PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 26862665-4 2016 To investigate which step(s) of the ATPase cycle is regulated by the N-terminal extension of cTnI, here we studied the calcium dependence of cardiac myosin II ATPase kinetics in isolated cardiac myofibrils. Calcium 119-126 dynein, axonemal, heavy chain 8 Mus musculus 159-165 6280042-3 1982 A small amount of calcium-insensitive ("basal") ATPase in the normal preparation and a higher value in the dystrophic were shown to be due to contamination by a lighter membrane fraction of probable surface membrane origin. Calcium 18-25 dynein, axonemal, heavy chain 8 Mus musculus 48-54 26862665-8 2016 These data from experiments using native cardiac myofibrils under physiological conditions indicate that modification of the N-terminal extension of cTnI plays a role in the calcium regulation of the kinetics of actomyosin ATPase. Calcium 174-181 dynein, axonemal, heavy chain 8 Mus musculus 223-229 16442703-1 2006 The sarcolemmal calcium pumps (PMCA for plasma membrane calcium/calmodulin dependent ATPase) are a family of 10 transmembrane domain proteins ejecting calcium from the cytosol. Calcium 16-23 dynein, axonemal, heavy chain 8 Mus musculus 85-91 16076902-0 2005 The E22K mutation of myosin RLC that causes familial hypertrophic cardiomyopathy increases calcium sensitivity of force and ATPase in transgenic mice. Calcium 91-98 dynein, axonemal, heavy chain 8 Mus musculus 124-130 8739238-2 1996 In order to determine if increased expression of the SR Ca2+ ATPase gene leads to alterations in calcium transients and in contractile behavior we constructed transgenic mice overexpressing the SERCA2 gene. Calcium 97-104 dynein, axonemal, heavy chain 8 Mus musculus 53-67 12424227-3 2003 The cardiac Ca2+ ATPase (SERCA2a) of the sarcoplasmic reticulum plays a dominant role in lowering cytoplasmic calcium levels during relaxation and is regulated by phospholamban (PLN). Calcium 110-117 dynein, axonemal, heavy chain 8 Mus musculus 4-23 9605008-3 1997 It is shown that AK-2123 injected at therapeutic dose inhibits active transport of calcium ions by the (Ca2+-Mg2+)-dependent ATP-ase. Calcium 83-90 dynein, axonemal, heavy chain 8 Mus musculus 125-132 9245088-3 1997 A therapeutic dose of AK-2123 has been shown to inhibit active transport of calcium ions across sarcoplasmic reticular cells effected by Ca(2+)-dependent Mg(2+)-activated ATPase. Calcium 76-83 dynein, axonemal, heavy chain 8 Mus musculus 171-177 1319155-5 1992 Increased calcium pool in pancreas along with Ca2+ activated ATPase was observed. Calcium 10-17 dynein, axonemal, heavy chain 8 Mus musculus 61-67 8682113-2 1995 Since systolic functional impairment and subsequent recovery are frequently observed in myocarditis, we reasoned that the development of autoimmunity to cardiac sarcoplasmic reticulum calcium ATPase (SR-Ca2+ ATPase), which could interfere with intracellular calcium regulation and therefore affect myocardial contractility, should lead to immune-mediated myocarditis in experimental animals. Calcium 184-191 dynein, axonemal, heavy chain 8 Mus musculus 200-214 8124810-2 1994 Since sarcoplasmic calcium overload is a recognized pathobiochemical finding in cardiomyopathy, we reasoned that there might be a causal relation between inhibition of sarcoplasmic calcium exclusion and pathogenesis of the disease and that immunization with sarcoplasmic reticulum calcium ATPase (SR-ATPase) or antibody specific for SR-ATPase, which can interfere with the regulation of the intracellular calcium content and the myocardial contractility, should lead to the development of cardiomyopathy and possibly myocarditis. Calcium 19-26 dynein, axonemal, heavy chain 8 Mus musculus 289-295 8124810-2 1994 Since sarcoplasmic calcium overload is a recognized pathobiochemical finding in cardiomyopathy, we reasoned that there might be a causal relation between inhibition of sarcoplasmic calcium exclusion and pathogenesis of the disease and that immunization with sarcoplasmic reticulum calcium ATPase (SR-ATPase) or antibody specific for SR-ATPase, which can interfere with the regulation of the intracellular calcium content and the myocardial contractility, should lead to the development of cardiomyopathy and possibly myocarditis. Calcium 19-26 dynein, axonemal, heavy chain 8 Mus musculus 297-306 8124810-2 1994 Since sarcoplasmic calcium overload is a recognized pathobiochemical finding in cardiomyopathy, we reasoned that there might be a causal relation between inhibition of sarcoplasmic calcium exclusion and pathogenesis of the disease and that immunization with sarcoplasmic reticulum calcium ATPase (SR-ATPase) or antibody specific for SR-ATPase, which can interfere with the regulation of the intracellular calcium content and the myocardial contractility, should lead to the development of cardiomyopathy and possibly myocarditis. Calcium 19-26 dynein, axonemal, heavy chain 8 Mus musculus 333-342 8124810-2 1994 Since sarcoplasmic calcium overload is a recognized pathobiochemical finding in cardiomyopathy, we reasoned that there might be a causal relation between inhibition of sarcoplasmic calcium exclusion and pathogenesis of the disease and that immunization with sarcoplasmic reticulum calcium ATPase (SR-ATPase) or antibody specific for SR-ATPase, which can interfere with the regulation of the intracellular calcium content and the myocardial contractility, should lead to the development of cardiomyopathy and possibly myocarditis. Calcium 181-188 dynein, axonemal, heavy chain 8 Mus musculus 289-295 8124810-2 1994 Since sarcoplasmic calcium overload is a recognized pathobiochemical finding in cardiomyopathy, we reasoned that there might be a causal relation between inhibition of sarcoplasmic calcium exclusion and pathogenesis of the disease and that immunization with sarcoplasmic reticulum calcium ATPase (SR-ATPase) or antibody specific for SR-ATPase, which can interfere with the regulation of the intracellular calcium content and the myocardial contractility, should lead to the development of cardiomyopathy and possibly myocarditis. Calcium 181-188 dynein, axonemal, heavy chain 8 Mus musculus 297-306 8124810-2 1994 Since sarcoplasmic calcium overload is a recognized pathobiochemical finding in cardiomyopathy, we reasoned that there might be a causal relation between inhibition of sarcoplasmic calcium exclusion and pathogenesis of the disease and that immunization with sarcoplasmic reticulum calcium ATPase (SR-ATPase) or antibody specific for SR-ATPase, which can interfere with the regulation of the intracellular calcium content and the myocardial contractility, should lead to the development of cardiomyopathy and possibly myocarditis. Calcium 181-188 dynein, axonemal, heavy chain 8 Mus musculus 333-342 8124810-2 1994 Since sarcoplasmic calcium overload is a recognized pathobiochemical finding in cardiomyopathy, we reasoned that there might be a causal relation between inhibition of sarcoplasmic calcium exclusion and pathogenesis of the disease and that immunization with sarcoplasmic reticulum calcium ATPase (SR-ATPase) or antibody specific for SR-ATPase, which can interfere with the regulation of the intracellular calcium content and the myocardial contractility, should lead to the development of cardiomyopathy and possibly myocarditis. Calcium 181-188 dynein, axonemal, heavy chain 8 Mus musculus 289-295 8124810-2 1994 Since sarcoplasmic calcium overload is a recognized pathobiochemical finding in cardiomyopathy, we reasoned that there might be a causal relation between inhibition of sarcoplasmic calcium exclusion and pathogenesis of the disease and that immunization with sarcoplasmic reticulum calcium ATPase (SR-ATPase) or antibody specific for SR-ATPase, which can interfere with the regulation of the intracellular calcium content and the myocardial contractility, should lead to the development of cardiomyopathy and possibly myocarditis. Calcium 181-188 dynein, axonemal, heavy chain 8 Mus musculus 297-306 8124810-2 1994 Since sarcoplasmic calcium overload is a recognized pathobiochemical finding in cardiomyopathy, we reasoned that there might be a causal relation between inhibition of sarcoplasmic calcium exclusion and pathogenesis of the disease and that immunization with sarcoplasmic reticulum calcium ATPase (SR-ATPase) or antibody specific for SR-ATPase, which can interfere with the regulation of the intracellular calcium content and the myocardial contractility, should lead to the development of cardiomyopathy and possibly myocarditis. Calcium 181-188 dynein, axonemal, heavy chain 8 Mus musculus 333-342 8124810-16 1994 Besides antigenic specificity, since antibody to cardiac SR-ATPase also inhibits energy-dependent processes in the myocardium, it is reasonable to associate the pathological evidence of myonecrosis with the interference of calcium regulation, which controls myocardial contractility. Calcium 223-230 dynein, axonemal, heavy chain 8 Mus musculus 57-66