Mutations in 2 distinct genetic pathways result in cerebral cavernous malformations in mice.
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Loss of CCM3 impairs DLL4-Notch signalling: implication in endothelial angiogenesis and in inherited cerebral cavernous malformationsCerebral cavernous malformation is a vascular disease associated with activated RhoA signalingMolecular mechanisms controlling vascular lumen formation in three-dimensional extracellular matricesEndothelial cell-cell adhesion during zebrafish vascular developmentVascular anomalies: from genetics toward models for therapeutic trialsLack of CCM1 induces hypersprouting and impairs response to flowMicro-CT Imaging Reveals Mekk3 Heterozygosity Prevents Cerebral Cavernous Malformations in Ccm2-Deficient MiceKLF4 is a key determinant in the development and progression of cerebral cavernous malformations.Exceptional aggressiveness of cerebral cavernous malformation disease associated with PDCD10 mutationsCCM1-ICAP-1 complex controls β1 integrin-dependent endothelial contractility and fibronectin remodelingDevelopmental timing of CCM2 loss influences cerebral cavernous malformations in mice.PDCD10 gene mutations in multiple cerebral cavernous malformationsThe pathobiology of vascular malformations: insights from human and model organism genetics.KRIT1 protein depletion modifies endothelial cell behavior via increased vascular endothelial growth factor (VEGF) signaling.Strategy for identifying repurposed drugs for the treatment of cerebral cavernous malformation.Downregulation of programmed cell death 10 is associated with tumor cell proliferation, hyperangiogenesis and peritumoral edema in human glioblastoma.ANKS1B Interacts with the Cerebral Cavernous Malformation Protein-1 and Controls Endothelial Permeability but Not Sprouting Angiogenesis.The cerebral cavernous malformation pathway controls cardiac development via regulation of endocardial MEKK3 signaling and KLF expression.Apicobasal polarity of brain endothelial cells.Minimal homozygous endothelial deletion of Eng with VEGF stimulation is sufficient to cause cerebrovascular dysplasia in the adult mouse.Nogo-B receptor deficiency causes cerebral vasculature defects during embryonic development in mice.Loss of endothelial programmed cell death 10 activates glioblastoma cells and promotes tumor growth.Endothelial exocytosis of angiopoietin-2 resulting from CCM3 deficiency contributes to cerebral cavernous malformation.A Novel CCM2 Gene Mutation Associated with Familial Cerebral Cavernous MalformationIntroduction to cerebral cavernous malformation: a brief review.Cerebral cavernous malformation proteins at a glance.STRIPAK complexes: structure, biological function, and involvement in human diseases.Ccm3, a gene associated with cerebral cavernous malformations, is required for neuronal migration.Signaling pathways and the cerebral cavernous malformations proteins: lessons from structural biology.Genetic and cellular basis of cerebral cavernous malformations: implications for clinical management.SOcK, MiSTs, MASK and STicKs: the GCKIII (germinal centre kinase III) kinases and their heterologous protein-protein interactions.A murine toolbox for imaging the neurovascular unit.PTEN/PI3K/Akt/VEGF signaling and the cross talk to KRIT1, CCM2, and PDCD10 proteins in cerebral cavernous malformations.Up-regulation of NADPH oxidase-mediated redox signaling contributes to the loss of barrier function in KRIT1 deficient endothelium.Oxidative stress and inflammation in cerebral cavernous malformation disease pathogenesis: Two sides of the same coin.Cerebral cavernous malformations arise independent of the heart of glass receptor.Focal defects in single-celled tubes mutant for Cerebral cavernous malformation 3, GCKIII, or NSF2.Decreased Krev interaction-trapped 1 expression leads to increased vascular permeability and modifies inflammatory responses in vivo.CCM-3/STRIPAK promotes seamless tube extension through endocytic recycling.KRIT1 loss-of-function induces a chronic Nrf2-mediated adaptive homeostasis that sensitizes cells to oxidative stress: Implication for Cerebral Cavernous Malformation disease.
P2860
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P2860
Mutations in 2 distinct genetic pathways result in cerebral cavernous malformations in mice.
description
2011 nî lūn-bûn
@nan
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
2011年论文
@zh
2011年论文
@zh-cn
name
Mutations in 2 distinct geneti ...... vernous malformations in mice.
@en
type
label
Mutations in 2 distinct geneti ...... vernous malformations in mice.
@en
prefLabel
Mutations in 2 distinct geneti ...... vernous malformations in mice.
@en
P2093
P2860
P356
P1476
Mutations in 2 distinct geneti ...... avernous malformations in mice
@en
P2093
Alexandra C H Smith
Allie H Grossmann
Amber N Stratman
Anastasia Sacharidou
Christopher C Gibson
George E Davis
Kevin J Whitehead
M Patricia Revelo
P2860
P304
P356
10.1172/JCI44393
P407
P577
2011-04-01T00:00:00Z