Open AccessClass IA Phosphatidylinositol 3-Kinase Isoform p110α Mediates Vascular Remodeling
Author(s) -
Marius Vantler,
Joana Jesus,
Olli Leppänen,
Maximilian Scherner,
Eva Berghausen,
Lenard Mustafov,
Xin Chen,
Tilmann Kramer,
Mario Zierden,
Maximilian Gerhardt,
Henrik ten Freyhaus,
Florian Blaschke,
Anja SternerKock,
Stephan Baldus,
Jean J. Zhao,
Stephan Rosenkranz
Publication year - 2015
Publication title -
arteriosclerosis thrombosis and vascular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.007
H-Index - 270
eISSN - 1524-4636
pISSN - 1079-5642
DOI - 10.1161/atvbaha.114.304887
Subject(s) - neointima , receptor tyrosine kinase , biology , p110α , vascular smooth muscle , microbiology and biotechnology , phosphatidylinositol , tyrosine kinase , kinase , gene isoform , signal transduction , endocrinology , medicine , biochemistry , restenosis , smooth muscle , gene , stent
Neointima formation after vascular injury remains a significant problem in clinical cardiology, and current preventive strategies are suboptimal. Phosphatidylinositol 3'-kinase is a central downstream mediator of growth factor signaling, but the role of phosphatidylinositol 3'-kinase isoforms in vascular remodeling remains elusive. We sought to systematically characterize the precise role of catalytic class IA phosphatidylinositol 3'-kinase isoforms (p110α, p110β, p110δ), which signal downstream of receptor tyrosine kinases, for vascular remodeling in vivo.
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