Featured Publications
CCM3 Loss-Induced Lymphatic Defect Is Mediated by the Augmented VEGFR3-ERK1/2 Signaling
Qin L, Zhang H, Li B, Jiang Q, Lopez F, Min W, Zhou JH. CCM3 Loss-Induced Lymphatic Defect Is Mediated by the Augmented VEGFR3-ERK1/2 Signaling. Arteriosclerosis Thrombosis And Vascular Biology 2021, 41: 2943-2960. PMID: 34670407, PMCID: PMC8613000, DOI: 10.1161/atvbaha.121.316707.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosis Regulatory ProteinsCells, CulturedEndothelial CellsEndothelium, LymphaticFemaleGene DeletionHemangioma, Cavernous, Central Nervous SystemHyperplasiaMaleMAP Kinase Signaling SystemMice, Inbred StrainsModels, AnimalNF-kappa BTranslocation, GeneticVascular Endothelial Growth Factor Receptor-3ConceptsLymphatic ECsLymphatic defectsCerebral cavernous malformationsPan-endothelial cellsGrowth factor receptorTranscriptional levelTransport assaysLymphatic hyperplasiaCCM genesLymphatic dysfunctionNuclear translocationGenesFactor receptorVEGFR3ERK1/2Nuclear factorDeletionEC proliferationInhibition of VEGFR3Dependent mannerVascular endothelial growth factor receptorEndothelial growth factor receptorEC deletionAbnormal valve structureKPNA2
2014
Novel action and mechanism of auranofin in inhibition of vascular endothelial growth factor receptor-3-dependent lymphangiogenesis.
Chen X, Zhou HJ, Huang Q, Lu L, Min W. Novel action and mechanism of auranofin in inhibition of vascular endothelial growth factor receptor-3-dependent lymphangiogenesis. Anti-Cancer Agents In Medicinal Chemistry 2014, 14: 946-54. PMID: 24913775, PMCID: PMC5055472, DOI: 10.2174/1871520614666140610102651.Peer-Reviewed Original ResearchConceptsVascular endothelial growth factor receptor 3Lysosome-dependent pathwayProteasomal inhibitor MG132Lysosome inhibitor chloroquineGrowth factor receptor 3Transcription factor NF-κBFactor NF-κBInhibitor MG132EC cell linesReceptor essentialThioredoxin reductaseVivo lymphangiogenesisInhibitor chloroquineNovel targetCancer metastasisEC apoptosisCell linesDose-dependent mannerEC proliferationPotent therapeutic agentMechanism of actionDownregulationLymphangiogenesisRheumatoid arthritisPrimary ECs