence mutationsHepatocellular carcinomaGene fusionsSequencing assayFISH analysisPancreatobiliary neoplasmsPCR technologyProtein kinase inhibitionStructural rearrangementsArginase-1MRNA in situ hybridizationAlbumin mRNA in situ hybridizationGenes
2009
C-Raf Is Associated with Disease Progression and Cell Proliferation in a Subset of Melanomas
Jilaveanu LB, Zito CR, Aziz SA, Conrad PJ, Schmitz JC, Sznol M, Camp RL, Rimm DL, Kluger HM. C-Raf Is Associated with Disease Progression and Cell Proliferation in a Subset of Melanomas. Clinical Cancer Research 2009, 15: 5704-5713. PMID: 19737955, PMCID: PMC2763114, DOI: 10.1158/1078-0432.ccr-09-0198.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAdultAgedAged, 80 and overBenzenesulfonatesCell Line, TumorCell ProliferationCell SurvivalCohort StudiesDisease ProgressionFemaleGene SilencingHumansIndolesMaleMelanomaMiddle AgedNevusNiacinamidePhenolsPhenylurea CompoundsProtein Kinase InhibitorsProto-Oncogene Proteins c-rafPyridinesRNA, Small InterferingSensitivity and SpecificitySkin NeoplasmsSorafenibYoung AdultConceptsExtracellular signal-regulated kinaseC-RafC-Raf expressionSubset of melanomasPhospho-c-RafSignal-regulated kinaseCell linesProtein kinase inhibitionMitogen-activated protein kinase inhibitionDecreased viabilityDecreased Bcl-2 expressionProtein kinaseCell signalingBcl-2 inhibitionRaf kinaseB-RafMelanoma cell linesPhospho-MEKSpecific siRNAsSitu protein expressionGW5074Major isoformsKinasePhospho-ERKBcl-2 expression
1994
Specificity of protein kinase inhibitor peptides and induction of long-term potentiation.
Hvalby O, Hemmings H, Paulsen O, Czernik A, Nairn A, Godfraind J, Jensen V, Raastad M, Storm J, Andersen P. Specificity of protein kinase inhibitor peptides and induction of long-term potentiation. Proceedings Of The National Academy Of Sciences Of The United States Of America 1994, 91: 4761-4765. PMID: 8197132, PMCID: PMC43868, DOI: 10.1073/pnas.91.11.4761.Peer-Reviewed Original ResearchConceptsProtein kinase CProtein kinase inhibitor peptideProtein kinase inhibitionInhibitor peptideDependent protein kinase IIInhibition of PKCKinase inhibitionProtein kinase IIPseudosubstrate domainAutoregulatory domainProtein kinasePhysiological assaysKinase IIKinase CLong-term potentiationSynthetic peptide analoguesInductionPeptide analoguesHippocampal neuronsPeptidesIntracellular deliveryBlockade of inductionInduction of LTPInhibitionVitro
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