Pathways of Ca²⁺ entry and cytoskeletal damage following eccentric contractions in mouse skeletal muscle
about
Classical Transient Receptor Potential 1 (TRPC1): Channel or Channel Regulator?L-arginine supplementation protects exercise performance and structural integrity of muscle fibers after a single bout of eccentric exercise in rats.SERCA1 overexpression minimizes skeletal muscle damage in dystrophic mouse models.Absence of Dystrophin Disrupts Skeletal Muscle Signaling: Roles of Ca2+, Reactive Oxygen Species, and Nitric Oxide in the Development of Muscular Dystrophy.Icaritin requires Phosphatidylinositol 3 kinase (PI3K)/Akt signaling to counteract skeletal muscle atrophy following mechanical unloading.Cardiac phenotype of Duchenne Muscular Dystrophy: insights from cellular studiesInhibition of iPLA2 β and of stretch-activated channels by doxorubicin alters dystrophic muscle function.Role of dystroglycan in limiting contraction-induced injury to the sarcomeric cytoskeleton of mature skeletal muscle.Blood flow restriction prevents muscle damage but not protein synthesis signaling following eccentric contractions.Evidence TRPV4 contributes to mechanosensitive ion channels in mouse skeletal muscle fibers.Utrophin regulates modal gating of mechanosensitive ion channels in dystrophic skeletal muscle.Ca2+-dependent proteolysis of junctophilin-1 and junctophilin-2 in skeletal and cardiac muscle.Partial opening and subconductance gating of mechanosensitive ion channels in dystrophic skeletal muscle.l-arginine ingestion inhibits eccentric contraction-induced proteolysis and force deficit via S-nitrosylation of calpain.Junctophilins and μ-calpain: partners in excitation-contraction uncoupling.Role of calpain in eccentric contraction-induced proteolysis of Ca2+-regulatory proteins and force depression in rat fast-twitch skeletal muscle.Blood flow restriction attenuates eccentric exercise-induced muscle damage without perceptual and cardiovascular overload.Impedance flow cytometry gauges proliferative capacity by detecting TRPC1 expression.Effect of eccentric contraction on satellite cell activation in human vastus lateralis muscle.The increase in surface EMG could be a misleading measure of neural adaptation during the early gains in strength.Past injurious exercise attenuates activation of primary calcium-dependent injury pathways in skeletal muscle during subsequent exercise.Resistance exercise-induced muscle fatigue is not accompanied by increased phosphorylation of ryanodine receptor 1 at serine 2843.
P2860
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P2860
Pathways of Ca²⁺ entry and cytoskeletal damage following eccentric contractions in mouse skeletal muscle
description
2012 nî lūn-bûn
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2012年の論文
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2012年論文
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2012年論文
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2012年論文
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2012年論文
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2012年論文
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2012年论文
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2012年论文
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2012年论文
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name
Pathways of Ca²⁺ entry and cyt ...... tions in mouse skeletal muscle
@ast
Pathways of Ca²⁺ entry and cyt ...... tions in mouse skeletal muscle
@en
type
label
Pathways of Ca²⁺ entry and cyt ...... tions in mouse skeletal muscle
@ast
Pathways of Ca²⁺ entry and cyt ...... tions in mouse skeletal muscle
@en
prefLabel
Pathways of Ca²⁺ entry and cyt ...... tions in mouse skeletal muscle
@ast
Pathways of Ca²⁺ entry and cyt ...... tions in mouse skeletal muscle
@en
P2093
P2860
P50
P1476
Pathways of Ca²⁺ entry and cyt ...... tions in mouse skeletal muscle
@en
P2093
Diane Fatkin
Molly Vale
Nicholas P Whitehead
Othon L Gervasio
Trent F Reardon
P2860
P304
P356
10.1152/JAPPLPHYSIOL.00770.2011
P407
P577
2012-03-29T00:00:00Z