about
Investigation of Debio 025, a cyclophilin inhibitor, in the dystrophic mdx mouse, a model for Duchenne muscular dystrophyInhibition of human immunodeficiency virus type 1 replication in human cells by Debio-025, a novel cyclophilin binding agentThe nonimmunosuppressive cyclosporin analogs NIM811 and UNIL025 display nanomolar potencies on permeability transition in brain-derived mitochondria.Role of TRPC1 channel in skeletal muscle function.Gene-mediated restoration of normal myofiber elasticity in dystrophic muscles.Diapocynin, a dimer of the NADPH oxidase inhibitor apocynin, reduces ROS production and prevents force loss in eccentrically contracting dystrophic musclePharmacological control of cellular calcium handling in dystrophic skeletal muscle.Calcium influx inhibition by steroids and analogs in C2C12 skeletal muscle cellsCharacterization and partial purification of solubilized active opiate receptors from toad brain.Role of superoxide as a signaling molecule.Modulation by prednisolone of calcium handling in skeletal muscle cells.Trpc1 ion channel modulates phosphatidylinositol 3-kinase/Akt pathway during myoblast differentiation and muscle regeneration.Quantitative evaluation of the beneficial effects in the mdx mouse of epigallocatechin gallate, an antioxidant polyphenol from green tea.Caloric restriction induces energy-sparing alterations in skeletal muscle contraction, fiber composition and local thyroid hormone metabolism that persist during catch-up fat upon refeeding.Characterization and Functional Analysis of Extracellular Vesicles and Muscle-Abundant miRNAs (miR-1, miR-133a, and miR-206) in C2C12 Myocytes and mdx MiceNav1.4 deregulation in dystrophic skeletal muscle leads to Na+ overload and enhanced cell death.Inhibition of iPLA2 β and of stretch-activated channels by doxorubicin alters dystrophic muscle function.Pharmacological prospects in the treatment of Duchenne muscular dystrophy.Agonist-induced mitochondrial Ca2+ transients in smooth muscle.Erythropoietin stimulates proliferation and interferes with differentiation of myoblasts.Vasopressin induced production of inositol trisphosphate and calcium efflux in a smooth muscle cell line.Biphasic effects of cyclosporin A on formyl-methionyl-leucyl-phenylalanine stimulated responses in HL-60 cells differentiated into neutrophils.Phospholipase A2-derived lysophosphatidylcholine triggers Ca2+ entry in dystrophic skeletal muscle fibers.Basal calcium entry in vascular smooth muscle.Regulation of the transforming growth factor beta-responsive transcription factor CTF-1 by calcineurin and calcium/calmodulin-dependent protein kinase IV.Melatonin prevents oxidative stress-mediated mitochondrial permeability transition and death in skeletal muscle cells.Vasopressin type 1A receptor up-regulation by cyclosporin A in vascular smooth muscle cells is mediated by superoxide.Involvement of inositol 1,4,5-trisphosphate in nicotinic calcium responses in dystrophic myotubes assessed by near-plasma membrane calcium measurement.Protection of dystrophic muscle cells with polyphenols from green tea correlates with improved glutathione balance and increased expression of 67LR, a receptor for (-)-epigallocatechin gallate.Green tea extract and its major polyphenol (-)-epigallocatechin gallate improve muscle function in a mouse model for Duchenne muscular dystrophy.Growth of dissociated neurons in culture dishes coated with synthetic polymeric amines.Inactivation and solubilization of opiate receptors by phospholipases A2.Mitochondria buffer NCX-mediated Ca2+-entry and limit its diffusion into vascular smooth muscle cells.Pharmacological actions of SDZ 218-135, a novel positive inotropic agent.The anticancer drug tamoxifen counteracts the pathology in a mouse model of duchenne muscular dystrophy.Urocortins improve dystrophic skeletal muscle structure and function through both PKA- and Epac-dependent pathways.Creatine supplementation improves intracellular Ca2+ handling and survival in mdx skeletal muscle cellsAlkylation of cysteine thiols with 1,3-propane sultoneReductive cleavage of S-sulfo groups with tributylphosphineLack of evidence for voltage dependent calcium channels on platelets
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