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The protein encoded by CASQ1 is a mitochondrial calcium-binding protein located in the luminal space of the terminal cisternae of the sarcoplasmic reticulum. 再加上，我们可以发Calsequestrin 蛋白 (13) 和 Calsequestrin 试剂盒 (11)和数多这个蛋白质的别的产品。
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Chicken Monoclonal Calsequestrin Primary Antibody for ICC, IF - ABIN266947
Leatherbury, Yu, Chatterjee, Walker, Yu, Tian, Lo: A novel mouse model of X-linked cardiac hypertrophy. in American journal of physiology. Heart and circulatory physiology 2008
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Mouse (Murine) Monoclonal Calsequestrin Primary Antibody for IF, WB - ABIN968625
Kobayashi, Alseikhan, Jones: Localization and characterization of the calsequestrin-binding domain of triadin 1. Evidence for a charged beta-strand in mediating the protein-protein interaction. in The Journal of biological chemistry 2000
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Dog (Canine) Polyclonal Calsequestrin Primary Antibody for ICC, IF - ABIN267179
Shankar, Messenberg, Chan, Underhill, Foster, Nabi: Pseudopodial actin dynamics control epithelial-mesenchymal transition in metastatic cancer cells. in Cancer research 2010
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Human Polyclonal Calsequestrin Primary Antibody for IHC, IHC (p) - ABIN4287523
Kato, Nicholson, Neiman, Rantalainen, Holmes, Barrett, Uhlén, Nilsson, Spector, Schwenk: Variance decomposition of protein profiles from antibody arrays using a longitudinal twin model. in Proteome science 2011
Calcium entry activated by ablation of both JP45 (显示 JSRP1 抗体)-CASQ1 and JP45 (显示 JSRP1 抗体)-CASQ2 (显示 CASQ2 抗体) complexes supports tetanic force development in slow twitch soleus muscles.
Transient knockdown of annexin A6 (显示 ANXA6 抗体) and calsequestrin 1 protein of high-active mice with vivo-morpholinos resulted in decreased physical activity levels (P = 0.001).
Ca(2 (显示 CA2 抗体)+) transients evoked by tetanic stimulation are the result of massive Ca(2 (显示 CA2 抗体)+) influx due to enhanced Ca(v)1.1 (显示 CACNA1S 抗体) channel activity, which restores muscle strength in JP45 (显示 JSRP1 抗体)/CASQ1 double knockout mice.
Protein levels of CSQ1, SERCA1 (显示 ATP2A1 抗体), and SERCA2 (显示 ATP2A2 抗体) are re-adjusted in skeletal muscles depending on the demands of diverse exercise training programs.
results support the view that in skeletal muscles, CASQ1 plays a key role in both Ca(2 (显示 CA2 抗体)+) homeostasis and terminal cisternae structure
The results presented in this paper unmask a differential effect of CASQ1&2 ablation in fast versus slow fibers
Calsequestrin not only stores Ca(2 (显示 CA2 抗体)+), but also varies its affinity in ways that progressively increase the ability of the store to deliver Ca(2 (显示 CA2 抗体)+) as it becomes depleted, a novel feedback mechanism of potentially valuable functional implications.
effect of nockdown of CSQ1 in adult mouse skeletal muscle on Store-operated Ca(2 (显示 CA2 抗体)+) entry
knocking down CSQ2, but not CSQ1, leads to reduced Ca2 (显示 CA2 抗体)+ storage and release in C2C12 myotubes
CSQ1 is essential for the normal development of the sarcoplasmic reticulum (SR) and its calcium release units and for the storage and release of appropriate amounts of SR Ca(2 (显示 CA2 抗体)+).
a mechanism for the observed in vitro and in vivo dynamic high-capacity and low-affinity Ca(2 (显示 CA2 抗体)+)-binding activity of calsequestrin
Purified skeletal ryanodine receptors are similarly activated by purified triadin (显示 TRDN 抗体) or purified junctin (显示 ASPH 抗体) added to their luminal side, although a lack of competition indicated that the proteins act at independent sites.
the p.D244G variant in CASQ1 is associated with a skeletal muscle disease and alters sarcoplasmic calcium release
Calsequestrin-1 monomers suppress Store-Operated Ca2 (显示 CA2 抗体)+ Entry by interacting with STIM1 (显示 STIM1 抗体) and attenuating STIM1 (显示 STIM1 抗体) aggregation via its C-terminal amino acid 362-396.
the protein aggregate myopathy with benign evolution and muscle inclusions composed of excess CASQ1 due to the D244G heterozygous missense mutation in the CASQ1 gene
Equilibrium dialysis and turbidity measurements showed that D244G and, to a lesser extent, M87T partially lose Ca(2 (显示 CA2 抗体)+) binding exhibited by wild type calsequestrin 1 at high Ca(2 (显示 CA2 抗体)+) concentrations.
Missense mutation in CASQ1 gene causes the formation of abnormal sarcoplasmic reticulum (SR) vacuoles containing aggregates of CASQ1 results in altered Ca2 (显示 CA2 抗体)+ release, and vacuolar myopathy patients phenotype.
The sarcoplasmic reticulum calcium content in human type II fibres is primarily determined by the CSQ1 abundance, and in type I fibres, by the combined amounts of both CSQ1 and CSQ2.
a direct interaction of dysferlin (显示 DYSF 抗体) with Trim72/MG53 (显示 TRIM72 抗体), AHNAK (显示 AHNAK 抗体), cytoplasmic dynein (显示 DYNC1H1 抗体), myomesin-2 (显示 MYOM2 抗体) and calsequestrin-1, but not with caveolin-3 (显示 CAV3 抗体) or dystrophin (显示 DMD 抗体), is reported.
CASQ1 is not a major malignant hyperthermia susceptibility locus in the North American population
Downregulation of CSQ-1 in diabetic platelets and impairment of CSQ-1 in normal cells leads to disturbed Ca(2 (显示 CA2 抗体)+) release, demonstrating a potential role for CSQ-1 in the regulation of the platelet Ca(2 (显示 CA2 抗体)+) release process
The protein encoded by this gene is a mitochondrial calcium-binding protein located in the luminal space of the terminal cisternae of the sarcoplasmic reticulum. The protein binds and putatively stores calcium ions. The protein is absent in patients with Duchenne and Becker types of muscular dystrophy.
, calsequestrin, skeletal muscle isoform
, laminin-binding protein
, skeletal muscle calsequestrin 1
, Laminin-binding protein
, calsquestrin 1
, calsequestrin homologue