The cerebral cavernous malformation signaling pathway promotes vascular integrity via Rho GTPases - Wikidata - awgldk - TriplyDB

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

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

http://www.wikidata.org/entity/Q34924413

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KRIT1 regulates the homeostasis of intracellular reactive oxygen species Structural studies of cerebral cavernous malformations 2 (CCM2) reveal a folded helical domain at its C-terminus Crystal structure of CCM3, a cerebral cavernous malformation protein critical for vascular integrity Cerebral cavernous malformation protein CCM1 inhibits sprouting angiogenesis by activating DELTA-NOTCH signaling.Cerebral cavernous malformation is a vascular disease associated with activated RhoA signaling Molecular mechanisms controlling vascular lumen formation in three-dimensional extracellular matrices Small G proteins in the cardiovascular system: physiological and pathological aspects Vascular anomalies: from genetics toward models for therapeutic trials Lack of CCM1 induces hypersprouting and impairs response to flow Mechanistic target of rapamycin (Mtor) is essential for murine embryonic heart development and growth Cdc42 and k-Ras Control Endothelial Tubulogenesis through Apical Membrane and Cytoskeletal Polarization: Novel Stimulatory Roles for GTPase Effectors, the Small GTPases, Rac2 and Rap1b, and Inhibitory Influence of Arhgap31 and Rasa1 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 Structural Basis for Small G Protein Effector Interaction of Ras-related Protein 1 (Rap1) and Adaptor Protein Krev Interaction Trapped 1 (KRIT1)Cerebral Cavernous Malformations: Review of the Genetic and Protein-Protein Interactions Resulting in Disease Pathogenesis Rho kinase as a target for cerebral vascular disorders Proteasome function is required for platelet production Rho kinase inhibition rescues the endothelial cell cerebral cavernous malformation phenotype.Dynamic regulation of the cerebral cavernous malformation pathway controls vascular stability and growth RHO binding to FAM65A regulates Golgi reorientation during cell migration KLF4 is a key determinant in the development and progression of cerebral cavernous malformations.Exceptional aggressiveness of cerebral cavernous malformation disease associated with PDCD10 mutations Phosphorylation sites in the cerebral cavernous malformations complex Rap1 and its effector KRIT1/CCM1 regulate beta-catenin signaling.Endothelial lumen signaling complexes control 3D matrix-specific tubulogenesis through interdependent Cdc42- and MT1-MMP-mediated events.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 Dynamic contrast-enhanced MRI evaluation of cerebral cavernous malformations.Recent insights into cerebral cavernous malformations: a complex jigsaw puzzle under construction.Endothelial adherens junctions and the actin cytoskeleton: an 'infinity net'?Biology of vascular malformations of the brain.Combined HMG-COA reductase and prenylation inhibition in treatment of CCM.Control of cell adhesion dynamics by Rap1 signaling.Systems biology and proteomic analysis of cerebral cavernous malformation Cerebral cavernous malformations proteins inhibit Rho kinase to stabilize vascular integrity.Recent insights into cerebral cavernous malformations: animal models of CCM and the human phenotype Mechanisms of vascular stability and the relationship to human disease Lesions from patients with sporadic cerebral cavernous malformations harbor somatic mutations in the CCM genes: evidence for a common biochemical pathway for CCM pathogenesis.

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P2860

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

http://www.wikidata.org/entity/Q34924413

description

2009 nî lūn-bûn

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2009 թուականի Յունուարին հրատարակուած գիտական յօդուած

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2009 թվականի հունվարին հրատարակված գիտական հոդված

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2009年の論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年论文

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name

The cerebral cavernous malform ...... ular integrity via Rho GTPases

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The cerebral cavernous malform ...... ular integrity via Rho GTPases

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The cerebral cavernous malform ...... ular integrity via Rho GTPases

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The cerebral cavernous malform ...... ular integrity via Rho GTPases

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Nature Medicine

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The cerebral cavernous malform ...... ular integrity via Rho GTPases

@en

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Anne H Mayo

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Aubrey C Chan

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Christopher A Jones

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Dean Y Li

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Douglas A Marchuk

http://www.w3.org/2001/XMLSchema#string

George E Davis

http://www.w3.org/2001/XMLSchema#string

Jing Ling

http://www.w3.org/2001/XMLSchema#string

Kevin J Whitehead

http://www.w3.org/2001/XMLSchema#string

Nyall R London

http://www.w3.org/2001/XMLSchema#string

Stavros G Drakos

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P2860

Mutations within the MGC4607 gene cause cerebral cavernous malformations

Mutations within the programmed cell death 10 gene cause cerebral cavernous malformations

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

Coregulation of vascular tube stabilization by endothelial cell TIMP-2 and pericyte TIMP-3.

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

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

HMG CoA reductase inhibition modulates VEGF-induced endothelial cell hyperpermeability by preventing RhoA activation and myosin regulatory light chain phosphorylation

Mechanisms of angiogenesis

Rho GTPases control polarity, protrusion, and adhesion during cell movement

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177-184

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10.1038/NM.1911

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2

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15

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1014416621

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2767168

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