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Effects of n−3 Polyunsaturated Fatty Acids on Cardiac Ion Channels
The effects of n−3 PUFAs on the cardiac APD and, therefore, on cardiac arrhythmias vary depending on the method of application, the animal model, and the underlying cardiac pathology. Expand
Irvalec Inserts into the Plasma Membrane Causing Rapid Loss of Integrity and Necrotic Cell Death in Tumor Cells
FRET experiments demonstrated that Irvalec molecules localize in the cell membrane close enough to each other as to suggest that the compound could self-organize, forming supramolecular structures that likely trigger cell death by necrosis through the disruption of membrane integrity. Expand
Celecoxib blocks cardiac Kv1.5, Kv4.3 and Kv7.1 (KCNQ1) channels: effects on cardiac action potentials.
It is demonstrated that celecoxib prolongs the action potential duration in mouse cardiac myocytes and shortens it in guinea pig cardiac myocyte, suggesting that Kv block induced by celecoxIB may be of clinical relevance. Expand
Stereoselective interactions between local anesthetics and ion channels.
The stereoselective effects of bupivacaine-like local anesthetics on cardiac sodium and potassium channels are reviewed and it is shown that in some cases, the pharmacological effects induced by the two enantiomers on the molecular target are opposite. Expand
Protein Kinase C (PKC) Activity Regulates Functional Effects of Kvβ1.3 Subunit on KV1.5 Channels
The results demonstrate that calphostin C-mediated abolishment of fast inactivation is not due to the dissociation of Kv1.5 and Kvβ1.3 and that PKC inhibition causes a dramatic positive shift of the inactivation curve. Expand
Modulation of Voltage-Dependent and Inward Rectifier Potassium Channels by 15-Epi-Lipoxin-A4 in Activated Murine Macrophages: Implications in Innate Immunity
Evidence is provided for a new mechanism by which e-LXA4 contributes to inflammation resolution, consisting of the reversion of LPS effects on Kv and Kir currents in macrophages. Expand
Kv1.5-Kv beta interactions: molecular determinants and pharmacological consequences.
Kv1.5 channels are homotetramers of alpha-pore subunits mainly present in human atrium and pulmonary vasculature. Thus, Kv1.5 is a pharmacological target for cardiovascular diseases. Kv beta 1.3Expand
Ceramide inhibits Kv currents and contributes to TP-receptor-induced vasoconstriction in rat and human pulmonary arteries.
The results suggest that ceramide represents a crucial signaling mediator in the pulmonary vasculature and a role for endogenous ceramide in K(v) channel regulation is identified. Expand
Kv1.5-Kvβ Interactions: Molecular Determinants and Pharmacological Consequences
Kv1.5 channels are homotetramers of α-pore subunits mainly present in human atrium and pulmonary vasculature. Thus, Kv1.5 is a pharmacological target for cardiovascular diseases. Kvβ1.3 assembliesExpand
Elisidepsin Interacts Directly with Glycosylceramides in the Plasma Membrane of Tumor Cells to Induce Necrotic Cell Death
It is shown that glycosylceramides act as membrane targets of elisidepsin, facilitating its insertion in the plasma membrane and the subsequent membrane permeabilization that leads to drug-induced cell death, indicating that cell membrane lipids are a plausible target for antineoplastic therapy. Expand