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1 ossreactive with streptococcal M protein and cardiac myosin.
2 heterozygous for the mutation R403Q in beta-cardiac myosin.
3 arbil, a small-molecule, direct activator of cardiac myosin.
4 matogenic epitopes in the S2 region of human cardiac myosin.
5 athy mutations have been identified in human cardiac myosin.
6 yte and Ab responses after immunization with cardiac myosin.
7 tained a sequence identical in human and rat cardiac myosin.
8 d-type (cWT) or mutant (D778G or G741R) beta-cardiac myosin.
9 s and delayed type hypersensitivity (DTH) to cardiac myosin.
10 fy regions of disease enrichment within beta-cardiac myosin.
11 chanical coordination between the 2 heads of cardiac myosin.
12 rg-712 in the converter domain of human beta-cardiac myosin.
13 sis for the kinetic and mechanical tuning of cardiac myosin.
14 hinery of the cardiac muscle, including beta-cardiac myosin.
15 utation, R453C, in the context of human beta-cardiac myosin.
16 osin, but this remains untested in mammalian cardiac myosins.
18 structurally and immunologically similar to cardiac myosin, a well-known mediator of inflammatory he
21 olecular motors.Omecamtiv mecarbil (OM) is a cardiac myosin activator that is currently in clinical t
24 othesis that omecamtiv mecarbil, a selective cardiac myosin activator, will augment cardiac function
25 Agents that target contractility, such as cardiac myosin activators and novel adenosine triphospha
26 ugs with novel mechanisms of action, such as cardiac myosin activators, are under investigation for p
28 n rheumatic carditis target the S2 region of cardiac myosin and are similar among populations with rh
29 ted intracellular biomarker antigens such as cardiac myosin and brain tubulin, while targeting extrac
32 treptococcal carbohydrate epitope GlcNAc and cardiac myosin and its peptides appear during progressio
33 in thymic epithelium conferred tolerance to cardiac myosin and prevented myocarditis, demonstrating
34 ry between streptococcal M protein and human cardiac myosin and represents some of the most well-defi
36 weaker than originally described for bovine cardiac myosin and thus the thermodynamic coupling betwe
39 rties of the regulatory light chain of human cardiac myosin are important for physiological function,
40 urements of Ca(2+) sensitivity of human beta-cardiac myosin ATPase activity are consistent with the h
41 tracardiac CD45(+) leukocytes, elevated anti-cardiac myosin autoantibodies, and increased cardiac fib
44 t affect humoral immunity against T cruzi or cardiac myosin (autoimmunity) but did decrease delayed-t
45 16 was characterized as a cryptic epitope of cardiac myosin because it did not recall lymphocyte and
47 uced protein kinase (PK)A phosphorylation of cardiac myosin binding protein (cMyBP)-C may regulate cr
49 n kinase A-mediated (PKA) phosphorylation of cardiac myosin binding protein C (cMyBP-C) accelerates t
54 scle contraction, and its accessory protein, cardiac myosin binding protein C (cMyBP-C), are the two
61 myopathy (FHC), individuals bearing a mutant cardiac myosin binding protein C (MyBP-C) gene usually h
64 ediated degradation of myosin heavy chain 6, cardiac myosin binding protein C, calcineurin (PPP3CB),
66 ene analyses revealed 8 sequence variants in cardiac myosin binding protein-C (1 nonsense, 1 splice a
75 microscopy, we examined the contribution of cardiac myosin binding protein-C (cMyBP-C) to thick-fila
76 Despite advances in the molecular biology of cardiac myosin binding protein-C (cMyBP-C), little is un
78 ions in the gene encoding cardiac C-protein [cardiac myosin binding protein-C (cMyBP-C)] are one of t
79 cohort studies suggest that mutations in the cardiac myosin binding protein-C (MYBPC3) gene cause lat
80 ges to the thin filament: phosphorylation of cardiac myosin binding protein-C accelerates cross bridg
81 d in over 170 normal chromosomes; 1 variant (cardiac myosin binding protein-C Arg326Gln) also occurre
83 evidence suggesting that phosphorylation of cardiac myosin binding protein-C is a key regulator of t
84 mutations in thick filament proteins such as cardiac myosin binding protein-C or titin, cause familia
86 ted a transgenic (TG) mouse model expressing cardiac myosin binding protein-C with a non-phosphorylat
89 us (Ser-23/24) of cardiac troponin I (cTnI), cardiac myosin-binding protein C (cMyBP-C) and titin.
96 e for a potential regulator of these motors, cardiac myosin-binding protein C (cMyBP-C), cause hypert
97 ns, to resolve the structure and dynamics of cardiac myosin-binding protein C (cMyBP-C), focusing on
100 olamban at Ser16, phospholemman at Ser68 and cardiac myosin-binding protein C at Ser282, was unaltere
102 on impairs phosphoregulation and function of cardiac myosin-binding protein C in human heart failure.
104 A stable 40-kDa fragment is produced from cardiac myosin-binding protein C when the heart is stres
105 eptide and disrupt the interaction of native cardiac myosin-binding protein C with the thin filament.
108 of cardiac myocyte proteins (alpha-actinin, cardiac myosin-binding protein C, and cardiac troponin I
109 th-old mice with gene targeted deficiency of cardiac myosin-binding protein-C (cMyBP-C(-/-), n=6) or
114 ples, ADP sensitivity highly correlated with cardiac myosin-binding protein-C (cMyBP-C) protein level
115 M-domain is the major regulatory subunit of cardiac myosin-binding protein-C (cMyBP-C) that modulate
118 ears have suggested that the interactions of cardiac myosin-binding protein-C with its binding partne
120 Dynamics study of the motor domain of human cardiac myosin bound to OM, where the effects of the dru
121 eater unloaded shortening velocity than beta-cardiac myosin but a 2-fold lower average isometric forc
122 dy the mechanochemical properties of mutated cardiac myosin, but mouse hearts express alpha-MHC, wher
128 al relevance of autoantibodies (Abs) against cardiac myosin (CM) in clinical idiopathic dilated cardi
132 e mechanisms by which autoantibodies against cardiac myosin (CM) may lead to heart dysfunction is unk
133 rafts triggers a CD4(+) Th1 cell response to cardiac myosin (CM), a major contractile protein of the
134 ssue-specific autoantigens such as vimentin, cardiac myosin (CM), collagen V (Col V), agrin, and angi
139 al muscle myosin, smooth muscle myosin, beta-cardiac myosin (CMIIB), Dictyostelium myosin II (DdMII),
140 om no loop to one that is abnormally shaped, cardiac myosin (cmlc2) is present and contraction occurs
144 erhaps more interesting, mice immunized with cardiac myosin developed T. cruzi-specific DTH and antib
145 g muscle motility, we demonstrate human beta-cardiac myosin-driven gliding of actin filaments on DNA
146 response, since C57BL/6 mice did not develop cardiac myosin DTH upon immunization with T. cruzi extra
147 proteolytic digestion of the C-loop in beta-cardiac myosin eliminates actin-activated myosin ATPase
150 ns, in which immunoglobulin G targeted human cardiac myosin epitopes in the S2 subfragment hinge regi
152 ctin-binding region at the N terminus of the cardiac myosin essential light chain (ELC) remains elusi
153 In an in vitro motility assay, both mutant cardiac myosins exhibited a reduced ability to transloca
154 he border zone was associated with increased cardiac myosin expression and cardiac myocyte size (30 m
157 ta gene switching and implicates the role of cardiac myosin gene organization with their function.
158 The expression patterns of two zebrafish cardiac myosin genes, cardiac myosin light chain 2 (cmlc
161 It is well-established that rabbit alpha-cardiac myosin has a 2-fold greater unloaded shortening
164 oimmunity to cardiac antigens, in particular cardiac myosin, has been observed in humans with myocard
170 ably transfected with cardiac-specific alpha-cardiac myosin heavy chain (MHC) promoter-driven enhance
171 diac alpha actin, atrial natriuretic factor, cardiac myosin heavy chain alpha, cardiac myosin heavy c
172 MNCs expressed the cardiac-specific antigens cardiac myosin heavy chain and cardiac troponin T, respe
173 nse mutations (S532P and F764L) in the alpha-cardiac myosin heavy chain and compared them with WT mic
174 for other loci, two muscle genes (Human beta-cardiac myosin heavy chain and myogenin) became localize
175 ic factor, cardiac myosin heavy chain alpha, cardiac myosin heavy chain beta, myosin light chain 1A,
176 action is disrupted when modeling human beta-cardiac myosin heavy chain cardiomyopathy mutations E497
177 sin binding protein-C, troponin I, and alpha-cardiac myosin heavy chain caused elderly-onset hypertro
184 a mouse model of FHC with an Arg403Gln alpha-cardiac myosin heavy chain missense mutation, and used n
186 banding of mice with or without an Arg403Gln cardiac myosin heavy chain mutation (alphaMHC403/+) prod
187 D2, or D3 under the regulation of the alpha cardiac myosin heavy chain promoter exhibited high rates
188 from cardiac myofilaments were identified on cardiac myosin heavy chain, actin, myosin light chains,
189 tion, circulating IgG autoantibodies against cardiac myosin heavy chain, and premature death due to h
191 the nucleus, whereas alpha-sarcomeric actin, cardiac myosin heavy chain, troponin I, and alpha-actini
192 notion, intracellular cardiac antigens, like cardiac myosin heavy chain-alpha, cardiac troponin-I, an
193 ncode truncated forms of MyBP-C in which the cardiac myosin heavy chain-binding and titin-binding dom
196 chemical differences between the 2 mammalian cardiac myosin heavy chains (MHCs), alpha-MHC and beta-M
197 rt here that a murine model of FHC bearing a cardiac myosin heavy-chain gene missense mutation (alpha
199 d by two bipolar arrays of the motor protein cardiac myosin II extending from the thick filament and
200 bstituted partially, and the CM-loop of beta-cardiac myosin II less well, for growth, capping of surf
201 ed Arg residue (whose mutation in human beta-cardiac myosin II results in familial hypertrophic cardi
202 This actin-binding loop is the site of a cardiac myosin-II mutation responsible for some forms of
207 dentified disease-specific epitopes of human cardiac myosin in the development of rheumatic carditis
208 ntracellular biomarkers of disease including cardiac myosin in the myocardium and tubulin, a protein
209 Here we determine the crystal structure of cardiac myosin in the pre-powerstroke state, the most re
210 primed position resulting in accumulation of cardiac myosin in the primed state prior to onset of car
211 pitopes were localized in fragments of human cardiac myosin, including heavy meromyosin (HMM), the S1
216 nal antibodies (MAbs) derived from mice with cardiac myosin-induced myocarditis were characterized.
217 dition of EMD 57033 to heat-inactivated beta-cardiac myosin is followed by refolding and reactivation
218 Mimicry between streptococcal M protein and cardiac myosin is important in the pathogenesis of rheum
219 ation of the regulatory light chain (RLC) of cardiac myosin is known to play a beneficial role in hea
222 chanism of mavacamten-mediated inhibition of cardiac myosin is the decrease of phosphate release from
223 heterozygous for this mutation in the alpha-cardiac myosin isoform display typical familial hypertro
224 Thus, nature has adapted the function of cardiac myosin isoforms to optimize power output for hea
227 irect evidence that immune responses against cardiac myosin lead to valvular heart disease and the in
228 autoimmune-susceptible SWXJ mice with whole cardiac myosin leads to T cell-mediated experimental aut
229 terns of two zebrafish cardiac myosin genes, cardiac myosin light chain 2 (cmlc2) and ventricular myo
232 c hypertrophy and failure, and a decrease in cardiac myosin light chain 2, an essential protein for c
233 her than the heart, we tested the use of the cardiac myosin light chain 2v (MLC-2v) promoter and the
234 single site to 0.45 mol of phosphate/mol by cardiac myosin light chain kinase (cMLCK) increases Ca(2
235 hosphorylated these recombinant species with cardiac myosin light chain kinase and zipper-interacting
236 hat changing the phosphorylation status of a cardiac myosin light chain might alter cardiac function
237 hat neural crest cells invade and contribute cardiac myosin light chain2 (cmlc2)-positive cardiomyocy
238 ntly phosphorylates MLC2v in cardiomyocytes, cardiac myosin light-chain kinase (cMLCK), yet the role(
239 est that the depressed molecular function in cardiac myosin may initiate the events that cause the he
240 rom the light meromyosin region of the human cardiac myosin molecule and had a different pattern of r
241 -dependent kinetics of individual human beta-cardiac myosin molecules interacting with an actin filam
245 tis (EAM) can be induced in the Lewis rat by cardiac myosin or its cryptic S2-16 peptide epitope (ami
246 n the T cell clones were stimulated by human cardiac myosin or other alpha-helical proteins, such as
247 These results suggest that immunization with cardiac myosin or T. cruzi antigen can induce specific,
251 itis (EAM), in which mice are immunized with cardiac myosin peptide, whereas IL-17A-deficient mice we
252 recruitment (100.9%, P<0.01), and increased cardiac myosin-positive area (39%, P<0.05) at 4, 7, and
253 vessels/mm2, P<0.01; SDF-1:MSC vs. MSC), and cardiac myosin-positive area (MSC: 49.5%; mSC:SDF-1: 162
255 osis factor-alpha (TNF-alpha) gene under the cardiac myosin promoter (TNF1.6 mice) develop dilated ca
256 loped computational models of the human beta-cardiac myosin protein before and after the myosin power
257 These transient kinetic studies on mouse cardiac myosins provide strong evidence that the functio
259 green fluorescent protein (GFP)-tagged human cardiac myosin regulatory light chain (HCRLC) was constr
260 22nd amino acid residue (E22K) in the human cardiac myosin regulatory light chain (RLC) gene causes
263 e in Lewis rats and have been linked to anti-cardiac myosin responses, we reacted myosin-sensitized l
264 We conclude that OM alters the energetics of cardiac myosin's mechanical cycle, causing the powerstro
265 e same exercise was repeated for human alpha-cardiac myosin S1 and rabbit fast skeletal muscle S1.
266 the decrease of phosphate release from beta-cardiac myosin-S1, a secondary mechanism decreases the n
267 biting the rate of phosphate release of beta-cardiac myosin-S1, but the molecular mechanism of action
269 from IFN-gamma-deficient mice immunized with cardiac myosin showed increased cellularity; greater num
270 urements using the expressed actins and beta-cardiac myosin showed that the mutation increased the K(
272 r immunity to T. cruzi antigens could induce cardiac myosin-specific autoimmunity in the absence of l
273 sitosis in the heart accompanied by vigorous cardiac myosin-specific delayed-type hypersensitivity (D
274 adjuvant and found that these mice developed cardiac myosin-specific delayed-type hypersensitivity (D
276 2, IL-4, and TNF-alpha production as well as cardiac myosin-specific IgG1 and IgG2b production, where
281 is a selective, small-molecule activator of cardiac myosin that is being developed as a potential tr
282 ) is a small molecule allosteric effector of cardiac myosin that is in clinical trials for treatment
283 discovered novel small-molecule modulator of cardiac myosin that targets the underlying sarcomere hyp
284 tic fever sera, contained Ab titers to human cardiac myosin that were significantly higher than those
287 t is linked to host immune responses against cardiac myosin, the most abundant protein in the heart.
288 In addition, pathogenic epitopes of human cardiac myosin, the S2 fragment peptides S2-16 and S2-28
289 with antibodies and T cell responses against cardiac myosin, there is no unifying hypothesis about ca
290 ach for the study of mutations in human beta-cardiac myosin using the hypertrophic myopathy mutation
291 accelerates the actin-activated activity of cardiac myosin was able to rescue processivity of the D1
292 erentiation for 5-7 days, cWT or mutant beta-cardiac myosin was expressed at 25 % of total myosin in
293 ardiac myosin with those expressing cWT beta-cardiac myosin, we found that ttp and t0.5 were signific
294 synthetic peptides of the S2 region of human cardiac myosin, we identified an amino acid sequence, S2
298 the crystal structure of OM bound to bovine cardiac myosin, which shows that OM stabilizes the pre-p
299 exchanged endogenous RLC from native porcine cardiac myosin with recombinant human ventricular wild t
300 we compared myotubes expressing mutant beta-cardiac myosin with those expressing cWT beta-cardiac my
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