2011
Loss of cerebral cavernous malformation 3 (Ccm3) in neuroglia leads to CCM and vascular pathology
Louvi A, Chen L, Two AM, Zhang H, Min W, Günel M. Loss of cerebral cavernous malformation 3 (Ccm3) in neuroglia leads to CCM and vascular pathology. Proceedings Of The National Academy Of Sciences Of The United States Of America 2011, 108: 3737-3742. PMID: 21321212, PMCID: PMC3048113, DOI: 10.1073/pnas.1012617108.Peer-Reviewed Original ResearchConceptsNeural cellsCerebral cavernous malformationsCell-nonautonomous mechanismsPathogenesis of CCMsRho GTPase signalingCell-autonomous mechanismsCell-autonomous roleCerebral cavernous malformation 3Cell death 10Central nervous systemConditional mouse mutantsNonautonomous functionsCytoskeletal remodelingRNA sequencingCCM3/Mouse mutantsNeurovascular unitNonautonomous mechanismsProper developmentVascular lesionsGene 1Function mutationsNervous systemAutonomous mechanismsLate functions
2008
PDCD10, the gene mutated in cerebral cavernous malformation 3, is expressed in the neurovascular unit.
Tanriover G, Boylan AJ, Diluna ML, Pricola KL, Louvi A, Gunel M. PDCD10, the gene mutated in cerebral cavernous malformation 3, is expressed in the neurovascular unit. Neurosurgery 2008, 62: 930-8; discussion 938. PMID: 18496199, DOI: 10.1227/01.neu.0000318179.02912.ca.Peer-Reviewed Original ResearchConceptsMultiple organ systemsNeurovascular unitPostnatal mouse brainCerebral cavernous malformation 3Mouse brainCell death 10 geneArterial endotheliumOrgan systemsGranule cell layerMessenger ribonucleic acid expressionRibonucleic acid expressionCCM3/PDCD10Brainstem tissueEmbryonic mouse brainSeptal nucleusCortical plateDentate gyrusHypothalamic nucleiOlfactory bulbHuman cerebralInferior colliculusSolid organ tissuesVenous structuresVenous endotheliumDisease pathogenesis