2017
Inflammation-dependent cerebrospinal fluid hypersecretion by the choroid plexus epithelium in posthemorrhagic hydrocephalus
Karimy JK, Zhang J, Kurland DB, Theriault BC, Duran D, Stokum JA, Furey CG, Zhou X, Mansuri MS, Montejo J, Vera A, DiLuna ML, Delpire E, Alper SL, Gunel M, Gerzanich V, Medzhitov R, Simard JM, Kahle KT. Inflammation-dependent cerebrospinal fluid hypersecretion by the choroid plexus epithelium in posthemorrhagic hydrocephalus. Nature Medicine 2017, 23: 997-1003. PMID: 28692063, DOI: 10.1038/nm.4361.Peer-Reviewed Original ResearchMeSH KeywordsAcetazolamideAnimalsAntioxidantsBlotting, WesternBumetanideCerebral HemorrhageCerebral VentriclesCerebrospinal FluidChoroid PlexusDiureticsGene Knockdown TechniquesGene Knockout TechniquesHydrocephalusImmunoblottingImmunohistochemistryImmunoprecipitationInflammationNF-kappa BProlineProtein Serine-Threonine KinasesRatsRats, WistarSalicylanilidesSolute Carrier Family 12, Member 2SulfonamidesThiocarbamatesToll-Like Receptor 4
2015
Augmentor α and β (FAM150) are ligands of the receptor tyrosine kinases ALK and LTK: Hierarchy and specificity of ligand–receptor interactions
Reshetnyak AV, Murray PB, Shi X, Mo ES, Mohanty J, Tome F, Bai H, Gunel M, Lax I, Schlessinger J. Augmentor α and β (FAM150) are ligands of the receptor tyrosine kinases ALK and LTK: Hierarchy and specificity of ligand–receptor interactions. Proceedings Of The National Academy Of Sciences Of The United States Of America 2015, 112: 15862-15867. PMID: 26630010, PMCID: PMC4702955, DOI: 10.1073/pnas.1520099112.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnaplastic Lymphoma KinaseAnimalsCell LineCell Line, TumorCell ProliferationCytokinesDoxycyclineEnzyme ActivationHEK293 CellsHeparinHumansImmunoblottingLigandsMiceMolecular Sequence DataNIH 3T3 CellsProtein BindingReceptor Protein-Tyrosine KinasesSequence Homology, Amino AcidConceptsLeukocyte tyrosine kinaseReceptor tyrosine kinasesTyrosine kinaseIL-3-independent growthCritical cellular functionsBa/F3 cellsCell surface receptorsAnaplastic lymphoma kinaseLigand-receptor interactionsCellular functionsLigand bindingF3 cellsReceptor tyrosineProtein ligandsNIH/3T3 cellsKinaseSurface receptorsIndependent growthSubnanomolar potencyCellsDisease statesHigh affinityLymphoma kinaseFAM150ANovel cytokine
2010
Stabilization of VEGFR2 Signaling by Cerebral Cavernous Malformation 3 Is Critical for Vascular Development
He Y, Zhang H, Yu L, Gunel M, Boggon TJ, Chen H, Min W. Stabilization of VEGFR2 Signaling by Cerebral Cavernous Malformation 3 Is Critical for Vascular Development. Science Signaling 2010, 3: ra26. PMID: 20371769, PMCID: PMC3052863, DOI: 10.1126/scisignal.2000722.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCardiovascular SystemEndothelial CellsFluorescent Antibody Technique, IndirectGene DeletionGene Expression ProfilingGene Knockdown TechniquesHematopoiesisHumansImmunoblottingImmunohistochemistryImmunoprecipitationMiceReverse Transcriptase Polymerase Chain ReactionSignal TransductionVascular Endothelial Growth Factor Receptor-2ConceptsCarboxyl-terminal domainVascular endothelial growth factor receptor 2Vascular developmentHuman vascular malformationsCerebral cavernous malformation 3Early embryonic stagesCerebral cavernous malformationsEndothelial cell-specific deletionApoptotic stimuliCell-specific deletionVivo functionEmbryonic angiogenesisEndothelial growth factor receptor 2Unknown functionVEGF stimulationVEGFR2 signalingEmbryonic stagesMessenger RNASmooth muscle cellsGrowth factor receptor 2DeletionCCM3 genesFactor receptor 2Muscle cellsGenes