Cerebral cavernous malformations proteins inhibit Rho kinase to stabilize vascular integrity. - Wikidata - awgldk - TriplyDB

Cerebral cavernous malformations proteins inhibit Rho kinase to stabilize vascular integrity.

Cerebral cavernous malformations proteins inhibit Rho kinase to stabilize vascular integrity.

http://www.wikidata.org/entity/Q33794968

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Tumor necrosis factor disrupts claudin-5 endothelial tight junction barriers in two distinct NF-κB-dependent phases MST kinases in development and disease Cerebral cavernous malformation is a vascular disease associated with activated RhoA signaling Molecular mechanisms controlling vascular lumen formation in three-dimensional extracellular matrices Endothelial cell-cell adhesion during zebrafish vascular development Small G proteins in the cardiovascular system: physiological and pathological aspects Vascular anomalies: from genetics toward models for therapeutic trials Micro-CT Imaging Reveals Mekk3 Heterozygosity Prevents Cerebral Cavernous Malformations in Ccm2-Deficient Mice Rap1 can bypass the FAK-Src-Paxillin cascade to induce cell spreading and focal adhesion formation Structural basis of the junctional anchorage of the cerebral cavernous malformations complex Mechanism for KRIT1 Release of ICAP1-Mediated Suppression of Integrin Activation Cerebral Cavernous Malformations: Review of the Genetic and Protein-Protein Interactions Resulting in Disease Pathogenesis Rho kinase as a target for cerebral vascular disorders Dynamic regulation of the cerebral cavernous malformation pathway controls vascular stability and growth Identification of the Kelch family protein Nd1-L as a novel molecular interactor of KRIT1 RHO binding to FAM65A regulates Golgi reorientation during cell migration KLF4 is a key determinant in the development and progression of cerebral cavernous malformations.Pediatric cerebral cavernous malformations: Genetics, pathogenesis, and management.Exceptional aggressiveness of cerebral cavernous malformation disease associated with PDCD10 mutations Phosphorylation sites in the cerebral cavernous malformations complex CCM3 signaling through sterile 20-like kinases plays an essential role during zebrafish cardiovascular development and cerebral cavernous malformations CCM1-ICAP-1 complex controls β1 integrin-dependent endothelial contractility and fibronectin remodeling Rap1 Spatially Controls ArhGAP29 To Inhibit Rho Signaling during Endothelial Barrier Regulation.Combined HMG-COA reductase and prenylation inhibition in treatment of CCM.Exophytic hypothalamic cavernous malformation mimicking an extra-axial suprasellar mass.Lesions from patients with sporadic cerebral cavernous malformations harbor somatic mutations in the CCM genes: evidence for a common biochemical pathway for CCM pathogenesis.Programmed cell death-10 enhances proliferation and protects malignant T cells from apoptosis.Developmental timing of CCM2 loss influences cerebral cavernous malformations in mice.A novel mouse model of cerebral cavernous malformations based on the two-hit mutation hypothesis recapitulates the human disease.The 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.Rap1 and Rap2 antagonistically control endothelial barrier resistance.ccm2-like is required for cardiovascular development as a novel component of the Heg-CCM pathway.A mechanism of Rap1-induced stabilization of endothelial cell--cell junctions.Dynamic permeability and quantitative susceptibility: related imaging biomarkers in cerebral cavernous malformations Strategy for identifying repurposed drugs for the treatment of cerebral cavernous malformation.Increased number of white matter lesions in patients with familial cerebral cavernous malformations.Regulation of mammalian physiology, development, and disease by the sphingosine 1-phosphate and lysophosphatidic acid receptors.Fasudil decreases lesion burden in a murine model of cerebral cavernous malformation disease Angiogenic sprouting requires the fine tuning of endothelial cell cohesion by the Raf-1/Rok-α complex

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P2860

Cerebral cavernous malformations proteins inhibit Rho kinase to stabilize vascular integrity.

http://www.wikidata.org/entity/Q33794968

description

2010 nî lūn-bûn

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2010 թուականի Մարտին հրատարակուած գիտական յօդուած

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2010 թվականի մարտին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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name

Cerebral cavernous malformatio ...... stabilize vascular integrity.

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Cerebral cavernous malformatio ...... stabilize vascular integrity.

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Cerebral cavernous malformatio ...... stabilize vascular integrity.

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Cerebral cavernous malformatio ...... stabilize vascular integrity.

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Journal of Experimental Medicine

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Cerebral cavernous malformatio ...... stabilize vascular integrity.

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P2093

Issam A Awad

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Mark H Ginsberg

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Rebecca A Stockton

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Robert Shenkar

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P2860

CCM1 and CCM2 protein interactions in cell signaling: implications for cerebral cavernous malformations pathogenesis

Association of Krev-1/rap1a with Krit1, a novel ankyrin repeat-containing protein encoded by a gene mapping to 7q21-22

CCM3 interacts with CCM2 indicating common pathogenesis for cerebral cavernous malformations

Mutations in a gene encoding a novel protein containing a phosphotyrosine-binding domain cause type 2 cerebral cavernous malformations.

A two-hit mechanism causes cerebral cavernous malformations: complete inactivation of CCM1, CCM2 or CCM3 in affected endothelial cells

Deletions in CCM2 are a common cause of cerebral cavernous malformations

Regulation of cardiovascular development and integrity by the heart of glass-cerebral cavernous malformation protein pathway

VEGF controls endothelial-cell permeability by promoting the beta-arrestin-dependent endocytosis of VE-cadherin

Mutations in the gene encoding KRIT1, a Krev-1/rap1a binding protein, cause cerebral cavernous malformations (CCM1)

KRIT-1/CCM1 is a Rap1 effector that regulates endothelial cell cell junctions

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10.1084/JEM.20091258

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207

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