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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.
17                                              Cardiac myosin, a heart autoantigen, induced experimenta
18  structurally and immunologically similar to cardiac myosin, a well-known mediator of inflammatory he
19                                              Cardiac myosin activation may provide a new therapeutic
20       Omecamtiv mecarbil (OM) is a selective cardiac myosin activator that increases myocardial funct
21 olecular motors.Omecamtiv mecarbil (OM) is a cardiac myosin activator that is currently in clinical t
22             We report the first study of the cardiac myosin activator, omecamtiv mecarbil, in patient
23 cts on cardiac function and structure of the cardiac myosin activator, omecamtiv mecarbil.
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
27 ight be improved by a new therapeutic class, cardiac myosin activators.
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
30                     Immune responses against cardiac myosin and group A streptococcal M protein have
31                        Our data suggest that cardiac myosin and its pathogenic T cell epitopes may li
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
35 treated rats proliferated in the presence of cardiac myosin and rM6 protein.
36  weaker than originally described for bovine cardiac myosin and thus the thermodynamic coupling betwe
37 s were reacted with streptococcal M protein, cardiac myosin, and cardiac tropomyosin.
38 atic carditis were cross-reactive with human cardiac myosin, and laminin, a valve protein.
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
42              Infection with T. cruzi induces cardiac myosin autoimmunity in susceptible humans and mi
43              To address how T. cruzi induces cardiac myosin autoimmunity, we investigated whether imm
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
46 ntractility of the molecular motor, the beta-cardiac myosin (betaCM).
47 uced protein kinase (PK)A phosphorylation of cardiac myosin binding protein (cMyBP)-C may regulate cr
48 in essential and regulatory light chains and cardiac myosin binding protein (cMyBP)-C.
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             We investigated the influence of cardiac myosin binding protein-C (cMyBP-C) and its const
68                        Although mutations in cardiac myosin binding protein-C (cMyBP-C) cause heart d
69                                              Cardiac myosin binding protein-C (cMyBP-C) is a member o
70                                              Cardiac myosin binding protein-C (cMyBP-C) is a thick fi
71                                              Cardiac myosin binding protein-C (cMyBP-C) is a thick-fi
72                    We examined the effect of cardiac myosin binding protein-C (cMyBP-C) on contractil
73                                              Cardiac myosin binding protein-C (cMyBP-C) phosphorylati
74                                  The role of cardiac myosin binding protein-C (cMyBP-C) phosphorylati
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
77 c proteins, most often MYBPC3, which encodes cardiac myosin binding protein-C (cMyBP-C).
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
82                             Mutations in the cardiac myosin binding protein-C gene (cMyBP-C) are amon
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
85                                              Cardiac myosin binding protein-C phosphorylation plays a
86 ted a transgenic (TG) mouse model expressing cardiac myosin binding protein-C with a non-phosphorylat
87                         Rather, mutations in cardiac myosin binding protein-C, troponin I, and alpha-
88 ilament proteins cardiac troponin (cTn)I and cardiac myosin-binding protein (cMyBP)-C.
89 us (Ser-23/24) of cardiac troponin I (cTnI), cardiac myosin-binding protein C (cMyBP-C) and titin.
90                                              Cardiac myosin-binding protein C (cMyBP-C) is a componen
91                                              Cardiac myosin-binding protein C (cMyBP-C) is a regulato
92                                              Cardiac myosin-binding protein C (cMyBP-C) is a sarcomer
93                                              Cardiac myosin-binding protein C (cMyBP-C) is a thick-fi
94                    The N-terminal modules of cardiac myosin-binding protein C (cMyBP-C) play a regula
95                                              Cardiac myosin-binding protein C (cMyBP-C) regulates act
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
98                                              Cardiac myosin-binding protein C (cMyC) is a cardiac-res
99                                 Mutations in cardiac myosin-binding protein C (MyBPC) gene have been
100 olamban at Ser16, phospholemman at Ser68 and cardiac myosin-binding protein C at Ser282, was unaltere
101        These results suggest that the 40-kDa cardiac myosin-binding protein C fragment, which is prod
102 on impairs phosphoregulation and function of cardiac myosin-binding protein C in human heart failure.
103                   In this G+LVH- population, cardiac myosin-binding protein C mutation carriers had t
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.
106                    MYBPC3, encoding cMyBP-C (cardiac myosin-binding protein C), is the most frequentl
107                                              Cardiac myosin-binding protein C, a cardiac-specific myo
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
110                           Phosphorylation of cardiac myosin-binding protein-C (cMyBP-C) by protein ki
111                                              Cardiac myosin-binding protein-C (cMyBP-C) is a thick fi
112                                              Cardiac myosin-binding protein-C (cMyBP-C) is a thick fi
113                                              Cardiac myosin-binding protein-C (cMyBP-C) is a thick-fi
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
116                     To elucidate the role of cardiac myosin-binding protein-C (MyBP-C) in myocardial
117 he unique myosin-binding motif (m-domain) of cardiac myosin-binding protein-C remains unclear.
118 ears have suggested that the interactions of cardiac myosin-binding protein-C with its binding partne
119 ransient time-resolved FRET on a ventricular cardiac myosin biosensor.
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
123 ats proliferated in the presence of purified cardiac myosin, but not skeletal myosin.
124          Syngeneic splenocytes, coupled with cardiac myosin by use of ethylene carbodiimide, were adm
125              We previously demonstrated that cardiac myosin can use 2-deoxy-ATP (dATP) as an energy s
126 alysis of the motor domain of the human beta-cardiac myosin carrying the R453C mutation.
127                    ELISA levels of preformed cardiac myosin (CM) autoantibodies (Abs) in patients wit
128 al relevance of autoantibodies (Abs) against cardiac myosin (CM) in clinical idiopathic dilated cardi
129          Miniature swine were immunized with cardiac myosin (CM) in Freund's adjuvant and received he
130                                      Because cardiac myosin (CM) is a dominant autoantigen in autoimm
131 sociated with an autoimmune process in which cardiac myosin (CM) is a major autoantigen.
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
135 e to graft-expressed autoantigens, including cardiac myosin (CM), could participate.
136          We tested the impact of preexisting cardiac myosin (CM)-specific immunity on murine heart tr
137 response to a heart tissue-specific protein, cardiac myosin (CM).
138 tively suppressed by nasal administration of cardiac myosin (CM).
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
141               F-actin sliding on human fetal cardiac myosin-coated surfaces slowed significantly from
142                                              Cardiac myosin cycling kinetics, which directly control
143         B cell-deficient mice immunized with cardiac myosin develop myocarditis comparable in inciden
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
148 ac myocyte performance by acute titration of cardiac myosin-embedded miR-208a.
149                     Our report suggests that cardiac myosin epitopes in rheumatic carditis target the
150 ns, in which immunoglobulin G targeted human cardiac myosin epitopes in the S2 subfragment hinge regi
151                                     In human cardiac myosin, epitopes were demonstrated in the S2 and
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
155                             The structure of cardiac myosin filaments and the alterations caused by H
156                                              Cardiac myosin filaments consist of the molecular motor
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
159  mouse orthologs of two human enhancers near cardiac myosin genes.
160 b 3.B6 with the valve was inhibited by human cardiac myosin > laminin > GlcNAc.
161     It is well-established that rabbit alpha-cardiac myosin has a 2-fold greater unloaded shortening
162 ound in the regulatory light chains of human cardiac myosin has been investigated.
163               A detailed kinetic analysis of cardiac myosin has shown that the drug accelerates phosp
164 oimmunity to cardiac antigens, in particular cardiac myosin, has been observed in humans with myocard
165           In this study we report that human cardiac myosin (HCM) acted as an endogenous ligand to di
166 , cardiac troponin I (2 missense), and alpha-cardiac myosin heavy chain (1 missense).
167 d by heterozygous missense mutations in beta-cardiac myosin heavy chain (beta-MHC).
168 tter prognosis than individuals bearing beta-cardiac myosin heavy chain (MHC) gene mutations.
169                                              Cardiac myosin heavy chain (MHC) isoforms are known to p
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
178                  Variation in the human beta-cardiac myosin heavy chain gene (MYH7) can lead to hyper
179           Over 40 different mutations in the cardiac myosin heavy chain gene (MYH7) have been associa
180  are caused by a premature stop codon in the cardiac myosin heavy chain gene myh6.
181                   The murine alpha- and beta-cardiac myosin heavy chain gene promoters were used to e
182                                              Cardiac myosin heavy chain isoform gene expression also
183                                      The two cardiac myosin heavy chain isoforms, alpha and beta, exh
184 a mouse model of FHC with an Arg403Gln alpha-cardiac myosin heavy chain missense mutation, and used n
185                Comparison of alpha- and beta-cardiac myosin heavy chain mRNA and protein levels in NC
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
190                      Whereas defects in beta-cardiac myosin heavy chain, cardiac troponin T, and alph
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
194  an Arg403Gln missense mutation in the alpha cardiac myosin heavy chain.
195 the adenosine triphosphatase activity of the cardiac myosin heavy chain.
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
198                           Using a human beta-cardiac myosin IHM quasi-atomic model, we defined intera
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
203 ntal autoimmune myocarditis (EAM) induced by cardiac myosin immunization.
204  dominant epitope recognized by T cells from cardiac myosin immunized rats.
205 ults were compared for reactivity with human cardiac myosin in ELISAs and Western blot assays.
206 ditis that is accompanied by autoimmunity to cardiac myosin in susceptible strains of mice.
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
212                                In our study, cardiac myosin induced valvulitis in the Lewis rat, and
213                                Human and rat cardiac myosins induced severe myocarditis in the Lewis
214                                              Cardiac myosin-induced experimental autoimmune myocardit
215                                     Although cardiac myosin-induced myocarditis has been reported in
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
220                                     Although cardiac myosin is known to produce myocarditis in suscep
221                                              Cardiac myosin is more radially displaced from the fiber
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
225 ffected only minor switches in the mammalian cardiac myosin isoforms.
226             The mammalian heart contains two cardiac myosin isoforms: beta-myosin heavy chain (MHC) i
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
230  MEF2 (or element B) binding site within the cardiac myosin light chain 2 (MLC2) gene promoter.
231                   Because phosphorylation of cardiac myosin light chain 2 (MLC2v), bound to myosin at
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
242  muscle performance, yet its impact on human cardiac myosin motor function is unclear.
243                                In human beta-cardiac myosin, mutation of arginine-403 to a glutamine
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 om rat myelin basic protein (RTL-200), or to cardiac myosin peptide CM-2 (RTL-203).
250 ing rat MBP69-89 peptide (RTL200), or to the cardiac myosin peptide CM-2 (RTL203).
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
254                  Low-duty cycle skeletal and cardiac myosin present challenges for a single-molecule
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
258          Experiments were performed on whole cardiac myosin purified from a mouse model of FHC to eli
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
261                            Understanding how cardiac myosin regulatory light chain (RLC) phosphorylat
262             Here, we studied the role of the cardiac myosin regulatory light chains (RLCs) in the cap
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
268                       Here, using human beta-cardiac myosin-S1, we combine published data from transi
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(
271                       Expression of cWT beta-cardiac myosin significantly increased ttp and t0.5 and
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
275                       Treatment also reduced cardiac myosin-specific DTH and antibody production.
276 2, IL-4, and TNF-alpha production as well as cardiac myosin-specific IgG1 and IgG2b production, where
277                     It also led to increased cardiac myosin-specific IL-1 and TNF-alpha production.
278                                         beta-cardiac myosin subfragment 1 (betaS1) tertiary structure
279         We expressed and purified human beta-cardiac myosin subfragment 1 (M2beta-S1) containing a C-
280 ct and substituted it for the VELC of bovine cardiac myosin subfragment 1.
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
285            A structured surface loop on beta-cardiac myosin, the cardiac or C-loop, was recently demo
286  with some resulting from point mutations in cardiac myosin, the molecular motor of the heart.
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
295 , autoantibodies against the primary antigen cardiac myosin were induced to the same extent.
296            We found that immune responses to cardiac myosin were similar in rheumatic carditis among
297           A/J mice, immunized with syngeneic cardiac myosin, were given 75 mg/L of captopril in their
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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