Rho kinase inhibition rescues the endothelial cell cerebral cavernous malformation phenotype. - Wikidata - awgldk - TriplyDB

Rho kinase inhibition rescues the endothelial cell cerebral cavernous malformation phenotype.

Rho kinase inhibition rescues the endothelial cell cerebral cavernous malformation phenotype.

http://www.wikidata.org/entity/Q28274176

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Cerebral cavernous malformation is a vascular disease associated with activated RhoA signaling Small G proteins in the cardiovascular system: physiological and pathological aspects Vascular anomalies: from genetics toward models for therapeutic trials 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 CCM2-CCM3 interaction stabilizes their protein expression and permits endothelial network formation RHO binding to FAM65A regulates Golgi reorientation during cell migration RhoA determines lineage fate of mesenchymal stem cells by modulating CTGF-VEGF complex in extracellular matrix.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 CCM1-ICAP-1 complex controls β1 integrin-dependent endothelial contractility and fibronectin remodeling Defining the functional domain of programmed cell death 10 through its interactions with phosphatidylinositol-3,4,5-trisphosphate.Role of cytoskeletal proteins in cerebral cavernous malformation signaling pathways: a proteomic analysis.Systems biology and proteomic analysis of cerebral cavernous malformation 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.A novel mouse model of cerebral cavernous malformations based on the two-hit mutation hypothesis recapitulates the human disease.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.Fasudil decreases lesion burden in a murine model of cerebral cavernous malformation disease 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.Structure and vascular function of MEKK3-cerebral cavernous malformations 2 complex.Phospholipase Cε Modulates Rap1 Activity and the Endothelial Barrier.Evaluating strategies for the treatment of cerebral cavernous malformations PDCD10 (CCM3) regulates brain endothelial barrier integrity in cerebral cavernous malformation type 3: role of CCM3-ERK1/2-cortactin cross-talk.Loss of endothelial programmed cell death 10 activates glioblastoma cells and promotes tumor growth.Cerebral cavernous malformations arise from endothelial gain of MEKK3-KLF2/4 signalling.Rap1 potentiates endothelial cell junctions by spatially controlling myosin II activity and actin organization.Introduction to cerebral cavernous malformation: a brief review.The Role of Ect2 Nuclear RhoGEF Activity in Ovarian Cancer Cell Transformation.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.Cerebral cavernous malformations: from molecular pathogenesis to genetic counselling and clinical management.Concepts and hypothesis: integrin cytoplasmic domain-associated protein-1 (ICAP-1) as a potential player in cerebral cavernous malformation.

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P2860

Rho kinase inhibition rescues the endothelial cell cerebral cavernous malformation phenotype.

http://www.wikidata.org/entity/Q28274176

description

2010 nî lūn-bûn

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2010 թուականի Փետրուարին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի փետրվարին հրատարակված գիտական հոդված

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2010年の論文

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2010年学术文章

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2010年学术文章

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2010年学术文章

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2010年学术文章

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2010年学术文章

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2010年學術文章

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name

Rho kinase inhibition rescues ...... vernous malformation phenotype

@nl

Rho kinase inhibition rescues ...... ernous malformation phenotype.

@ast

Rho kinase inhibition rescues ...... ernous malformation phenotype.

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type

label

Rho kinase inhibition rescues ...... vernous malformation phenotype

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Rho kinase inhibition rescues ...... ernous malformation phenotype.

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Rho kinase inhibition rescues ...... ernous malformation phenotype.

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prefLabel

Rho kinase inhibition rescues ...... vernous malformation phenotype

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Rho kinase inhibition rescues ...... ernous malformation phenotype.

@ast

Rho kinase inhibition rescues ...... ernous malformation phenotype.

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Rho kinase inhibition rescues ...... ernous malformation phenotype.

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Amy N Abell

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Asya L Borikova

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Christopher F Dibble

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Christopher M Welch

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Gary L Johnson

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Noah Sciaky

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Sompop Bencharit

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P2860

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

Rho GTPases: biochemistry and biology

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

Truncating mutations in CCM1, encoding KRIT1, cause hereditary cavernous angiomas

Coordination of Rho GTPase activities during cell protrusion

Spatiotemporal dynamics of RhoA activity in migrating cells

Cooperative effects of Rho and mechanical stretch on stress fiber organization.

Activation of Rho GTPases in Smith-Lemli-Opitz syndrome: pathophysiological and clinical implications.

Rac-MEKK3-MKK3 scaffolding for p38 MAPK activation during hyperosmotic shock.

The cerebral cavernous malformation signaling pathway promotes vascular integrity via Rho GTPases

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20181950

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