Cerebral cavernous malformations arise from endothelial gain of MEKK3–KLF2/4 signalling

Zinan Zhou, Alan T. Tang, Weng-Yew Wong, Sharika Bamezai, Lauren M. Goddard, Robert Shenkar, Su Zhou, Jisheng Yang, Alexander C. Wright, Matthew Foley, J. Simon C. Arthur, Kevin J. Whitehead, Issam A. Awad, Dean Y. Li, Xiangjian Zheng and Mark L. Kahn ()
Additional contact information
Zinan Zhou: University of Pennsylvania, 3400 Civic Center Blvd
Alan T. Tang: University of Pennsylvania, 3400 Civic Center Blvd
Weng-Yew Wong: Laboratory of Cardiovascular Signaling, Centenary Institute
Sharika Bamezai: University of Pennsylvania, 3400 Civic Center Blvd
Lauren M. Goddard: University of Pennsylvania, 3400 Civic Center Blvd
Robert Shenkar: Neurovascular Surgery Program, Section of Neurosurgery, The University of Chicago Medicine and Biological Sciences
Su Zhou: University of Pennsylvania, 3400 Civic Center Blvd
Jisheng Yang: University of Pennsylvania, 3400 Civic Center Blvd
Alexander C. Wright: University of Pennsylvania Medical Center
Matthew Foley: Sydney Microscopy & Microanalysis, University of Sydney
J. Simon C. Arthur: University of Dundee
Kevin J. Whitehead: University of Utah
Issam A. Awad: Neurovascular Surgery Program, Section of Neurosurgery, The University of Chicago Medicine and Biological Sciences
Dean Y. Li: University of Utah
Xiangjian Zheng: Laboratory of Cardiovascular Signaling, Centenary Institute
Mark L. Kahn: University of Pennsylvania, 3400 Civic Center Blvd

Nature, 2016, vol. 532, issue 7597, 122-126

Abstract: Gain of MEKK3 signalling is shown to cause cerebral cavernous malformations (CCMs) via activation of the target genes Klf2 and Klf4; endothelial-specific loss of MEKK3, KLF2 or KLF4 prevents lesion formation and lethality in a mouse CCM model.

Date: 2016
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DOI: 10.1038/nature17178

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