Minimal homozygous endothelial deletion of Eng with VEGF stimulation is sufficient to cause cerebrovascular dysplasia in the adult mouse.
about
Targeting BMP signalling in cardiovascular disease and anaemiaAnimal Models in Studying Cerebral Arteriovenous MalformationMononuclear cells and vascular repair in HHTBrain arteriovenous malformation modeling, pathogenesis, and novel therapeutic targets.Molecular pathways: can activin-like kinase pathway inhibition enhance the limited efficacy of VEGF inhibitors?Novel brain arteriovenous malformation mouse models for type 1 hereditary hemorrhagic telangiectasia.Endoglin deficiency in bone marrow is sufficient to cause cerebrovascular dysplasia in the adult mouse after vascular endothelial growth factor stimulation.Mouse Models of Cerebral Arteriovenous Malformation.Endothelial signaling and the molecular basis of arteriovenous malformation.Induction of brain arteriovenous malformation in the adult mouse.Mouse models of hereditary hemorrhagic telangiectasia: recent advances and future challenges.Pericytes as targets in hereditary hemorrhagic telangiectasia.Integrin β8 Deletion Enhances Vascular Dysplasia and Hemorrhage in the Brain of Adult Alk1 Heterozygous Mice.Pathogenesis of Brain Arteriovenous Malformations.Endoglin inhibition leads to intussusceptive angiogenesis via activation of factors related to COUP-TFII signaling pathway.Adult mouse venous hypertension model: common carotid artery to external jugular vein anastomosis.Executive summary of the 11th HHT international scientific conference.Endoglin prevents vascular malformation by regulating flow-induced cell migration and specification through VEGFR2 signalling.Endoglin and activin receptor-like kinase 1 heterozygous mice have a distinct pulmonary and hepatic angiogenic profile and response to anti-VEGF treatment.The roles of endoglin gene in cerebrovascular diseases.ALK1 signaling in development and disease: new paradigms.Endoglin and alk1 as therapeutic targets for hereditary hemorrhagic telangiectasia.Angiogenic stimuli and endoglin absence induces brain arteriovenous malformations: are local endoglin deletion and angiogenesis the 'second hit' that is necessary for arteriovenous malformations formation in HHT-1?
P2860
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P2860
Minimal homozygous endothelial deletion of Eng with VEGF stimulation is sufficient to cause cerebrovascular dysplasia in the adult mouse.
description
2012 nî lūn-bûn
@nan
2012年の論文
@ja
2012年論文
@yue
2012年論文
@zh-hant
2012年論文
@zh-hk
2012年論文
@zh-mo
2012年論文
@zh-tw
2012年论文
@wuu
2012年论文
@zh
2012年论文
@zh-cn
name
Minimal homozygous endothelial ...... dysplasia in the adult mouse.
@ast
Minimal homozygous endothelial ...... dysplasia in the adult mouse.
@en
type
label
Minimal homozygous endothelial ...... dysplasia in the adult mouse.
@ast
Minimal homozygous endothelial ...... dysplasia in the adult mouse.
@en
prefLabel
Minimal homozygous endothelial ...... dysplasia in the adult mouse.
@ast
Minimal homozygous endothelial ...... dysplasia in the adult mouse.
@en
P2093
P2860
P356
P1476
Minimal homozygous endothelial ...... dysplasia in the adult mouse.
@en
P2093
Espen J Walker
Eun-Jung Choi
Fanxia Shen
William L Young
P2860
P304
P356
10.1159/000337762
P577
2012-05-09T00:00:00Z