Calsequestrin
Mostrando 1-12 de 41 artigos, teses e dissertações.
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1. Cardiac function and intracellular Ca2+ handling proteins are not impaired by high-saturated-fat diet-induced obesity
Obesity is often associated with changes in cardiac function; however, the mechanisms responsible for functional abnormalities have not yet been fully clarified. Considering the lack of information regarding high-saturated-fat diet-induced obesity, heart function, and the proteins involved in myocardial calcium (Ca2+) handling, the aim of this study was to t
Braz J Med Biol Res. Publicado em: 27/05/2019
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2. Mecanismos de proteção da distrofia muscular : estudo proteômico e terapia farmacológica / Protective mechanisms of muscular dystrophy : proteomic study and pharmacological therapy
In Duchenne Muscular Dystrophy (DMD) and in the mdx mice model of DMD, the lack of dystrophin leads to muscle degeneration. The pathogenesis of DMD is related to sarcolemmal fragility, mechanical stress and increased influx of calcium in muscle fibers, due to dysfunction of ion channels, such as the stretch-activated calcium channels. The knowledge of the pr
IBICT - Instituto Brasileiro de Informação em Ciência e Tecnologia. Publicado em: 30/07/2012
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3. Mechanisms of protection against myonecrosis in extraocular muscles of the mdx mice / Mecanismos de proteção a mionecrose nos musculos extra-oculares de camundongos distroficos mdx
Duchenne muscular dystrophy is one of the most common hereditary diseases. Abnormal calcium ion handling renders dystrophic muscle fibers more susceptible to necrosis. In the mdx mice, extraocular muscles (EOM) are protected and do not undergo myonecrosis. We investigated whether this protection is related to an increased expression of calcium-binding protei
Publicado em: 2008
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4. Influencia de bloqueadores de canais de calcio no processo de degeneração/regeneração muscular em camundongos ditroficos MDX / The influence iof calcium channel blockers in the process of muscular degeneration/regeneration in mdx mice
The lack of dystrophin in dystrophin-deficient fibers of mdx mice and in Duchenne muscular dystrophy leads to sarcolemmal breakdown and enhanced calcium influx followed by muscle degeneration.In this work, we examined whether the calcium channel blockers diltiazem and verapamil could protect dystrophic muscles from degeneration/regeneration. Mdx mice (n=32;
Publicado em: 2008
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5. Protection from myonecrosis, and expression of SERCA1 and calsequestrin in dystrophic laryngeal muscles / Musculos laringeos distroficos : proteção a mionecrose, expressao de SERCA1 e calsequestrina
Duchenne muscular dystrophy (DMD) and mdx mice, a model for DMD, is characterized by the lack of dystrophin expression and muscle fiber necrosis. Some muscle are enigmatically protected and admitted that an elevated expression of calcium-binding proteins. The intrinsic laryngeal muscles (ILMs) share many anatomical and physiological properties with extra-ocu
Publicado em: 2007
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6. Protons induce calsequestrin conformational changes.
Calsequestrin, a high-capacity, intermediate-affinity, calcium-binding protein present in the lumen of sarcoplasmic reticulum, undergoes extensive calcium-induced conformational changes at neutral pH that cause distinct intrinsic fluorescence changes. The results reported in this work indicate that pH has a marked effect on these calcium-induced intrinsic fl
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7. Regulation of Ca2+ signaling in transgenic mouse cardiac myocytes overexpressing calsequestrin.
To probe the physiological role of calsequestrin in excitation-contraction coupling, transgenic mice overexpressing cardiac calsequestrin were developed. Transgenic mice exhibited 10-fold higher levels of calsequestrin in myocardium and survived into adulthood, but had severe cardiac hypertrophy, with a twofold increase in heart mass and cell size. In whole
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8. Deconstructing calsequestrin. Complex buffering in the calcium store of skeletal muscle
Since its discovery in 1971, calsequestrin has been recognized as the main Ca2+ binding protein inside the sarcoplasmic reticulum (SR), the organelle that stores and upon demand mobilizes Ca2+ for contractile activation of muscle. This article reviews the potential roles of calsequestrin in excitation–contraction coupling of skeletal muscle. It first consi
Blackwell Science Inc.
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9. Cardiac calsequestrin: quest inside the SR
Blackwell Science Inc.
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10. Calsequestrin, triadin and more: the molecules that modulate calcium release in cardiac and skeletal muscle
Blackwell Science Inc.
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11. Amino acid sequence of rabbit fast-twitch skeletal muscle calsequestrin deduced from cDNA and peptide sequencing.
Partial amino acid sequence analysis of rabbit fast-twitch skeletal muscle calsequestrin permitted the construction of synthetic oligonucleotides that were used as both primers and probes for the synthesis and isolation of cDNAs encoding calsequestrin from neonatal rabbit skeletal muscle libraries. The cDNA sequence encodes a processed protein of 367 residue
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12. Ryanodine Receptor Luminal Ca2+ Regulation: Swapping Calsequestrin and Channel Isoforms
Sarcoplasmic reticulum (SR) Ca2+ release in striated muscle is mediated by a multiprotein complex that includes the ryanodine receptor (RyR) Ca2+ channel and the intra-SR Ca2+ buffering protein calsequestrin (CSQ). Besides its buffering role, CSQ is thought to regulate RyR channel function. Here, CSQ-dependent luminal Ca2+ regulation of skeletal (RyR1) and c
The Biophysical Society.