Fasudil decreases lesion burden in a murine model of cerebral cavernous malformation disease - Wikidata - awgldk - TriplyDB

Fasudil decreases lesion burden in a murine model of cerebral cavernous malformation disease

Fasudil decreases lesion burden in a murine model of cerebral cavernous malformation disease

http://www.wikidata.org/entity/Q35693325

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Micro-CT Imaging Reveals Mekk3 Heterozygosity Prevents Cerebral Cavernous Malformations in Ccm2-Deficient Mice Structural basis of the junctional anchorage of the cerebral cavernous malformations complex The RhoA-ROCK pathway in the regulation of T and B cell responses Rho kinase as a target for cerebral vascular disorders Exceptional aggressiveness of cerebral cavernous malformation disease associated with PDCD10 mutations CCM1-ICAP-1 complex controls β1 integrin-dependent endothelial contractility and fibronectin remodeling Dynamic contrast-enhanced MRI evaluation of cerebral cavernous malformations.Combined HMG-COA reductase and prenylation inhibition in treatment of CCM.Lesions from patients with sporadic cerebral cavernous malformations harbor somatic mutations in the CCM genes: evidence for a common biochemical pathway for CCM pathogenesis.The pathobiology of vascular malformations: insights from human and model organism genetics.Evaluation of iron content in human cerebral cavernous malformation using quantitative susceptibility mapping Dynamic permeability and quantitative susceptibility: related imaging biomarkers in cerebral cavernous malformations Strategy for identifying repurposed drugs for the treatment of cerebral cavernous malformation.Sulindac metabolites decrease cerebrovascular malformations in CCM3-knockout mice.The cerebral cavernous malformation pathway controls cardiac development via regulation of endocardial MEKK3 signaling and KLF expression.Vascular permeability in cerebral cavernous malformations.Cerebral cavernous malformations arise from endothelial gain of MEKK3-KLF2/4 signalling.Quantitative Susceptibility Mapping in Cerebral Cavernous Malformations: Clinical Correlations.Introduction to cerebral cavernous malformation: a brief review.Rho kinases in cardiovascular physiology and pathophysiology: the effect of fasudil.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.Cerebral cavernous malformations: natural history and clinical management.Beyond multiple mechanisms and a unique drug: Defective autophagy as pivotal player in cerebral cavernous malformation pathogenesis and implications for targeted therapies.Synopsis of Guidelines for the Clinical Management of Cerebral Cavernous Malformations: Consensus Recommendations Based on Systematic Literature Review by the Angioma Alliance Scientific Advisory Board Clinical Experts Panel.KRIT1 loss of function causes a ROS-dependent upregulation of c-Jun B-Cell Depletion Reduces the Maturation of Cerebral Cavernous Malformations in Murine Models.Oxidative stress and inflammation in cerebral cavernous malformation disease pathogenesis: Two sides of the same coin.Rap1 signaling in endothelial barrier control.Micro-computed tomography in murine models of cerebral cavernous malformations as a paradigm for brain disease.KRIT1 mutations in three Japanese pedigrees with hereditary cavernous malformation.Fasudil, a clinically safe ROCK inhibitor, decreases disease burden in a Cbl/Cbl-b deficiency-driven murine model of myeloproliferative disorders.Thrombospondin1 (TSP1) replacement prevents cerebral cavernous malformations.Blood-brain barrier dysfunction and recovery after ischemic stroke.Induction and Micro-CT Imaging of Cerebral Cavernous Malformations in Mouse Model.RhoA Kinase Inhibition With Fasudil Versus Simvastatin in Murine Models of Cerebral Cavernous Malformations.ROCK as a therapeutic target for ischemic stroke.

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Fasudil decreases lesion burden in a murine model of cerebral cavernous malformation disease

http://www.wikidata.org/entity/Q35693325

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2011 nî lūn-bûn

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2011年の論文

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2011年論文

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2011年论文

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name

Fasudil decreases lesion burde ...... cavernous malformation disease

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Fasudil decreases lesion burde ...... cavernous malformation disease

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Fasudil decreases lesion burde ...... cavernous malformation disease

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Fasudil decreases lesion burde ...... cavernous malformation disease

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Fasudil decreases lesion burde ...... cavernous malformation disease

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STROKEAHA.111.625467

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Fasudil decreases lesion burde ...... cavernous malformation disease

@en

P2093

Changbin Shi

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Douglas A Marchuk

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Feifei Liu

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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

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

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

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

Specificity and mechanism of action of some commonly used protein kinase inhibitors

Advanced magnetic resonance imaging of cerebral cavernous malformations: part II. Imaging of lesions in murine models.

Cerebral cavernous malformations: somatic mutations in vascular endothelial cells

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

A novel mouse model of cerebral cavernous malformations based on the two-hit mutation hypothesis recapitulates the human disease.

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571-574

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scholarly article

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10.1161/STROKEAHA.111.625467

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2

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David A McDonald

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2011-10-27T00:00:00Z

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22034008

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3265629

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