Loss of p53 sensitizes mice with a mutation in Ccm1 (KRIT1) to development of cerebral vascular malformations. - Wikidata - awgldk - TriplyDB

Loss of p53 sensitizes mice with a mutation in Ccm1 (KRIT1) to development of cerebral vascular malformations.

Loss of p53 sensitizes mice with a mutation in Ccm1 (KRIT1) to development of cerebral vascular malformations.

http://www.wikidata.org/entity/Q35103397

about

Cerebral cavernous malformation protein CCM1 inhibits sprouting angiogenesis by activating DELTA-NOTCH signaling.A two-hit mechanism causes cerebral cavernous malformations: complete inactivation of CCM1, CCM2 or CCM3 in affected endothelial cells Vascular anomalies: from genetics toward models for therapeutic trials Chromosome 8p as a potential hub for developmental neuropsychiatric disorders: implications for schizophrenia, autism and cancer Cerebral cavernous malformation: new molecular and clinical insights.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 Biology of vascular malformations of the brain.Control of cell adhesion dynamics by Rap1 signaling.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 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.Pathogenesis of vascular anomalies.The pathobiology of vascular malformations: insights from human and model organism genetics.Loss of cerebral cavernous malformation 3 (Ccm3) in neuroglia leads to CCM and vascular pathology.Polymorphisms in inflammatory and immune response genes associated with cerebral cavernous malformation type 1 severity.Conditional deletion of Ccm2 causes hemorrhage in the adult brain: a mouse model of human cerebral cavernous malformations.Strategy for identifying repurposed drugs for the treatment of cerebral cavernous malformation.Genetics of cerebral cavernous malformations: current status and future prospects Small GTPase Rap1 Is Essential for Mouse Development and Formation of Functional Vasculature.Genetics of cerebral cavernous malformations.Biallelic somatic and germline mutations in cerebral cavernous malformations (CCMs): evidence for a two-hit mechanism of CCM pathogenesis.From germline towards somatic mutations in the pathophysiology of vascular anomalies.Genetics, epigenetics and pharmaco-(epi)genomics in angiogenesis Introduction to cerebral cavernous malformation: a brief review.Immune response in human cerebral cavernous malformations.Cerebral cavernous malformation proteins at a glance.STRIPAK complexes: structure, biological function, and involvement in human diseases.Advances in the biology of cerebral cavernous malformations.Distinct functions for Rap1 signaling in vascular morphogenesis and dysfunction.CCM1 and the second life of proteins in adhesion complexes.B-Cell Depletion Reduces the Maturation of Cerebral Cavernous Malformations in Murine Models.Management of brainstem cavernous malformations.Novel loss of function mutation in KRIT1/CCM1 is associated with distinctly progressive cerebral and spinal cavernous malformations after radiochemotherapy for intracranial malignant germ cell tumor.Genotype-phenotype correlations in cerebral cavernous malformations patients.RhoA Kinase Inhibition With Fasudil Versus Simvastatin in Murine Models of Cerebral Cavernous Malformations.Neuronal expression of the Ccm2 gene in a new mouse model of cerebral cavernous malformations.

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P2860

Loss of p53 sensitizes mice with a mutation in Ccm1 (KRIT1) to development of cerebral vascular malformations.

http://www.wikidata.org/entity/Q35103397

description

2004 nî lūn-bûn

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2004 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած

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2004 թվականի նոյեմբերին հրատարակված գիտական հոդված

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2004年の論文

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2004年論文

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Loss of p53 sensitizes mice wi ...... rebral vascular malformations.

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Loss of p53 sensitizes mice wi ...... rebral vascular malformations.

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Loss of p53 sensitizes mice wi ...... rebral vascular malformations.

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Loss of p53 sensitizes mice wi ...... rebral vascular malformations.

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Loss of p53 sensitizes mice wi ...... rebral vascular malformations.

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Loss of p53 sensitizes mice wi ...... rebral vascular malformations.

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S0002-9440(10)63409-8

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The American Journal of Pathology

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Loss of p53 sensitizes mice wi ...... erebral vascular malformations

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P2093

Carol J Gallione

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David N Louis

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Douglas A Marchuk

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Jon S Zawistowski

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P2860

The integrin cytoplasmic domain-associated protein ICAP-1 binds and regulates Rho family GTPases during cell spreading

Mutations within the MGC4607 gene cause cerebral cavernous malformations

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

Mapping a gene causing cerebral cavernous malformation to 7q11.2-q21

Krit1 missense mutations lead to splicing errors in cerebral cavernous malformation

KRIT1 is mutated in hyperkeratotic cutaneous capillary-venous malformation associated with cerebral capillary malformation

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)

KRIT1 association with the integrin-binding protein ICAP-1: a new direction in the elucidation of cerebral cavernous malformations (CCM1) pathogenesis

Interaction between krit1 and icap1alpha infers perturbation of integrin beta1-mediated angiogenesis in the pathogenesis of cerebral cavernous malformation

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