Featured Publications
Glioblastoma mutations alter EGFR dimer structure to prevent ligand bias
Hu C, Leche CA, Kiyatkin A, Yu Z, Stayrook SE, Ferguson KM, Lemmon MA. Glioblastoma mutations alter EGFR dimer structure to prevent ligand bias. Nature 2022, 602: 518-522. PMID: 35140400, PMCID: PMC8857055, DOI: 10.1038/s41586-021-04393-3.Peer-Reviewed Original Research
2020
Comparison of tyrosine kinase domain properties for the neurotrophin receptors TrkA and TrkB.
Artim SC, Kiyatkin A, Lemmon MA. Comparison of tyrosine kinase domain properties for the neurotrophin receptors TrkA and TrkB. Biochemical Journal 2020, 477: 4053-4070. PMID: 33043964, PMCID: PMC7606831, DOI: 10.1042/bcj20200695.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBrain-Derived Neurotrophic FactorCatalytic DomainCell DifferentiationCell ProliferationGene Knockdown TechniquesKineticsMutationNerve Growth FactorsNerve Tissue ProteinsNeuroblastomaPC12 CellsPhosphorylationProtein DomainsRatsReceptor, trkAReceptor, trkBReceptors, Growth FactorRecombinant ProteinsRNA, Small InterferingSignal Transduction
2013
Immunogenicity, Efficacy, Safety, and Mechanism of Action of Epitope Vaccine (Lu AF20513) for Alzheimer's Disease: Prelude to a Clinical Trial
Davtyan H, Ghochikyan A, Petrushina I, Hovakimyan A, Davtyan A, Poghosyan A, Marleau AM, Movsesyan N, Kiyatkin A, Rasool S, Larsen AK, Madsen PJ, Wegener KM, Ditlevsen DK, Cribbs DH, Pedersen LO, Agadjanyan MG. Immunogenicity, Efficacy, Safety, and Mechanism of Action of Epitope Vaccine (Lu AF20513) for Alzheimer's Disease: Prelude to a Clinical Trial. Journal Of Neuroscience 2013, 33: 4923-4934. PMID: 23486963, PMCID: PMC3634356, DOI: 10.1523/jneurosci.4672-12.2013.Peer-Reviewed Original ResearchMeSH KeywordsAge FactorsAlzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnalysis of VarianceAnimalsAntibodies, Anti-IdiotypicAntibody FormationBrainCells, CulturedCytokinesDisease Models, AnimalDose-Response Relationship, ImmunologicEnzyme-Linked Immunosorbent AssayEpitopes, B-LymphocyteEpitopes, T-LymphocyteFemaleGuinea PigsHumansImmunologic MemoryMacaca fascicularisMaleMiceMice, TransgenicMutationNeurogliaPeptide FragmentsPlaque, AmyloidProtein BindingSurface Plasmon ResonanceT-LymphocytesVaccinationVaccinesConceptsAnti-Aβ antibodiesMemory T helper cellsT cell responsesT helper cellsClinical trialsMild ADDisease processAutoreactive T cell responsesAD mouse modelAD-like pathologyCerebral amyloid angiopathyRecent clinical trialsTetanus toxoid vaccineStrong humoral immunityStrong humoral responseAlzheimer's disease processNeurotoxic Aβ peptidesMechanism of actionMicroglial activationAmyloid angiopathyImmunotherapeutic approachesSingle immunizationHumoral immunityHumoral responseToxoid vaccine
2010
PI3K/Akt-sensitive MEK-independent compensatory circuit of ERK activation in ER-positive PI3K-mutant T47D breast cancer cells
Aksamitiene E, Kholodenko BN, Kolch W, Hoek JB, Kiyatkin A. PI3K/Akt-sensitive MEK-independent compensatory circuit of ERK activation in ER-positive PI3K-mutant T47D breast cancer cells. Cellular Signalling 2010, 22: 1369-1378. PMID: 20471474, PMCID: PMC2893265, DOI: 10.1016/j.cellsig.2010.05.006.Peer-Reviewed Original ResearchMeSH KeywordsBreast NeoplasmsCarcinoma, Ductal, BreastCell Line, TumorEpidermal Growth FactorExtracellular Signal-Regulated MAP KinasesFemaleHumansIntercellular Signaling Peptides and ProteinsMAP Kinase Signaling SystemMitogen-Activated Protein Kinase KinasesMutationPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktReceptors, EstrogenConceptsERK activationERK phosphorylationEpidermal growth factorRas/mitogen-activated protein kinase cascadeMitogen-activated protein kinase cascadeEGF-induced ERK phosphorylationT47D breast cancer cellsBreast cancer cellsProtein kinase cascadeErbB-family ligandsClass I PI3KMCF7 cellsCancer cellsErbB receptor ligandsSmall molecule inhibitorsPI3K/AktKinase cascadeProtein kinasePI3K inhibitionCandidate proteinsPD 098059Cellular growthCell survivalFamily ligandsMolecule inhibitors