Developmental timing of CCM2 loss influences cerebral cavernous malformations in mice. - Wikidata - wikimedia - TriplyDB

Developmental timing of CCM2 loss influences cerebral cavernous malformations in mice.

Developmental timing of CCM2 loss influences cerebral cavernous malformations in mice.

http://www.wikidata.org/entity/Q34209951

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Endothelial cell-cell adhesion during zebrafish vascular development Lack of CCM1 induces hypersprouting and impairs response to flow 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 KLF4 is a key determinant in the development and progression of cerebral cavernous malformations.CCM1-ICAP-1 complex controls β1 integrin-dependent endothelial contractility and fibronectin remodeling Network-based analysis of omics data: the LEAN method Combined HMG-COA reductase and prenylation inhibition in treatment of CCM.Sulindac metabolites decrease cerebrovascular malformations in CCM3-knockout mice.Small GTPase Rap1 Is Essential for Mouse Development and Formation of Functional Vasculature.The cerebral cavernous malformation pathway controls cardiac development via regulation of endocardial MEKK3 signaling and KLF expression.Defective autophagy is a key feature of cerebral cavernous malformations.The cerebral cavernous malformation proteins CCM2L and CCM2 prevent the activation of the MAP kinase MEKK3.Apicobasal polarity of brain endothelial cells.Nogo-B receptor deficiency causes cerebral vasculature defects during embryonic development in mice.Cytochrome P450 and matrix metalloproteinase genetic modifiers of disease severity in Cerebral Cavernous Malformation type 1.Recent advances in vascular development.Cerebral cavernous malformations arise from endothelial gain of MEKK3-KLF2/4 signalling.Introduction to cerebral cavernous malformation: a brief review.Cerebral cavernous malformation proteins at a glance.STRIPAK complexes: structure, biological function, and involvement in human diseases.Signaling pathways and the cerebral cavernous malformations proteins: lessons from structural biology.Distinct functions for Rap1 signaling in vascular morphogenesis and dysfunction.CCM1 and the second life of proteins in adhesion complexes.A murine toolbox for imaging the neurovascular unit.Neural Regulation of CNS Angiogenesis During Development.Up-regulation of NADPH oxidase-mediated redox signaling contributes to the loss of barrier function in KRIT1 deficient endothelium.Role of Delta-Notch signaling in cerebral cavernous malformations.KRIT1 loss of function causes a ROS-dependent upregulation of c-Jun Oxidative stress and inflammation in cerebral cavernous malformation disease pathogenesis: Two sides of the same coin.Cerebral cavernous malformations arise independent of the heart of glass receptor.Vascular heterogeneity and specialization in development and disease.Thrombospondin1 (TSP1) replacement prevents cerebral cavernous malformations.Endothelial TLR4 and the microbiome drive cerebral cavernous malformations.KRIT1 loss-of-function induces a chronic Nrf2-mediated adaptive homeostasis that sensitizes cells to oxidative stress: Implication for Cerebral Cavernous Malformation disease.Induction and Micro-CT Imaging of Cerebral Cavernous Malformations in Mouse Model.Heg1 and Ccm1/2 proteins control endocardial mechanosensitivity during zebrafish valvulogenesis.Systematic pharmacological screens uncover novel pathways involved in cerebral cavernous malformations

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P2860

Developmental timing of CCM2 loss influences cerebral cavernous malformations in mice.

http://www.wikidata.org/entity/Q34209951

description

2011 nî lūn-bûn

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2011 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

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2011 թվականի օգոստոսին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年论文

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name

Developmental timing of CCM2 loss influences cerebral cavernous malformations in mice.

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Developmental timing of CCM2 loss influences cerebral cavernous malformations in mice.

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Developmental timing of CCM2 loss influences cerebral cavernous malformations in mice.

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type

label

Developmental timing of CCM2 loss influences cerebral cavernous malformations in mice.

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Developmental timing of CCM2 loss influences cerebral cavernous malformations in mice.

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Developmental timing of CCM2 loss influences cerebral cavernous malformations in mice.

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Developmental timing of CCM2 loss influences cerebral cavernous malformations in mice.

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Developmental timing of CCM2 loss influences cerebral cavernous malformations in mice.

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Developmental timing of CCM2 loss influences cerebral cavernous malformations in mice.

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Developmental timing of CCM2 loss influences cerebral cavernous malformations in mice.

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Anne Blécon

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Françoise Chapon

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Luigi Maddaluno

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Minh Arnould

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Noemi Rudini

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P2860

Akt promotes cell survival by phosphorylating and inhibiting a Forkhead transcription factor

SOX-18 controls endothelial-specific claudin-5 gene expression and barrier function

CCM1 regulates vascular-lumen organization by inducing endothelial polarity

Mutations within the MGC4607 gene cause cerebral cavernous malformations

Phosphorylation of serine 256 suppresses transactivation by FKHR (FOXO1) by multiple mechanisms. Direct and indirect effects on nuclear/cytoplasmic shuttling and DNA binding

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

Molecular distinction and angiogenic interaction between embryonic arteries and veins revealed by ephrin-B2 and its receptor Eph-B4

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.

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

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1835-1847

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10.1084/JEM.20110571

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9

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208

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Gwénola Boulday

Elisabeth Tournier-Lasserve

Elisabetta Dejana

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51588593

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21859843

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3171098

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