Loss of CCM3 impairs DLL4-Notch signalling: implication in endothelial angiogenesis and in inherited cerebral cavernous malformations
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Title
Loss of CCM3 impairs DLL4-Notch signalling: implication in endothelial angiogenesis and in inherited cerebral cavernous malformations
Authors
Keywords
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Journal
JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
Volume 17, Issue 3, Pages 407-418
Publisher
Wiley
Online
2013-02-07
DOI
10.1111/jcmm.12022
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Note: Only part of the references are listed.- Adaptor Protein Cerebral Cavernous Malformation 3 (CCM3) Mediates Phosphorylation of the Cytoskeletal Proteins Ezrin/Radixin/Moesin by Mammalian Ste20-4 to Protect Cells from Oxidative Stress
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- The Dll4/Notch pathway controls postangiogenic blood vessel remodeling and regression by modulating vasoconstriction and blood flow
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- CCM3/PDCD10 Heterodimerizes with Germinal Center Kinase III (GCKIII) Proteins Using a Mechanism Analogous to CCM3 Homodimerization
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- Crystal Structure of CCM3, a Cerebral Cavernous Malformation Protein Critical for Vascular Integrity
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- KRIT1 Regulates the Homeostasis of Intracellular Reactive Oxygen Species
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- (2009) Purnima Narasimhan et al. STROKE
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- Suppressed NFAT-dependent VEGFR1 expression and constitutive VEGFR2 signaling in infantile hemangioma
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