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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. Zusätzlich bieten wir Ihnen Calsequestrin Proteine (13) und Calsequestrin Kits (11) und viele weitere Produktgruppen zu diesem Protein an.
Showing 10 out of 27 products:
Chicken Monoclonal Calsequestrin Primary Antibody für 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 für 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 für 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 für 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 (zeige JSRP1 Antikörper)-CASQ1 and JP45 (zeige JSRP1 Antikörper)-CASQ2 (zeige CASQ2 Antikörper) complexes supports tetanic force development in slow twitch soleus muscles.
Transient knockdown of annexin A6 (zeige ANXA6 Antikörper) and calsequestrin 1 protein of high-active mice with vivo-morpholinos resulted in decreased physical activity levels (P = 0.001).
Ca(2 (zeige CA2 Antikörper)+) transients evoked by tetanic stimulation are the result of massive Ca(2 (zeige CA2 Antikörper)+) influx due to enhanced Ca(v)1.1 (zeige CACNA1S Antikörper) channel activity, which restores muscle strength in JP45 (zeige JSRP1 Antikörper)/CASQ1 double knockout mice.
Protein levels of CSQ1, SERCA1 (zeige ATP2A1 Antikörper), and SERCA2 (zeige ATP2A2 Antikörper) 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 (zeige CA2 Antikörper)+) 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 (zeige CA2 Antikörper)+), but also varies its affinity in ways that progressively increase the ability of the store to deliver Ca(2 (zeige CA2 Antikörper)+) 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 (zeige CA2 Antikörper)+) entry
knocking down CSQ2, but not CSQ1, leads to reduced Ca2 (zeige CA2 Antikörper)+ 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 (zeige CA2 Antikörper)+).
a mechanism for the observed in vitro and in vivo dynamic high-capacity and low-affinity Ca(2 (zeige CA2 Antikörper)+)-binding activity of calsequestrin
Purified skeletal ryanodine receptors are similarly activated by purified triadin (zeige TRDN Antikörper) or purified junctin (zeige ASPH Antikörper) 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 (zeige CA2 Antikörper)+ Entry by interacting with STIM1 (zeige STIM1 Antikörper) and attenuating STIM1 (zeige STIM1 Antikörper) 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 (zeige CA2 Antikörper)+) binding exhibited by wild type calsequestrin 1 at high Ca(2 (zeige CA2 Antikörper)+) concentrations.
Missense mutation in CASQ1 gene causes the formation of abnormal sarcoplasmic reticulum (SR) vacuoles containing aggregates of CASQ1 results in altered Ca2 (zeige CA2 Antikörper)+ 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 (zeige DYSF Antikörper) with Trim72/MG53 (zeige TRIM72 Antikörper), AHNAK (zeige AHNAK Antikörper), cytoplasmic dynein (zeige DYNC1H1 Antikörper), myomesin-2 (zeige MYOM2 Antikörper) and calsequestrin-1, but not with caveolin-3 (zeige CAV3 Antikörper) or dystrophin (zeige DMD Antikörper), 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 (zeige CA2 Antikörper)+) release, demonstrating a potential role for CSQ-1 in the regulation of the platelet Ca(2 (zeige CA2 Antikörper)+) 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