Keigi Fujiwara

Vascular endothelial cells that express dystroglycan are involved in angiogenesis.

Evidence for a role of platelet endothelial cell adhesion molecule-1 in endothelial cell mechanosignal transduction: is it a mechanoresponsive molecule?

Mechanical stresses keep endothelial cells healthy: beneficial effects of a physiological level of cyclic stretch on endothelial barrier function.

Endothelial cell-cell adhesion and mechanosignal transduction.

Serum response factor: master regulator of the actin cytoskeleton and contractile apparatus.

Down-regulation of ERK but not MEK phosphorylation in cultured endothelial cells by repeated changes in cyclic stretch.

ECM remodeling in hypertensive heart disease.

Phosphorylation and localization of protein-zero related (PZR) in cultured endothelial cells.

Mechanotransduction in an extracted cell model: Fyn drives stretch- and flow-elicited PECAM-1 phosphorylation.

Physiologic stress-mediated signaling in the endothelium.

Collagen I matrix turnover is regulated by fibronectin polymerization.

PKCzeta decreases eNOS protein stability via inhibitory phosphorylation of ERK5.

MK2 SUMOylation regulates actin filament remodeling and subsequent migration in endothelial cells by inhibiting MK2 kinase and HSP27 phosphorylation.

PKCζ mediates disturbed flow-induced endothelial apoptosis via p53 SUMOylation.

Cyclic nucleotide phosphodiesterase 1A: a key regulator of cardiac fibroblast activation and extracellular matrix remodeling in the heart.

Disturbed-flow-mediated vascular reactive oxygen species induce endothelial dysfunction.

p90RSK targets the ERK5-CHIP ubiquitin E3 ligase activity in diabetic hearts and promotes cardiac apoptosis and dysfunction.

Thioredoxin interacting protein promotes endothelial cell inflammation in response to disturbed flow by increasing leukocyte adhesion and repressing Kruppel-like factor 2.

Glucagon-like peptide-1 and its cardiovascular effects.

Reactive Oxygen Species, SUMOylation, and Endothelial Inflammation.

p62 binding to protein kinase C ζ regulates tumor necrosis factor α-induced apoptotic pathway in endothelial cells.

Phosphorylation of protein inhibitor of activated STAT1 (PIAS1) by MAPK-activated protein kinase-2 inhibits endothelial inflammation via increasing both PIAS1 transrepression and SUMO E3 ligase activity.

A crucial role for p90RSK-mediated reduction of ERK5 transcriptional activity in endothelial dysfunction and atherosclerosis.

De-SUMOylation enzyme of sentrin/SUMO-specific protease 2 regulates disturbed flow-induced SUMOylation of ERK5 and p53 that leads to endothelial dysfunction and atherosclerosis.

Shear stress and atherosclerosis.

Intima modifier locus 2 controls endothelial cell activation and vascular permeability.

ERK5 activation in macrophages promotes efferocytosis and inhibits atherosclerosis.

Identification of activators of ERK5 transcriptional activity by high-throughput screening and the role of endothelial ERK5 in vasoprotective effects induced by statins and antimalarial agents.

Disturbed flow-activated p90RSK kinase accelerates atherosclerosis by inhibiting SENP2 function.

Mitochondrial dynamics regulate neointima formation.

Mechanosignaling in the vasculature: emerging concepts in sensing, transduction and physiological responses.

PECAM1 regulates flow-mediated Gab1 tyrosine phosphorylation and signaling.

Flow signaling and atherosclerosis.

Sub-cellular localization specific SUMOylation in the heart.

Coordination of Cellular Localization-Dependent Effects of Sumoylation in Regulating Cardiovascular and Neurological Diseases.

STING-IRF3 Triggers Endothelial Inflammation in Response to Free Fatty Acid-Induced Mitochondrial Damage in Diet-Induced Obesity.