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1 y supported by rabbit skeletal and by bovine cardiac myosin.
2 hinery of the cardiac muscle, including beta-cardiac myosin.
3 utation, R453C, in the context of human beta-cardiac myosin.
4 therapeutic approaches to target human beta-cardiac myosin.
5 ossreactive with streptococcal M protein and cardiac myosin.
6 heterozygous for the mutation R403Q in beta-cardiac myosin.
7 arbil, a small-molecule, direct activator of cardiac myosin.
8 matogenic epitopes in the S2 region of human cardiac myosin.
9 CM-causing mutations are found in human beta-cardiac myosin.
10 cur within <200 mus of actin binding by beta-cardiac myosin.
11 athy mutations have been identified in human cardiac myosin.
12 yte and Ab responses after immunization with cardiac myosin.
13 tained a sequence identical in human and rat cardiac myosin.
14 d-type (cWT) or mutant (D778G or G741R) beta-cardiac myosin.
15 fy regions of disease enrichment within beta-cardiac myosin.
16 rg-712 in the converter domain of human beta-cardiac myosin.
17 sis for the kinetic and mechanical tuning of cardiac myosin.
18 osin, but this remains untested in mammalian cardiac myosins.
20 structurally and immunologically similar to cardiac myosin, a well-known mediator of inflammatory he
23 olecular motors.Omecamtiv mecarbil (OM) is a cardiac myosin activator that is currently in clinical t
26 othesis that omecamtiv mecarbil, a selective cardiac myosin activator, will augment cardiac function
27 Agents that target contractility, such as cardiac myosin activators and novel adenosine triphospha
28 ugs with novel mechanisms of action, such as cardiac myosin activators, are under investigation for p
30 n rheumatic carditis target the S2 region of cardiac myosin and are similar among populations with rh
31 ted intracellular biomarker antigens such as cardiac myosin and brain tubulin, while targeting extrac
34 treptococcal carbohydrate epitope GlcNAc and cardiac myosin and its peptides appear during progressio
35 in thymic epithelium conferred tolerance to cardiac myosin and prevented myocarditis, demonstrating
36 ry between streptococcal M protein and human cardiac myosin and represents some of the most well-defi
37 weaker than originally described for bovine cardiac myosin and thus the thermodynamic coupling betwe
39 urements of Ca(2+) sensitivity of human beta-cardiac myosin ATPase activity are consistent with the h
40 tracardiac CD45(+) leukocytes, elevated anti-cardiac myosin autoantibodies, and increased cardiac fib
43 t affect humoral immunity against T cruzi or cardiac myosin (autoimmunity) but did decrease delayed-t
44 16 was characterized as a cryptic epitope of cardiac myosin because it did not recall lymphocyte and
46 uced protein kinase (PK)A phosphorylation of cardiac myosin binding protein (cMyBP)-C may regulate cr
48 proteoform identification, endogenous human cardiac myosin binding protein C (140 kDa) was identifie
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
77 microscopy, we examined the contribution of cardiac myosin binding protein-C (cMyBP-C) to thick-fila
78 Despite advances in the molecular biology of cardiac myosin binding protein-C (cMyBP-C), little is un
80 ions in the gene encoding cardiac C-protein [cardiac myosin binding protein-C (cMyBP-C)] are one of t
81 cohort studies suggest that mutations in the cardiac myosin binding protein-C (MYBPC3) gene cause lat
82 ges to the thin filament: phosphorylation of cardiac myosin binding protein-C accelerates cross bridg
83 d in over 170 normal chromosomes; 1 variant (cardiac myosin binding protein-C Arg326Gln) also occurre
85 o a downregulation of S-glutathionylation of cardiac myosin binding protein-C in FTY720-treated Tm-E1
86 evidence suggesting that phosphorylation of cardiac myosin binding protein-C is a key regulator of t
87 mutations in thick filament proteins such as cardiac myosin binding protein-C or titin, cause familia
89 ted a transgenic (TG) mouse model expressing cardiac myosin binding protein-C with a non-phosphorylat
90 lly encoded] N'-terminal domains C0 to C7 of cardiac myosin binding protein-C) fragment and an insolu
91 recombinant] N'-terminal domains C0 to C7 of cardiac myosin binding protein-C)-sc returned pCa(50) an
94 us (Ser-23/24) of cardiac troponin I (cTnI), cardiac myosin-binding protein C (cMyBP-C) and titin.
103 e for a potential regulator of these motors, cardiac myosin-binding protein C (cMyBP-C), cause hypert
104 ns, to resolve the structure and dynamics of cardiac myosin-binding protein C (cMyBP-C), focusing on
107 olamban at Ser16, phospholemman at Ser68 and cardiac myosin-binding protein C at Ser282, was unaltere
109 on impairs phosphoregulation and function of cardiac myosin-binding protein C in human heart failure.
111 A stable 40-kDa fragment is produced from cardiac myosin-binding protein C when the heart is stres
112 eptide and disrupt the interaction of native cardiac myosin-binding protein C with the thin filament.
116 of cardiac myocyte proteins (alpha-actinin, cardiac myosin-binding protein C, and cardiac troponin I
117 th-old mice with gene targeted deficiency of cardiac myosin-binding protein-C (cMyBP-C(-/-), n=6) or
123 ples, ADP sensitivity highly correlated with cardiac myosin-binding protein-C (cMyBP-C) protein level
124 M-domain is the major regulatory subunit of cardiac myosin-binding protein-C (cMyBP-C) that modulate
126 ears have suggested that the interactions of cardiac myosin-binding protein-C with its binding partne
129 Dynamics study of the motor domain of human cardiac myosin bound to OM, where the effects of the dru
130 eater unloaded shortening velocity than beta-cardiac myosin but a 2-fold lower average isometric forc
131 dy the mechanochemical properties of mutated cardiac myosin, but mouse hearts express alpha-MHC, wher
132 yopathy (DCM) mutation (F764L) in human beta-cardiac myosin by determining its motor properties in th
135 al relevance of autoantibodies (Abs) against cardiac myosin (CM) in clinical idiopathic dilated cardi
139 e mechanisms by which autoantibodies against cardiac myosin (CM) may lead to heart dysfunction is unk
140 rafts triggers a CD4(+) Th1 cell response to cardiac myosin (CM), a major contractile protein of the
141 ssue-specific autoantigens such as vimentin, cardiac myosin (CM), collagen V (Col V), agrin, and angi
145 al muscle myosin, smooth muscle myosin, beta-cardiac myosin (CMIIB), Dictyostelium myosin II (DdMII),
146 om no loop to one that is abnormally shaped, cardiac myosin (cmlc2) is present and contraction occurs
150 erhaps more interesting, mice immunized with cardiac myosin developed T. cruzi-specific DTH and antib
151 g muscle motility, we demonstrate human beta-cardiac myosin-driven gliding of actin filaments on DNA
152 response, since C57BL/6 mice did not develop cardiac myosin DTH upon immunization with T. cruzi extra
153 proteolytic digestion of the C-loop in beta-cardiac myosin eliminates actin-activated myosin ATPase
156 ns, in which immunoglobulin G targeted human cardiac myosin epitopes in the S2 subfragment hinge regi
158 ctin-binding region at the N terminus of the cardiac myosin essential light chain (ELC) remains elusi
159 In an in vitro motility assay, both mutant cardiac myosins exhibited a reduced ability to transloca
160 he border zone was associated with increased cardiac myosin expression and cardiac myocyte size (30 m
164 he corresponding mutations in the human beta-cardiac myosin gene are associated with hypertrophic and
165 ta gene switching and implicates the role of cardiac myosin gene organization with their function.
167 ntamination by ~1:100 000 TF/myosin, whereas cardiac myosin had TF-like activity >10-fold higher.
168 It is well-established that rabbit alpha-cardiac myosin has a 2-fold greater unloaded shortening
171 tivity of the catalytic domain of human beta-cardiac myosin have not shown clear trends leading to hy
176 ably transfected with cardiac-specific alpha-cardiac myosin heavy chain (MHC) promoter-driven enhance
177 diac alpha actin, atrial natriuretic factor, cardiac myosin heavy chain alpha, cardiac myosin heavy c
178 MNCs expressed the cardiac-specific antigens cardiac myosin heavy chain and cardiac troponin T, respe
179 nse mutations (S532P and F764L) in the alpha-cardiac myosin heavy chain and compared them with WT mic
180 for other loci, two muscle genes (Human beta-cardiac myosin heavy chain and myogenin) became localize
181 ic factor, cardiac myosin heavy chain alpha, cardiac myosin heavy chain beta, myosin light chain 1A,
182 action is disrupted when modeling human beta-cardiac myosin heavy chain cardiomyopathy mutations E497
183 sin binding protein-C, troponin I, and alpha-cardiac myosin heavy chain caused elderly-onset hypertro
189 banding of mice with or without an Arg403Gln cardiac myosin heavy chain mutation (alphaMHC403/+) prod
190 D2, or D3 under the regulation of the alpha cardiac myosin heavy chain promoter exhibited high rates
191 eat systolic heart failure via targeting the cardiac myosin heavy chain to increase myocardial contra
192 from cardiac myofilaments were identified on cardiac myosin heavy chain, actin, myosin light chains,
193 tion, circulating IgG autoantibodies against cardiac myosin heavy chain, and premature death due to h
195 the nucleus, whereas alpha-sarcomeric actin, cardiac myosin heavy chain, troponin I, and alpha-actini
196 notion, intracellular cardiac antigens, like cardiac myosin heavy chain-alpha, cardiac troponin-I, an
199 chemical differences between the 2 mammalian cardiac myosin heavy chains (MHCs), alpha-MHC and beta-M
200 in, which shares sequence identity with beta-cardiac myosin-heavy chain, was used because of its stab
202 d by two bipolar arrays of the motor protein cardiac myosin II extending from the thick filament and
203 bstituted partially, and the CM-loop of beta-cardiac myosin II less well, for growth, capping of surf
204 ed Arg residue (whose mutation in human beta-cardiac myosin II results in familial hypertrophic cardi
205 This actin-binding loop is the site of a cardiac myosin-II mutation responsible for some forms of
208 Omecamtiv mecarbil (OM)-a novel activator of cardiac myosin-improves left ventricular systolic functi
211 dentified disease-specific epitopes of human cardiac myosin in the development of rheumatic carditis
212 ntracellular biomarkers of disease including cardiac myosin in the myocardium and tubulin, a protein
213 Here we determine the crystal structure of cardiac myosin in the pre-powerstroke state, the most re
214 primed position resulting in accumulation of cardiac myosin in the primed state prior to onset of car
220 y and safety of mavacamten, a first-in-class cardiac myosin inhibitor, in symptomatic obstructive hyp
221 dition of EMD 57033 to heat-inactivated beta-cardiac myosin is followed by refolding and reactivation
222 Mimicry between streptococcal M protein and cardiac myosin is important in the pathogenesis of rheum
223 ation of the regulatory light chain (RLC) of cardiac myosin is known to play a beneficial role in hea
226 chanism of mavacamten-mediated inhibition of cardiac myosin is the decrease of phosphate release from
227 heterozygous for this mutation in the alpha-cardiac myosin isoform display typical familial hypertro
228 Thus, nature has adapted the function of cardiac myosin isoforms to optimize power output for hea
231 irect evidence that immune responses against cardiac myosin lead to valvular heart disease and the in
232 autoimmune-susceptible SWXJ mice with whole cardiac myosin leads to T cell-mediated experimental aut
234 c hypertrophy and failure, and a decrease in cardiac myosin light chain 2, an essential protein for c
235 her than the heart, we tested the use of the cardiac myosin light chain 2v (MLC-2v) promoter and the
236 single site to 0.45 mol of phosphate/mol by cardiac myosin light chain kinase (cMLCK) increases Ca(2
237 ly in vitro and in vivo, the precise role of cardiac myosin light chain kinase (cMLCK), the primary k
238 hosphorylated these recombinant species with cardiac myosin light chain kinase and zipper-interacting
239 hat neural crest cells invade and contribute cardiac myosin light chain2 (cmlc2)-positive cardiomyocy
240 ntly phosphorylates MLC2v in cardiomyocytes, cardiac myosin light-chain kinase (cMLCK), yet the role(
241 est that the depressed molecular function in cardiac myosin may initiate the events that cause the he
242 -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,
250 itis (EAM), in which mice are immunized with cardiac myosin peptide, whereas IL-17A-deficient mice we
251 recruitment (100.9%, P<0.01), and increased cardiac myosin-positive area (39%, P<0.05) at 4, 7, and
252 vessels/mm2, P<0.01; SDF-1:MSC vs. MSC), and cardiac myosin-positive area (MSC: 49.5%; mSC:SDF-1: 162
254 osis factor-alpha (TNF-alpha) gene under the cardiac myosin promoter (TNF1.6 mice) develop dilated ca
255 loped computational models of the human beta-cardiac myosin protein before and after the myosin power
256 These transient kinetic studies on mouse cardiac myosins provide strong evidence that the functio
257 green fluorescent protein (GFP)-tagged human cardiac myosin regulatory light chain (HCRLC) was constr
258 22nd amino acid residue (E22K) in the human cardiac myosin regulatory light chain (RLC) gene causes
261 e in Lewis rats and have been linked to anti-cardiac myosin responses, we reacted myosin-sensitized l
262 We conclude that OM alters the energetics of cardiac myosin's mechanical cycle, causing the powerstro
263 e same exercise was repeated for human alpha-cardiac myosin S1 and rabbit fast skeletal muscle S1.
264 the decrease of phosphate release from beta-cardiac myosin-S1, a secondary mechanism decreases the n
265 biting the rate of phosphate release of beta-cardiac myosin-S1, but the molecular mechanism of action
267 urements using the expressed actins and beta-cardiac myosin showed that the mutation increased the K(
269 r immunity to T. cruzi antigens could induce cardiac myosin-specific autoimmunity in the absence of l
270 sitosis in the heart accompanied by vigorous cardiac myosin-specific delayed-type hypersensitivity (D
271 adjuvant and found that these mice developed cardiac myosin-specific delayed-type hypersensitivity (D
273 2, IL-4, and TNF-alpha production as well as cardiac myosin-specific IgG1 and IgG2b production, where
278 reports indicate that suspended skeletal and cardiac myosin, such as might be released during injury,
279 s indicate that purified skeletal muscle and cardiac myosins support the prothrombinase complex indir
280 ly administered, small-molecule modulator of cardiac myosin, targets underlying biomechanical abnorma
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
286 t is linked to host immune responses against cardiac myosin, the most abundant protein in the heart.
287 In addition, pathogenic epitopes of human cardiac myosin, the S2 fragment peptides S2-16 and S2-28
288 with antibodies and T cell responses against cardiac myosin, there is no unifying hypothesis about ca
289 c native thin filaments and the S2 domain of cardiac myosin to show that site-specific phosphorylatio
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
297 en is a first-in-class targeted inhibitor of cardiac myosin, which has been shown to reduce LV outflo
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