Involvement of TRPC in the abnormal calcium influx observed in dystrophic (mdx) mouse skeletal muscle fibers.
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Calcium antagonists for Duchenne muscular dystrophyHypernitrosylated ryanodine receptor calcium release channels are leaky in dystrophic muscleDiacylglycerol kinase-zeta localization in skeletal muscle is regulated by phosphorylation and interaction with syntrophinsCaveolae regulation of mechanosensitive channel function in myotubesEarly pathogenesis of Duchenne muscular dystrophy modelled in patient-derived human induced pluripotent stem cells.Interaction between mitsugumin 29 and TRPC3 participates in regulating Ca(2+) transients in skeletal muscleInhibitory control over Ca(2+) sparks via mechanosensitive channels is disrupted in dystrophin deficient muscle but restored by mini-dystrophin expressionGenetic evidence in the mouse solidifies the calcium hypothesis of myofiber death in muscular dystrophyRat hypocretin/orexin neurons are maintained in a depolarized state by TRPC channelsIncreasing the expression of calcium-permeable TRPC3 and TRPC7 channels enhances constitutive secretionMice lacking Homer 1 exhibit a skeletal myopathy characterized by abnormal transient receptor potential channel activityTissue-specific expression of TRP channel genes in the mouse and its variation in three different mouse strainsL-type Ca2+ channel function is linked to dystrophin expression in mammalian muscleRapid Ca2+ flux through the transverse tubular membrane, activated by individual action potentials in mammalian skeletal muscle.Role of TRPC1 channel in skeletal muscle function.Skeletal muscle NADPH oxidase is increased and triggers stretch-induced damage in the mdx mouse.Enhanced Ca²⁺ influx from STIM1-Orai1 induces muscle pathology in mouse models of muscular dystrophy.TRPC3 cation channel plays an important role in proliferation and differentiation of skeletal muscle myoblasts.High-frequency fatigue of skeletal muscle: role of extracellular Ca(2+).Compromised store-operated Ca2+ entry in aged skeletal muscle.Impaired Orai1-mediated resting Ca2+ entry reduces the cytosolic [Ca2+] and sarcoplasmic reticulum Ca2+ loading in quiescent junctophilin 1 knock-out myotubesLong-term blocking of calcium channels in mdx mice results in differential effects on heart and skeletal muscleOrai1 mediates exacerbated Ca(2+) entry in dystrophic skeletal muscleClassical Transient Receptor Potential 1 (TRPC1): Channel or Channel Regulator?Mechanosensitive channels in striated muscle and the cardiovascular system: not quite a stretch anymore.Expression and localization of TRPC proteins in rat ventricular myocytes at various developmental stages.Ca(2+) permeation and/or binding to CaV1.1 fine-tunes skeletal muscle Ca(2+) signaling to sustain muscle function.TRPC1 expression and distribution in rat heartsQuantitative proteomic analysis reveals metabolic alterations, calcium dysregulation, and increased expression of extracellular matrix proteins in laminin α2 chain-deficient muscle.Whole body periodic acceleration is an effective therapy to ameliorate muscular dystrophy in mdx mice.TRPC3 channels confer cellular memory of recent neuromuscular activity.The dynamic complexity of the TRPC1 channelosome.Sarcoplasmic reticulum Ca2+ permeation explored from the lumen side in mdx muscle fibers under voltage control4-IBP, a sigma1 receptor agonist, decreases the migration of human cancer cells, including glioblastoma cells, in vitro and sensitizes them in vitro and in vivo to cytotoxic insults of proapoptotic and proautophagic drugsHypertrophy in skeletal myotubes induced by junctophilin-2 mutant, Y141H, involves an increase in store-operated Ca2+ entry via Orai1.Mutation of delta-sarcoglycan is associated with Ca(2+) -dependent vascular remodeling in the Syrian hamster.Increased resting intracellular calcium modulates NF-κB-dependent inducible nitric-oxide synthase gene expression in dystrophic mdx skeletal myotubesPathways of Ca²⁺ entry and cytoskeletal damage following eccentric contractions in mouse skeletal muscleMechanisms of stretch-induced muscle damage in normal and dystrophic muscle: role of ionic changes.Characterization and Functional Analysis of Extracellular Vesicles and Muscle-Abundant miRNAs (miR-1, miR-133a, and miR-206) in C2C12 Myocytes and mdx Mice
P2860
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P2860
Involvement of TRPC in the abnormal calcium influx observed in dystrophic (mdx) mouse skeletal muscle fibers.
description
2002 nî lūn-bûn
@nan
2002年の論文
@ja
2002年論文
@yue
2002年論文
@zh-hant
2002年論文
@zh-hk
2002年論文
@zh-mo
2002年論文
@zh-tw
2002年论文
@wuu
2002年论文
@zh
2002年论文
@zh-cn
name
Involvement of TRPC in the abn ...... mouse skeletal muscle fibers.
@en
type
label
Involvement of TRPC in the abn ...... mouse skeletal muscle fibers.
@en
prefLabel
Involvement of TRPC in the abn ...... mouse skeletal muscle fibers.
@en
P2093
P2860
P356
P1476
Involvement of TRPC in the abn ...... mouse skeletal muscle fibers.
@en
P2093
Clarisse Vandebrouck
Dominique Martin
Huguette Debaix
Monique Colson-Van Schoor
Philippe Gailly
P2860
P304
P356
10.1083/JCB.200203091
P407
P577
2002-09-16T00:00:00Z