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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.
19                                              Cardiac myosin, a heart autoantigen, induced experimenta
20  structurally and immunologically similar to cardiac myosin, a well-known mediator of inflammatory he
21                                              Cardiac myosin activation may provide a new therapeutic
22       Omecamtiv mecarbil (OM) is a selective cardiac myosin activator that increases myocardial funct
23 olecular motors.Omecamtiv mecarbil (OM) is a cardiac myosin activator that is currently in clinical t
24             We report the first study of the cardiac myosin activator, omecamtiv mecarbil, in patient
25 cts on cardiac function and structure of the cardiac myosin activator, omecamtiv mecarbil.
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
29 ight be improved by a new therapeutic class, cardiac myosin activators.
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
32                     Immune responses against cardiac myosin and group A streptococcal M protein have
33                        Our data suggest that cardiac myosin and its pathogenic T cell epitopes may li
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
38 atic carditis were cross-reactive with human cardiac myosin, and laminin, a valve protein.
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
41              Infection with T. cruzi induces cardiac myosin autoimmunity in susceptible humans and mi
42              To address how T. cruzi induces cardiac myosin autoimmunity, we investigated whether imm
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
45 ntractility of the molecular motor, the beta-cardiac myosin (betaCM).
46 uced protein kinase (PK)A phosphorylation of cardiac myosin binding protein (cMyBP)-C may regulate cr
47 in essential and regulatory light chains and cardiac myosin binding protein (cMyBP)-C.
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
50               In the cardiac sarcomere, both cardiac myosin binding protein C (cMyBP-C) and troponin-
51                                              Cardiac myosin binding protein C (cMyBP-C) appears to mo
52                                              Cardiac myosin binding protein C (cMyBP-C) has a key reg
53                                              Cardiac myosin binding protein C (cMyBP-C) has three pho
54 scle contraction, and its accessory protein, cardiac myosin binding protein C (cMyBP-C), are the two
55                                              Cardiac myosin binding protein C (cMyBP-C), bound to the
56                         The cardiac isoform [cardiac myosin binding protein C (cMyBP-C)] is essential
57                      Decreased expression of cardiac myosin binding protein C (cMyBPC) as a result of
58                      Decreased expression of cardiac myosin binding protein C (cMyBPC) in the heart h
59                                              Cardiac myosin binding protein C (cMyBPC) phosphorylatio
60        beta-adrenergic stimulation increases cardiac myosin binding protein C (MyBP-C) and troponin I
61 myopathy (FHC), individuals bearing a mutant cardiac myosin binding protein C (MyBP-C) gene usually h
62 ylated protein was identified as the 140-kDa cardiac myosin binding protein C (MyBPC).
63 d in several sarcomeric genes, including the cardiac myosin binding protein C (MYBPC3) gene.
64 ediated degradation of myosin heavy chain 6, cardiac myosin binding protein C, calcineurin (PPP3CB),
65                                   Homozygous cardiac myosin binding protein C-deficient (Mybpc(t/t))
66 ene analyses revealed 8 sequence variants in cardiac myosin binding protein-C (1 nonsense, 1 splice a
67                           Phosphorylation of cardiac myosin binding protein-C (cMyBP-C) accelerates c
68             We investigated the influence of cardiac myosin binding protein-C (cMyBP-C) and its const
69                        Although mutations in cardiac myosin binding protein-C (cMyBP-C) cause heart d
70                  Although phosphorylation of cardiac myosin binding protein-C (cMyBP-C) has been reco
71                                              Cardiac myosin binding protein-C (cMyBP-C) is a member o
72                                              Cardiac myosin binding protein-C (cMyBP-C) is a thick fi
73                                              Cardiac myosin binding protein-C (cMyBP-C) is a thick-fi
74                    We examined the effect of cardiac myosin binding protein-C (cMyBP-C) on contractil
75                                              Cardiac myosin binding protein-C (cMyBP-C) phosphorylati
76                                  The role of cardiac myosin binding protein-C (cMyBP-C) phosphorylati
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
79 c proteins, most often MYBPC3, which encodes cardiac myosin binding protein-C (cMyBP-C).
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
84                             Mutations in the cardiac myosin binding protein-C gene (cMyBP-C) are amon
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
88                                              Cardiac myosin binding protein-C phosphorylation plays a
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
92                         Rather, mutations in cardiac myosin binding protein-C, troponin I, and alpha-
93 ilament proteins cardiac troponin (cTn)I and cardiac myosin-binding protein (cMyBP)-C.
94 us (Ser-23/24) of cardiac troponin I (cTnI), cardiac myosin-binding protein C (cMyBP-C) and titin.
95                                              Cardiac myosin-binding protein C (cMyBP-C) is a componen
96                                              Cardiac myosin-binding protein C (cMyBP-C) is a regulato
97                                              Cardiac myosin-binding protein C (cMyBP-C) is a sarcomer
98                                              Cardiac myosin-binding protein C (cMyBP-C) is a thick fi
99                                              Cardiac myosin-binding protein C (cMyBP-C) is a thick-fi
100                    The N-terminal modules of cardiac myosin-binding protein C (cMyBP-C) play a regula
101                                              Cardiac myosin-binding protein C (cMyBP-C) plays a modul
102                                              Cardiac myosin-binding protein C (cMyBP-C) regulates act
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
105                                              Cardiac myosin-binding protein C (cMyC) is a cardiac-res
106                                 Mutations in cardiac myosin-binding protein C (MyBPC) gene have been
107 olamban at Ser16, phospholemman at Ser68 and cardiac myosin-binding protein C at Ser282, was unaltere
108        These results suggest that the 40-kDa cardiac myosin-binding protein C fragment, which is prod
109 on impairs phosphoregulation and function of cardiac myosin-binding protein C in human heart failure.
110                   In this G+LVH- population, cardiac myosin-binding protein C mutation carriers had t
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.
113                    MYBPC3, encoding cMyBP-C (cardiac myosin-binding protein C), is the most frequentl
114 compared with cardiac troponins and cMyBP-C (cardiac myosin-binding protein C).
115                                              Cardiac myosin-binding protein C, a cardiac-specific myo
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
118                           Phosphorylation of cardiac myosin-binding protein-C (cMyBP-C) by protein ki
119                                              Cardiac myosin-binding protein-C (cMyBP-C) is a thick fi
120                                              Cardiac myosin-binding protein-C (cMyBP-C) is a thick fi
121                                              Cardiac myosin-binding protein-C (cMyBP-C) is a thick-fi
122                                              Cardiac myosin-binding protein-C (cMyBP-C) is highly pho
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
125 he unique myosin-binding motif (m-domain) of cardiac myosin-binding protein-C remains unclear.
126 ears have suggested that the interactions of cardiac myosin-binding protein-C with its binding partne
127                                     cMyBP-C (cardiac myosin-binding protein-C) is a critical regulato
128 ransient time-resolved FRET on a ventricular cardiac myosin biosensor.
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
133              We previously demonstrated that cardiac myosin can use 2-deoxy-ATP (dATP) as an energy s
134 alysis of the motor domain of the human beta-cardiac myosin carrying the R453C mutation.
135 al relevance of autoantibodies (Abs) against cardiac myosin (CM) in clinical idiopathic dilated cardi
136          Miniature swine were immunized with cardiac myosin (CM) in Freund's adjuvant and received he
137                                      Because cardiac myosin (CM) is a dominant autoantigen in autoimm
138 sociated with an autoimmune process in which cardiac myosin (CM) is a major autoantigen.
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
142 e to graft-expressed autoantigens, including cardiac myosin (CM), could participate.
143          We tested the impact of preexisting cardiac myosin (CM)-specific immunity on murine heart tr
144 response to a heart tissue-specific protein, cardiac myosin (CM).
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
147               F-actin sliding on human fetal cardiac myosin-coated surfaces slowed significantly from
148 ivity (>=12-fold) for skeletal myosin versus cardiac myosin compared to BHC.
149                                              Cardiac myosin cycling kinetics, which directly control
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
154 ac myocyte performance by acute titration of cardiac myosin-embedded miR-208a.
155                     Our report suggests that cardiac myosin epitopes in rheumatic carditis target the
156 ns, in which immunoglobulin G targeted human cardiac myosin epitopes in the S2 subfragment hinge regi
157                                     In human cardiac myosin, epitopes were demonstrated in the S2 and
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
161                             The structure of cardiac myosin filaments and the alterations caused by H
162                                              Cardiac myosin filaments consist of the molecular motor
163 reviously unstudied affinity of skeletal and cardiac myosin for phospholipid membranes.
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.
166  mouse orthologs of two human enhancers near cardiac myosin genes.
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
169                                   Human beta-cardiac myosin has proved to be an excellent target for
170               A detailed kinetic analysis of cardiac myosin has shown that the drug accelerates phosp
171 tivity of the catalytic domain of human beta-cardiac myosin have not shown clear trends leading to hy
172           In this study we report that human cardiac myosin (HCM) acted as an endogenous ligand to di
173 , cardiac troponin I (2 missense), and alpha-cardiac myosin heavy chain (1 missense).
174 d by heterozygous missense mutations in beta-cardiac myosin heavy chain (beta-MHC).
175 tter prognosis than individuals bearing beta-cardiac myosin heavy chain (MHC) gene mutations.
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
184                        Mutations in the beta-cardiac myosin heavy chain gene (beta-MyHC) are a major
185                  Variation in the human beta-cardiac myosin heavy chain gene (MYH7) can lead to hyper
186  are caused by a premature stop codon in the cardiac myosin heavy chain gene myh6.
187                                              Cardiac myosin heavy chain isoform gene expression also
188                                      The two cardiac myosin heavy chain isoforms, alpha and beta, exh
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
194                      Whereas defects in beta-cardiac myosin heavy chain, cardiac troponin T, and alph
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
197  an Arg403Gln missense mutation in the alpha cardiac myosin heavy chain.
198 the adenosine triphosphatase activity of the cardiac myosin heavy chain.
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
201                           Using a human beta-cardiac myosin IHM quasi-atomic model, we defined intera
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
206 ntal autoimmune myocarditis (EAM) induced by cardiac myosin immunization.
207  dominant epitope recognized by T cells from cardiac myosin immunized rats.
208 Omecamtiv mecarbil (OM)-a novel activator of cardiac myosin-improves left ventricular systolic functi
209 ced by immunizing rats (n = 18) with porcine cardiac myosin in complete Freund adjuvant.
210 ditis that is accompanied by autoimmunity to cardiac myosin in susceptible strains of mice.
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
215 electrostatic interactions between actin and cardiac myosin in vitro.
216                                In our study, cardiac myosin induced valvulitis in the Lewis rat, and
217                                Human and rat cardiac myosins induced severe myocarditis in the Lewis
218                                              Cardiac myosin-induced experimental autoimmune myocardit
219                                     Although cardiac myosin-induced myocarditis has been reported in
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
224                                     Although cardiac myosin is known to produce myocarditis in suscep
225                                              Cardiac myosin is more radially displaced from the fiber
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
229 ffected only minor switches in the mammalian cardiac myosin isoforms.
230             The mammalian heart contains two cardiac myosin isoforms: beta-myosin heavy chain (MHC) i
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
233                   Because phosphorylation of cardiac myosin light chain 2 (MLC2v), bound to myosin at
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
243  muscle performance, yet its impact on human cardiac myosin motor function is unclear.
244  heavy meromyosin (sHMM) or full-length beta-cardiac myosin (MYH7).
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,
248 skeletal heavy meromyosin (rsHMM) or porcine cardiac myosin (pcMyosin).
249 ing rat MBP69-89 peptide (RTL200), or to the cardiac myosin peptide CM-2 (RTL203).
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
253                  Low-duty cycle skeletal and cardiac myosin present challenges for a single-molecule
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
259                            Understanding how cardiac myosin regulatory light chain (RLC) phosphorylat
260             Here, we studied the role of the cardiac myosin regulatory light chains (RLCs) in the cap
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
266                       Here, using human beta-cardiac myosin-S1, we combine published data from transi
267 urements using the expressed actins and beta-cardiac myosin showed that the mutation increased the K(
268                       Expression of cWT beta-cardiac myosin significantly increased ttp and t0.5 and
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
272                       Treatment also reduced cardiac myosin-specific DTH and antibody production.
273 2, IL-4, and TNF-alpha production as well as cardiac myosin-specific IgG1 and IgG2b production, where
274                     It also led to increased cardiac myosin-specific IL-1 and TNF-alpha production.
275         We expressed and purified human beta-cardiac myosin subfragment 1 (M2beta-S1) containing a C-
276         We expressed and purified human beta-cardiac myosin subfragment 1 (M2beta-S1) containing the
277 ct and substituted it for the VELC of bovine cardiac myosin subfragment 1.
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
284            A structured surface loop on beta-cardiac myosin, the cardiac or C-loop, was recently demo
285  with some resulting from point mutations in cardiac myosin, the molecular motor of the heart.
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
295            We found that immune responses to cardiac myosin were similar in rheumatic carditis among
296           A/J mice, immunized with syngeneic cardiac myosin, were given 75 mg/L of captopril in their
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

 
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