Irena Levitan

Dual effect of fluid shear stress on volume-regulated anion current in bovine aortic endothelial cells.

Modulation of endothelial inward-rectifier K+ current by optical isomers of cholesterol.

Shear stress increases expression of a KATP channel in rat and bovine pulmonary vascular endothelial cells.

Sensitivity of volume-regulated anion current to cholesterol structural analogues.

Plasma membrane surface increases with tonic stretch of alveolar epithelial cells.

Cholesterol depletion increases membrane stiffness of aortic endothelial cells.

Cholesterol sensitivity and lipid raft targeting of Kir2.1 channels.

Functional expression of Kir2.x in human aortic endothelial cells: the dominant role of Kir2.2.

OxLDL increases endothelial stiffness, force generation, and network formation.

Hypercholesterolemia suppresses inwardly rectifying K+ channels in aortic endothelium in vitro and in vivo.

Relationship between Kir2.1/Kir2.3 activity and their distributions between cholesterol-rich and cholesterol-poor membrane domains.

Hypercholesterolemia suppresses Kir channels in porcine bone marrow progenitor cells in vivo.

Use of cyclodextrins to manipulate plasma membrane cholesterol content: evidence, misconceptions and control strategies.

The effect of cellular cholesterol on membrane-cytoskeleton adhesion.

Lipid rafts in membrane-cytoskeleton interactions and control of cellular biomechanics: actions of oxLDL.

oxLDL facilitates flow-induced realignment of aortic endothelial cells.

Endothelial actin and cell stiffness is modulated by substrate stiffness in 2D and 3D.

Identification of a C-terminus domain critical for the sensitivity of Kir2.1 to cholesterol.

Cholesterol and Kir channels.

Direct regulation of prokaryotic Kir channel by cholesterol.

Oxidized LDL: diversity, patterns of recognition, and pathophysiology.

Comparative analysis of cholesterol sensitivity of Kir channels: role of the CD loop.

Cholesterol and ion channels.

oxLDL-induced decrease in lipid order of membrane domains is inversely correlated with endothelial stiffness and network formation.

Cholesterol sensitivity of KIR2.1 is controlled by a belt of residues around the cytosolic pore.

Anthrax lethal factor activates K(+) channels to induce IL-1β secretion in macrophages.

Modification of Cellular Cholesterol Content Affects Traction Force, Adhesion and Cell Spreading.

Impact of oxLDL on Cholesterol-Rich Membrane Rafts.

Cholesterol regulates prokaryotic Kir channel by direct binding to channel protein.

Novel role of p66Shc in ROS-dependent VEGF signaling and angiogenesis in endothelial cells.

Hypercholesterolemia induces up-regulation of KACh cardiac currents via a mechanism independent of phosphatidylinositol 4,5-bisphosphate and Gβγ.

Cholesterol depletion facilitates recovery from hypotonic cell swelling in CHO cells.

New mechanisms of pulmonary arterial hypertension: role of Ca²⁺ signaling.

The role of oxysterols in control of endothelial stiffness.

OxLDL and substrate stiffness promote neutrophil transmigration by enhanced endothelial cell contractility and ICAM-1.

Distant cytosolic residues mediate a two-way molecular switch that controls the modulation of Kir channels by cholesterol and PI(4,5)P2.

Regulation of ion channels by membrane lipids.

Cholesterol sensitivity of KIR2.1 depends on functional inter-links between the N and C termini.

Identification of novel cholesterol-binding regions in Kir2 channels.

Upregulated copper transporters in hypoxia-induced pulmonary hypertension.

Cholesterol binding to ion channels.

Oxidized low-density lipoprotein alters the effect of matrix stiffness on the formation of endothelial networks and capillary lumens.

Silencing of Kir2 channels by caveolin-1: cross-talk with cholesterol.

Interplay Between Lipid Modulators of Kir2 Channels: Cholesterol and PIP2.

Cholesterol increases the open probability of cardiac KACh currents.

Oxidized LDL signals through Rho-GTPase to induce endothelial cell stiffening and promote capillary formation.

Paradoxical impact of cholesterol on lipid packing and cell stiffness.

Inwardly rectifying K channels are major contributors to flow-induced vasodilatation in resistance arteries.

Orthogonal lipid sensors identify transbilayer asymmetry of plasma membrane cholesterol.

Molecular-Scale Biophysical Modulation of an Endothelial Membrane by Oxidized Phospholipids.

oxLDL induces endothelial cell proliferation via Rho/ROCK/Akt/p27 signaling: opposite effects of oxLDL and cholesterol loading.

Differential Effects of Sterols on Ion Channels: Stereospecific Binding vs Stereospecific Response.

Proatherogenic Flow Increases Endothelial Stiffness via Enhanced CD36-Mediated Uptake of Oxidized Low-Density Lipoproteins.

Hypotonic Challenge of Endothelial Cells Increases Membrane Stiffness with No Effect on Tether Force.

Hypercholesterolemia-Induced Loss of Flow-Induced Vasodilation and Lesion Formation in Apolipoprotein E-Deficient Mice Critically Depend on Inwardly Rectifying K Channels.

Comparative analysis of endothelial cell and sub-endothelial cell elastic moduli in young and aged mice: Role of CD36.

Molecular Dynamics Simulations of Kir2.2 Interactions with an Ensemble of Cholesterol Molecules.

Membrane Stiffening in Osmotic Swelling: Analysis of Membrane Tension and Elastic Modulus.

Potential Strategies to Reduce Blood Pressure in Treatment-Resistant Hypertension Using Food and Drug Administration-Approved Nanodrug Delivery Platforms.

Role of matrix metalloproteinases and histone deacetylase in oxidative stress-induced degradation of the endothelial glycocalyx.

Chiral Specificity of Cholesterol Orientation Within Cholesterol Binding Sites in Inwardly Rectifying K Channels.

Endothelial stiffening in dyslipidemia.

Comparative docking analysis of cholesterol analogs to ion channels to discriminate between stereospecific binding vs. stereospecific response.

Shear-Stress Sensitive Inwardly-Rectifying K Channels Regulate Developmental Retinal Angiogenesis by Vessel Regression.