Somatic Gain of KRAS Function in the Endothelium Is Sufficient to Cause Vascular Malformations That Require MEK but Not PI3K Signaling
Abstract
We previously identified somatic activating mutations in the KRAS ( Kirsten rat sarcoma viral oncogene homologue ) gene in the endothelium of the majority of human sporadic brain arteriovenous malformations; a disorder characterized by direct connections between arteries and veins. However, whether this genetic abnormality alone is sufficient for lesion formation, as well as how active KRAS signaling contributes to arteriovenous malformations, remains unknown.
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- Aug 28, 2020
- Source ID
- 10.1161/circresaha.119.316500
Entities
People
- Alexander M. Herman
- Carlos Perfecto Flores Suarez
- Christopher S. Ward
- Dakota Gustafson
- Emilie Boudreau
- Ivan Radovanovic
- Joshua D Wythe
- Karen Berman De Ruiz
- Manuel Cantu Gutierrez
- Meng Cui
- Peter V. Distefano
- Taylor S. Schexnayder
- Zhiqi Chen
Organizations
- American Heart Association
- Baylor College of Medicine
- Canadian Institutes of Health Research
- National Heart, Lung, and Blood Institute
- National Human Genome Research Institute
- National Institute of Diabetes and Digestive and Kidney Diseases
- United States Department of Defense
- University Health Network
- University of Toronto