The cerebral cavernous malformation proteins CCM2L and CCM2 prevent the activation of the MAP kinase MEKK3

The Cerebral Cavernous Malformation Pathway Controls Cardiac Development via Regulation of Endocardial MEKK3 Signaling and KLF Expression

(2015) Zinan Zhou et al.   DEVELOPMENTAL CELL

Regulation of β1 Integrin-Klf2-Mediated Angiogenesis by CCM Proteins

(2015) Marc Renz et al.   DEVELOPMENTAL CELL

Structural Insights into the Molecular Recognition between Cerebral Cavernous Malformation 2 and Mitogen-Activated Protein Kinase Kinase Kinase 3

(2015) Xiaoyan Wang et al.   STRUCTURE

Identification of a New Modulator of the Intercalated Disc in a Zebrafish Model of Arrhythmogenic Cardiomyopathy

(2014) A. Asimaki et al.   Science Translational Medicine

Signaling pathways and the cerebral cavernous malformations proteins: lessons from structural biology

(2013) Oriana S. Fisher et al.   CELLULAR AND MOLECULAR LIFE SCIENCES

ccm2-like is required for cardiovascular development as a novel component of the Heg-CCM pathway

(2013) Jonathan N. Rosen et al.   DEVELOPMENTAL BIOLOGY

MEKK2 Kinase Association with 14-3-3 Protein Regulates Activation of c-Jun N-terminal Kinase

(2013) Adi E. Matitau et al.   JOURNAL OF BIOLOGICAL CHEMISTRY

EndMT contributes to the onset and progression of cerebral cavernous malformations

(2013) Luigi Maddaluno et al.   NATURE

Cerebral cavernous malformations: from CCM genes to endothelial cell homeostasis

(2013) Andreas Fischer et al.   TRENDS IN MOLECULAR MEDICINE

Cerebral cavernous malformation is a vascular disease associated with activated RhoA signaling

(2012) Bryan T. Richardson et al.   BIOLOGICAL CHEMISTRY

Vascular endothelium, hemodynamics, and the pathobiology of atherosclerosis

(2012) Michael A. Gimbrone et al.   CARDIOVASCULAR PATHOLOGY

Dynamic Regulation of the Cerebral Cavernous Malformation Pathway Controls Vascular Stability and Growth

(2012) Xiangjian Zheng et al.   DEVELOPMENTAL CELL

Role of shear-stress-induced VEGF expression in endothelial cell survival

(2012) Nathaniel G. dela Paz et al.   JOURNAL OF CELL SCIENCE

MEK5/ERK5 pathway: The first fifteen years

(2011) Barbara A. Drew et al.   BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER

Ccm3 functions in a manner distinct from Ccm1 and Ccm2 in a zebrafish model of CCM vascular disease

(2011) Bilge Yoruk et al.   DEVELOPMENTAL BIOLOGY

Developmental timing of CCM2 loss influences cerebral cavernous malformations in mice

(2011) Gwénola Boulday et al.   JOURNAL OF EXPERIMENTAL MEDICINE

CCM3 signaling through sterile 20–like kinases plays an essential role during zebrafish cardiovascular development and cerebral cavernous malformations

(2010) Xiangjian Zheng et al.   JOURNAL OF CLINICAL INVESTIGATION

Differential angiogenesis function ofCCM2andCCM3in cerebral cavernous malformations

(2010) Yuan Zhu et al.   Neurosurgical Focus

Mitogen-Activated Protein Kinase Signaling in the Heart: Angels Versus Demons in a Heart-Breaking Tale

(2010) Beth A. Rose et al.   PHYSIOLOGICAL REVIEWS

Cerebral cavernous malformation protein CCM1 inhibits sprouting angiogenesis by activating DELTA-NOTCH signaling

(2010) Joycelyn Wüstehube et al.   PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA

Tissue-specific conditional CCM2 knockout mice establish the essential role of endothelial CCM2 in angiogenesis: implications for human cerebral cavernous malformations

(2009) G. Boulday et al.   Disease Models & Mechanisms

The small molecule Mek1/2 inhibitor U0126 disrupts the chordamesoderm to notochord transition in zebrafish

(2008) Thomas A Hawkins et al.   BMC DEVELOPMENTAL BIOLOGY

Phosphorylation of MEKK3 at Threonine 294 Promotes 14-3-3 Association to Inhibit Nuclear Factor κB Activation

(2008) Adi E. Matitau et al.   JOURNAL OF BIOLOGICAL CHEMISTRY

Endothelial adherens junctions control tight junctions by VE-cadherin-mediated upregulation of claudin-5

(2008) Andrea Taddei et al.   NATURE CELL BIOLOGY

Homeostatic interactions between MEKK3 and TAK1 involved in NF-κB signaling

(2007) Yuwei Di et al.   CELLULAR SIGNALLING