2015
Endothelial-to-mesenchymal transition drives atherosclerosis progression
Chen PY, Qin L, Baeyens N, Li G, Afolabi T, Budatha M, Tellides G, Schwartz MA, Simons M. Endothelial-to-mesenchymal transition drives atherosclerosis progression. Journal Of Clinical Investigation 2015, 125: 4514-4528. PMID: 26517696, PMCID: PMC4665771, DOI: 10.1172/jci82719.Peer-Reviewed Original ResearchConceptsProgression of atherosclerosisTGF-β signalingFGF receptor 1Left main coronary arteryMesenchymal transitionFGFR1 expressionDevelopment of EndMTMain coronary arteryTotal plaque burdenHigh-fat dietCultured human endothelial cellsDouble knockout miceEndothelial-specific deletionEarly time pointsCoronary atherosclerosisCoronary diseaseHuman endothelial cellsAtherosclerosis progressionPlaque burdenAtherosclerotic miceCoronary arteryInflammatory cytokinesAtherosclerotic lesionsNeointima formationClinical relevance
2012
Syndecan 4 Regulates FGFR1 Signaling in Endothelial Cells by Directing Macropinocytosis
Elfenbein A, Lanahan A, Zhou TX, Yamasaki A, Tkachenko E, Matsuda M, Simons M. Syndecan 4 Regulates FGFR1 Signaling in Endothelial Cells by Directing Macropinocytosis. Science Signaling 2012, 5: ra36. PMID: 22569333, PMCID: PMC3827948, DOI: 10.1126/scisignal.2002495.Peer-Reviewed Original ResearchConceptsFGF receptor 1Mitogen-activated protein kinaseFibroblast growth factor-2MAPK signalingSyndecan-4Inhibition of Rab5Receptor tyrosine kinasesEndothelial cell migrationHeparan sulfate proteoglycanSignal transductionProtein kinaseFGF2 stimulationEndothelial cellsMAPK activationTyrosine kinaseGrowth factor 2Genetic knockoutCell migrationReceptor complexMacropinocytosisClasses of receptorsSignalingRab5Factor 2Sulfate proteoglycan
2009
Increased Bone Volume and Correction of HYP Mouse Hypophosphatemia in the Klotho/HYP Mouse
Brownstein CA, Zhang J, Stillman A, Ellis B, Troiano N, Adams DJ, Gundberg CM, Lifton RP, Carpenter TO. Increased Bone Volume and Correction of HYP Mouse Hypophosphatemia in the Klotho/HYP Mouse. Endocrinology 2009, 151: 492-501. PMID: 19952276, PMCID: PMC2817612, DOI: 10.1210/en.2009-0564.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCalciumCrosses, GeneticDNA PrimersDNA-Binding ProteinsFamilial Hypophosphatemic RicketsFemaleFemurFibroblast Growth Factor-23Genetic Diseases, X-LinkedGenotypeGlucuronidaseHeterozygoteHomozygoteHumansKlotho ProteinsMaleMiceMice, KnockoutNuclear ProteinsPolymerase Chain ReactionTibiaTomography, X-Ray ComputedTranscription FactorsConceptsTrabecular bone densityHyp miceBone densityGreater trabecular bone volume fractionFibroblast growth factor 23Serum PTH levelsDihydroxyvitamin D levelsGrowth factor 23Vitamin D metabolismTrabecular bone volume fractionDouble knockout miceKlotho null miceFGF23 effectsKlotho lossPhosphaturic activityPTH levelsFGF23 actionFGF23 levelsBone volume fractionFactor 23D metabolismD levelsFGF receptor 1Osteoid volumeBone volume
2002
Chronic hypoxia up-regulates fibroblast growth factor ligands in the perinatal brain and induces fibroblast growth factor-responsive radial glial cells in the sub-ependymal zone
Ganat Y, Soni S, Chacon M, Schwartz ML, Vaccarino FM. Chronic hypoxia up-regulates fibroblast growth factor ligands in the perinatal brain and induces fibroblast growth factor-responsive radial glial cells in the sub-ependymal zone. Neuroscience 2002, 112: 977-991. PMID: 12088755, DOI: 10.1016/s0306-4522(02)00060-x.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBlotting, WesternCerebral CortexCerebral VentriclesEnzyme-Linked Immunosorbent AssayEpendymaFibroblast Growth Factor 1Fibroblast Growth Factor 2HypoxiaImmunohistochemistryNeurogliaRatsReceptor Protein-Tyrosine KinasesReceptor, Fibroblast Growth Factor, Type 1Receptor, Fibroblast Growth Factor, Type 2Receptors, Fibroblast Growth FactorRegenerationUp-RegulationConceptsRadial glial cellsRadial gliaChronic hypoxiaGlial cellsFibroblast growth factor 1Periventricular regionBrain lipid binding proteinMajor receptorChronic hypoxic damageGlial fibrillary acidic proteinHypoxia/ischemiaSub-ventricular zoneImmature glial cellsFibrillary acidic proteinGrowth factor-1Ependymal zoneChronic hypoxemiaCerebral cortexHypoxic damageNeurotrophin familyPerinatal brainFGF receptor 1Rat pupsPostnatal weekGlial phenotype
1997
Suppression of autocrine cell proliferation and tumorigenesis of human melanoma cells and fibroblast growth factor transformed fibroblasts by a kinase-deficient FGF receptor 1: evidence for the involvement of Src-family kinases
Yayon A, Ma Y, Safran M, Klagsbrun M, Halaban R. Suppression of autocrine cell proliferation and tumorigenesis of human melanoma cells and fibroblast growth factor transformed fibroblasts by a kinase-deficient FGF receptor 1: evidence for the involvement of Src-family kinases. Oncogene 1997, 14: 2999-3009. PMID: 9223663, DOI: 10.1038/sj.onc.1201159.Peer-Reviewed Original ResearchMeSH Keywords3T3 CellsAnimalsCell DivisionCell Line, TransformedFibroblast Growth Factor 2FibroblastsFilaggrin ProteinsGenes, DominantHumansMelanomaMicePhenotypeProtein-Tyrosine KinasesReceptor Protein-Tyrosine KinasesReceptor, Fibroblast Growth Factor, Type 1Receptors, Fibroblast Growth FactorRecombinant Proteinssrc Homology DomainsTumor Cells, CulturedConceptsSrc family kinasesFGF receptor 1FGF receptorsTyrosyl-phosphorylated proteinsHuman melanoma cellsMelanoma cellsImmune kinase assayIntracellular kinase domainDominant negative mutantActivated FGF receptorCell proliferationMetastatic melanoma cellsMelanoma tumor progressionGrowth factorTransmembrane domainKinase assaysSrc familyKinase domainDownstream targetsReceptor 1Fibroblast growth factorBasic fibroblast growth factorGrowth advantageNormal melanocytesAutocrine activation
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