ライフサイエンスコーパス: myofilament

1 actile function directly at the level of the myofilament.

2 BP-HL protein failed to incorporate into the myofilament.

3 elaxation has been proposed to reside in the myofilament.

4 ensitizing effect of HCM-cTnC mutants on the myofilament.

5 sly increasing the Ca(2+) sensitivity of the myofilament.

6 mately 21%) into the KI-TnC-A8V(+/-) cardiac myofilament.

7 rdiomyocytes, allowing an in vivo imaging of myofilaments.

8 resembled that found previously in mammalian myofilaments.

9 omyosin ATPase activity and contractility of myofilaments.

10 ns, indicating cross-bridge association with myofilaments.

11 mic inclusions, and focal disorganization of myofilaments.

12 y allowing for local Ca(2+) release near the myofilaments.

13 attributable to changes at the level of the myofilaments.

14 onal "cracking" of the crystal-like array of myofilaments.

15 hostatin A, enhances contractile activity of myofilaments.

16 functions to modulate activation of cardiac myofilaments.

17 -dependent increased contractile activity of myofilaments.

18 ltered by the OM-mediated effects on cardiac myofilaments.

19 talytic subunit content in the cytoplasm and myofilaments.

20 hostatin A, enhances contractile activity of myofilaments.

21 ants increased the Ca(2+) sensitivity of the myofilament; 2) the effects of the mutations on the Ca(2

22 BSO-induced mitochondrial loss and myofilament aberration.

23 n the length-dependent Ca(2+) sensitivity of myofilament activation and consequently the mechanism un

24 lude that this occurs primarily via enhanced myofilament activation and contraction, with similar or

25 es in our understanding of the biophysics of myofilament activation, coupled to the emerging evidence

26 Moreover, modulation of myofilament activation-relaxation and force redevelopmen

27 contributes to several properties of cardiac myofilament activation.

28 on and negative lusitropy via persistence of myofilament active state.

29 se in calcium-independent persistence of the myofilament active state.

30 he regulation of myocyte calcium cycling and myofilament activity.

31 Myofilament ADP sensitivity was higher in IDCM and HCM c

32 ls of cMyBPC in the intact heart can improve myofilament and in vivo contractile function and attenua

33 the cMyBPC-deficient myocardium can improve myofilament and in vivo contractile function, suggesting

34 roperties and, in vivo, can drive asymmetric myofilament and sarcomere formation.

35 Glc-6-PD decreased Ca(2+) sensitivity to the myofilaments and diminished Ca(2+)-independent and -depe

36 own about the interaction between individual myofilaments and membrane-bound actin filaments.

37 to define the mechanical characteristics of myofilaments and myosin heads that underpin refined mode

38 The link between myofilaments and SCD has been known for over 25 years, b

39 ignal by preventing PKA signal access to the myofilaments and to restore contractile response to adre

40 first evidence for localization of HDAC3 at myofilaments and uncover a novel mechanism modulating th

41 first evidence for localization of HDAC3 at myofilaments and uncover a novel mechanism modulating th

42 argeted proteomic analysis of mitochondrial, myofilament, and extracellular subproteomes in pathologi

43 rporated 24.9% of the mutant cTnI within the myofilament; and 2) the R21C mutation abolished the in v

44 Electron microscopy (EM) showed that the myofilament architecture was disrupted in skeletal muscl

45 Although extensible myofilaments are implicated as sites of energy storage,

46 We determined that MyBP-HL protein was myofilament associated in the atria, and truncated MyBP-

47 pendent of any beta-adrenergic compensation, myofilament-based molecular manipulation of inotropy by

48 e ionization states in vitro by studying the myofilament biophysics of amino acid substitutions that

49 moval of thin filament proteins also reduced myofilament-bound PKA-type II.

50 Troponin mutations that increase myofilament Ca sensitivity are associated with familial

51 -F110I, TnT-R278C), we found that increasing myofilament Ca sensitivity produced a proportional incre

52 Myofilament Ca sensitization increases cytosolic Ca bind

53 Myofilament Ca(2+) desensitization with blebbistatin pre

54 sensitizing agent EMD 57033 and prevented by myofilament Ca(2+) desensitization with blebbistatin.

55 ressed cardiomyocyte contractility caused by myofilament Ca(2+) desensitization.

56 ase force development by directly depressing myofilament Ca(2+) responsiveness and have binding sites

57 uncation of the N-terminal tail, "resetting" myofilament Ca(2+) responsiveness back to control levels

58 t on cardiac myofilament proteins increasing myofilament Ca(2+) responsiveness by promoting disulfide

59 this study, we determined whether decreasing myofilament Ca(2+) responsiveness underlies anesthesia-i

60 iously documented ssTnI-mediated increase in myofilament Ca(2+) sensitivity (pCa(50)) was blunted whe

61 TnT(45-74Delta) attenuated tension (19%) and myofilament Ca(2+) sensitivity (pCa50=5.93 vs. 6.00 in t

62 thalene-6-sulfonic acid showed a decrease in myofilament Ca(2+) sensitivity and Ca(2+) binding affini

63 lic and diastolic dysfunction with decreased myofilament Ca(2+) sensitivity and cardiomyocyte contrac

64 This may result in higher myofilament Ca(2+) sensitivity and increased basal contr

65 To test the hypothesis that aberrant myofilament Ca(2+) sensitivity and its related function

66 conformational change induces an increase in myofilament Ca(2+) sensitivity and, moreover, uncoupling

67 ink cellular stretch to the length-dependent myofilament Ca(2+) sensitivity are poorly understood.

68 versatile target to reset disease-associated myofilament Ca(2+) sensitivity back to normal.

69 the heart is due, in part, to modulation of myofilament Ca(2+) sensitivity by sarcomere length (SL)

70 sion of cTnC at lower temperatures increases myofilament Ca(2+) sensitivity by this mechanism, despit

71 TnI-PP mice demonstrated a reduced myofilament Ca(2+) sensitivity compared with wild-type m

72 taN100/DeltaE101:cTnT3-WT also increased the myofilament Ca(2+) sensitivity compared with WT.

73 However, myofilament Ca(2+) sensitivity depends on protein phosph

74 Given that interventions that increase myofilament Ca(2+) sensitivity have the potential to alt

75 rdiomyocyte force measurements showed higher myofilament Ca(2+) sensitivity in all HCM samples and lo

76 we found markedly impaired length-dependent myofilament Ca(2+) sensitivity in beta-arrestin 1, beta-

77 a suggested the presence of abnormalities in myofilament Ca(2+) sensitivity in SOCS3 cKO mice.

78 ablated the H276N-induced desensitization of myofilament Ca(2+) sensitivity in Tm(DM)+TnT(1-44Delta)

79 To test our hypothesis, we reduced myofilament Ca(2+) sensitivity in Tm180 mice by generati

80 High-myofilament Ca(2+) sensitivity is a common characteristi

81 Aberrant myofilament Ca(2+) sensitivity is commonly observed with

82 reduced maximal tension and abnormally high myofilament Ca(2+) sensitivity observed in D166V-mutated

83 roteins, but can be explained by the reduced myofilament Ca(2+) sensitivity of force generation that

84 Myofilament Ca(2+) sensitivity of force, tension cost, L

85 ing protein-C from skinned muscle normalized myofilament Ca(2+) sensitivity of the KO extensor digito

86 he range of pacing frequencies and increased myofilament Ca(2+) sensitivity thereby enhancing contrac

87 After exogenous PKA treatment, myofilament Ca(2+) sensitivity was similar (MYBPC3mut, T

88 sion led to a marked decrease in contractile myofilament Ca(2+) sensitivity with an unexpected electr

89 eart:body weight ratios, fibrosis, increased myofilament Ca(2+) sensitivity, and contractile defects.

90 ertrophy, diastolic heart failure, increased myofilament Ca(2+) sensitivity, and high susceptibility

91 Myofilament Ca(2+) sensitivity, as measured by pCa50 (-l

92 Myofilament Ca(2+) sensitivity, as measured by pCa50 (-l

93 pomyosin (Tm180) that demonstrates increased myofilament Ca(2+) sensitivity, severe hypertrophy, and

94 cular mechanism responsible for the enhanced myofilament Ca(2+) sensitivity, we measured Ca(2+) bindi

95 t not long, SL, decreasing maximal force and myofilament Ca(2+) sensitivity.

96 of the cTnC molecule are key in determining myofilament Ca(2+) sensitivity.

97 den cardiac death in diseases with increased myofilament Ca(2+) sensitivity.

98 ts cardiac contractile function by enhancing myofilament Ca(2+) sensitivity.

99 action and prolongs relaxation by increasing myofilament Ca(2+) sensitivity.

100 olve length-dependent enhancement of cardiac myofilament Ca(2+) sensitivity.

101 , DCM, and ISHD samples all showed increased myofilament Ca(2+) sensitivity.

102 Myofilament Ca(2+) sensitization rapidly leads to focal

103 nergy deprivation as a direct consequence of myofilament Ca(2+) sensitization.

104 7.2+/-2.3 kN/m(2), respectively), and higher myofilament Ca(2+)-sensitivity (EC(50)=2.5+/-0.2, 2.4+/-

105 Protein kinase A treatment restored myofilament Ca(2+)-sensitivity and length-dependent acti

106 ated with cap myopathy characterized by high myofilament Ca(2+)-sensitivity and muscle weakness.

107 cardiac function using echocardiography, the myofilament-Ca(2)(+) response of detergent-extracted fib

108 o improving cardiac function by altering the myofilament-Ca(2)(+) response via beta-arrestin signalin

109 dilated cardiomyopathy is a reduction in the myofilament-Ca(2)(+) response, we hypothesized that beta

110 that beta-arrestin signaling would increase myofilament-Ca(2)(+) responsiveness in a model of famili

111 ated Tm-E54K mice had significantly improved myofilament-Ca(2)(+) responsiveness, which was depressed

112 sensitizing agent EMD 57033 and prevented by myofilament Ca2+ desensitization with blebbistatin.

113 Here we have shown that increased myofilament Ca2+ sensitivity, also a common feature in b

114 cient of steady-state force while increasing myofilament Ca2+ sensitivity.

115 here are no alterations in cardiac function, myofilament calcium (Ca(2+)) sensitivity, cooperativity,

116 transients, suggesting that CRT may enhance myofilament calcium responsiveness.

117 nd in vitro studies suggest that it enhances myofilament calcium sensitivity and alters calpain-media

118 ed similar cellular contractile function and myofilament calcium sensitivity between myocytes express

119 We hypothesized that titrating myofilament calcium sensitivity by a single histidine su

120 , a class I and II HDAC inhibitor, increases myofilament calcium sensitivity of wild-type, but not of

121 ting systems were functionally examined, and myofilament calcium sensitivity was studied.

122 lic and diastolic dysfunction, and decreased myofilament calcium sensitivity with no change in maximu

123 , whereas the A164R variant showed increased myofilament calcium sensitivity.

124 ibitors or anti-HDAC4 antibody) enhanced the myofilament calcium sensitivity.

125 technique and observed reduced function and myofilament calcium sensitivity.

126 ractility in the face of impaired postarrest myofilament calcium sensitivity.

127 ponses to positive inotropic agents, such as myofilament calcium sensitizers.

128 force of the myocardium, whereas the lack of myofilament changes from L29Q-CTnC may preserve diastoli

129 The Ca(2+) sensitivity of the myofilaments containing the K206I variant was significan

130 Consistent with the changes toward more fast myofilament contents, ssTnT-KD diaphragm muscle required

131 r273 and Ser302 residues, and thereby govern myofilament contractile acceleration in response to prot

132 he regulation of cardiac metabolic demand to myofilament contractile energetics.

133 nase (cMLCK) increases Ca(2+) sensitivity of myofilament contraction necessary for normal cardiac per

134 f Ca(2+) from internal stores and subsequent myofilament contraction, although these structures becom

135 It is not known whether the myofilament contributes to diastolic dysfunction in pati

136 ta2 adrenergic receptor signaling toward the myofilaments contributes to elevated PKA activity and PK

137 e improvements are achieved by correction of myofilament deficits is not known.

138 mutation in eight genes commonly mutated in myofilament disease.

139 modeling during cell division is a result of myofilament-driven contractility of the cortical membran

140 incorporates a biophysical representation of myofilament dynamics.

141 ely matured over 30 days in culture based on myofilament expression pattern and mitotic activity.

142 that CRT improves calcium responsiveness of myofilaments following HF(dys) through GSK-3beta reactiv

143 In the presence of Ca(2+), ADP increased myofilament force development and sarcomere stiffness.

144 been shown to alter both calcium binding and myofilament force generation.

145 orted effects of nonfunctional troponin C on myofilament force generation.

146 Myofilament force-calcium relationships were measured in

147 iomyocyte proliferation, differentiation and myofilament formation from the repopulated human multipo

148 at was localized mainly in the cytoplasm and myofilament fraction.

149 luble fraction, with reduced presence in the myofilament fraction.

150 We show that synthetic myofilaments fragment and compact membrane-bound actin w

151 nd current paradigms, the desensitization of myofilaments from G159D-CTnC is expected to weaken the c

152 sarcomere is sufficient to induce depressed myofilament function and Ca(2+) sensitivity in otherwise

153 ysiological hypertrophy, but not to enhanced myofilament function as determined by simultaneous measu

154 y, our results indicate that improvements in myofilament function in sedentary elderly with and witho

155 the LKB1 complex desensitizes and suppresses myofilament function independently of AMPK.

156 dyssynchrony displays decreased myocyte and myofilament function, calcium handling, beta-adrenergic

157 le the impact of S23D/S24D phosphomimetic on myofilament function, including LDA.

158 ansients, suggesting targeted improvement of myofilament function.

159 s multiple sarcomeric substrates to regulate myofilament function.

160 clude that cTnI truncation induces depressed myofilament function.

161 ivator complex to AMPK would uniquely impact myofilament function.

162 tivity is shifted from the sarcolemma to the myofilaments in hypertrophic failing rabbit myocytes.

163 e and blunted length-dependent activation of myofilaments in PPCM samples.

164 n kinase A (PKA) biosensor anchored onto the myofilaments in rabbit cardiac myocytes to examine PKA a

165 diac myocytes to examine PKA activity at the myofilaments in responses to adrenergic stimulation.

166 f and altered contractility in human cardiac myofilaments in vitro.

167 comparison between the two proposed rates of myofilament inactivation.

168 C (TnC) have been hypothesized to rate-limit myofilament inactivation.

169 ot be a simple, single rate-limiting step of myofilament inactivation.

170 , probably resulting from a direct effect on myofilaments, indicating that cardiac oxidative stress m

171 ence that reduction of Ca(2+) sensitivity in myofilaments is antiarrhythmic and might be beneficial t

172 nistically, the enhanced PKA activity on the myofilaments is associated with downregulation of caveol

173 articular, the increased PKA activity on the myofilaments is because of an enhanced beta2 adrenergic

174 The Ca(2+) sensitivity of the myofilaments is increased in hypertrophic cardiomyopathy

175 dysregulation of protein phosphorylation on myofilaments is not clear.

176 and phosphorylation on Ca(2+) dependence of myofilament isometric force production, isometric ATPase

177 t results in a progressive disruption of the myofilament lattice and flight ability.

178 egulation, causing abnormal hydration of the myofilament lattice and its proteins.

179 result is consistent with the idea that the myofilament lattice expands after PKA phosphorylation of

180 lopment and detachment are modulated more by myofilament lattice geometry than protein hydration.

181 diffusion of adenine nucleotides through the myofilament lattice has been shown to be anisotropic, wi

182 ncludes terms representing protein crowding, myofilament lattice hindrance, and binding to the cytoma

183 e radial and longitudinal stiffnesses of the myofilament lattice in chemically skinned myocardial str

184 llP-(t/t) resulted in a compressible cardiac myofilament lattice induced by rigor not observed in the

185 ctural and functional consequences of varied myofilament lattice spacing and protein hydration on cro

186 Myofilament lattice spacing from TEM was significantly g

187 These data emphasize that SL and/or myofilament lattice spacing modulation of the cross-brid

188 The myofilament lattice spacing was measured in the A-band (

189 muscle at near-physiological temperature and myofilament lattice spacing, the majority of the myosin

190 [Ca(2+)] relations to changes in both SL and myofilament lattice spacing.

191 that cMyBP-C provides radial rigidity to the myofilament lattice through the N-terminus, and that dis

192 embryogenesis and display disruption of the myofilament lattice.

193 tructural support and radial rigidity to the myofilament lattice.

194 rayed myofibrils with some disruption of the myofilament lattice.

195 ow that PKA-type II is troponin-bound in the myofilament lattice.

196 yed reduced passive force, twitch force, and myofilament LDA.

197 laments that correlate with titin strain and myofilament LDA.

198 of increased levels of TPM1kappa protein in myofilaments leads to dilated cardiomyopathy.

199 uggests that this mutation induces perturbed myofilament length-dependent activation (LDA) under cond

200 bilized myocardium with PKA induces enhanced myofilament length-dependent activation (LDA), the cellu

201 Myofilament length-dependent activation is a universal p

202 TnI each independently contribute to enhance myofilament length-dependent activation properties of th

203 meabilized cells/myofibrils, we found robust myofilament length-dependent activation.

204 s for this relationship is in large part the myofilament length-tension relationship.

205 Myofilament length-tension relationships were considerab

206 ions to improve cardiac contractility at the myofilament level and improve overall cardiac function.

207 lead to abnormal contractile function at the myofilament level, thereby contributing to the developme

208 Examination of myofilament longitudinal stiffness under rigor condition

209 We develop a point model of the cardiac myofilament (MF) to simulate a wide variety of experimen

210 Briefly, hearts were fractionated into myofilament-, mitochondrial- and cytosol-enriched fracti

211 esentation of this phenomenon to an existing myofilament model, which allowed predictions of CIA-depe

212 omyopathy, but many patients lack sarcomeric/myofilament mutations.

213 Myofilaments of TRV120067-treated Tm-E54K mice had signi

214 directly visualize the action of individual myofilaments on membrane-bound actin filaments using TIR

215 The alteration in myofilament organization was associated with decreased e

216 rements and dependent on lattice spacing and myofilament overlap.

217 ationships by protein kinase A (PKA)-induced myofilament phosphorylation.

218 were unaffected, implying that CRT enhances myofilament phosphorylation.

219 ation cross-talk can uncouple the effects of myofilament PKA-dependent phosphorylation from beta-adre

220 In myofilaments PKA targets troponin I (cTnI), myosin bindi

221 lls is driven by the sliding displacement of myofilaments powered by the cycling myosin crossbridges.

222 These perturbed biophysical and biochemical myofilament properties are likely to significantly contr

223 Changes in myofilament properties, when considered in isolation, we

224 emonstrated that PKCdelta phosphorylates the myofilament protein cardiac troponin I (cTnI) at Ser(23)

225 tion by ROS-activated signaling enzymes, and myofilament protein cleavage by ROS-activated proteases)

226 tients may be partially explained by altered myofilament protein content and function.

227 th a reduced cross-bridge detachment rate as myofilament protein hydration decreased.

228 Expression of a single fetal myofilament protein into adulthood in the ssTnI-transgen

229 th the slow fibre atrophy and the changes in myofilament protein isoform contents, ssTnT deficiency s

230 the contributions of variable expression of myofilament protein isoforms in mediating the timing of

231 ing open questions about how a mutation in a myofilament protein leads to an increased risk for sudde

232 ative modifications of myofilament proteins, myofilament protein phosphorylation by ROS-activated sig

233 Enhanced myofilament protein phosphorylation detected after hRFRP

234 heart during identical infusions to measure myofilament protein phosphorylation.

235 This minireview focuses on myofilament protein post-translational modifications ind

236 myosin-binding protein C, a cardiac-specific myofilament protein, is proteolyzed post-MI in humans, w

237 S-induced posttranslational modifications of myofilament proteins (including direct oxidative modific

238 ned with low PKA-mediated phosphorylation of myofilament proteins and increased compliant titin isofo

239 ated whether atomistic-resolution details of myofilament proteins can refine coarse-grain estimates o

240 Mass spectrometry of myofilament proteins from HF(dys) animals incubated with

241 anisms underlying altered phosphorylation of myofilament proteins in heart failure.

242 HNO exerts a direct effect on cardiac myofilament proteins increasing myofilament Ca(2+) respo

243 A phospho-proteomic analysis of myofilament proteins revealed site-specific changes in c

244 abundance or phosphorylation status of other myofilament proteins were detected.

245 ilament proteins whereas fast fibre-specific myofilament proteins were increased correspondingly.

246 ecreased levels of other slow fibre-specific myofilament proteins whereas fast fibre-specific myofila

247 nt mouse hearts expressed normal isoforms of myofilament proteins whereas the phosphorylation of vent

248 Photoaffinity labeling of myofilament proteins with meta-Azi-propofol (AziPm) and

249 specific sites of O-GlcNAcylation in cardiac myofilament proteins, a recently developed methodology b

250 MYH7mut was caused by low phosphorylation of myofilament proteins, as it was normalized to donors by

251 yl acetate, was found to act directly on the myofilament proteins, increasing maximum force (F(max))

252 (including direct oxidative modifications of myofilament proteins, myofilament protein phosphorylatio

253 -handling proteins, RyR2 and SERCA2, and the myofilament proteins, myosin heavy chain, myosin light c

254 or post-translational modifications of major myofilament proteins.

255 ression of cardiac transcription factors and myofilament proteins.

256 ated PKA activity and PKA phosphorylation of myofilament proteins.

257 the mechanism of dysfunction at the level of myofilament proteins.

258 Two key myofilaments proteins, troponin I (TnI) and myosin bindi

259 fic N-terminal modulatory extension to alter myofilament regulation.

260 each amino acid in the inhibitory region to myofilament regulation.

261 nhibitory subunit of cardiac troponin, a key myofilament regulatory protein complex located on the th

262 sphorylation of cardiac troponin I (cTnI), a myofilament regulatory protein.

263 filament activation and result in increased myofilament relaxation kinetics, the latter of which cou

264 irectly affects thin filament activation and myofilament relaxation kinetics.

265 sults indicate that the inability to enhance myofilament relaxation through cTnI phosphorylation pred

266 restricted Ca(2+) microdomains that regulate myofilament remodeling and activate spatially segregated

267 An altered cardiac myofilament response to activating Ca(2+) is a hallmark

268 specific removal of O-GlcNAcylation restores myofilament response to Ca(2+) in diabetic hearts and th

269 from DOCA-salt hearts demonstrated increased myofilament response to Ca(2+) with glutathionylation of

270 e cTnT variant results in a temporally split myofilament response to calcium, which causes decreased

271 erminal amino acids 1-91 (cTnT-del) enhances myofilament responsiveness to nonsaturating Ca(2+) level

272 , removes site-specific O-GlcNAcylation from myofilaments, restoring Ca(2+) sensitivity in streptozot

273 which tension builds up between the ends of myofilaments, resulting in compressive stress exerted to

274 wing hypothesis: correction of the increased myofilament sensitivity can delay or prevent the develop

275 Our data strongly indicate that reduction of myofilament sensitivity to Ca(2+) and associated correct

276 underway to treat heart failure by enhancing myofilament sensitivity to Ca(2+); transfer of the gene

277 Biochemical studies with myofilaments showed that RLC phosphorylation up to 90% w

278 ete plasmalemmal, sarcoplasmic reticular and myofilament sites, reveals differential kinetics and amp

279 h triggers the cross-bridge power stroke and myofilament sliding in sarcomeres.

280 a(50) shifts were associated with changes in myofilament spacing (d(1,0)) or thick-thin filament inte

281 muscle that may also be limited by immature myofilament structure.

282 ac isoform alters contractile properties and myofilament structure.

283 -ray diffraction study revealed that altered myofilament structures present in HCM-D166V mice were mi

284 cMyBP-C) and troponin-I (cTnI) are prominent myofilament targets of PKA.

285 into a computational model, the integral of myofilament tension development predicts hypertrophic an

286 Myocardial sarcomeres also contain a third myofilament, titin, and it is unknown whether titin can

287 mutation alters the function/ability of the myofilament to bind Ca(2+) as a result of modifications

288 nI induces an increase in the sensitivity of myofilament to Ca(2+), but the detailed mechanism is unk

289 roximately 20 pN) can be generated by single myofilaments to buckle and break actin filaments.

290 expression resulted in sensitization of the myofilaments to Ca(2+) and blocked stimulus-dependent in

291 tion of myosin could be an early response of myofilaments to increase contractile performance of the

292 tion of myosin could be an early response of myofilaments to increase contractile performance of the

293 and then fall, during diastole, to allow the myofilaments to relax and the heart to refill with blood

294 ks, and transmit forces from the contracting myofilaments to the cell surface through costameres at t

295 receptor signal selectively directed to the myofilaments together with a reduced phosphodiesterase a

296 -1 impaired myocyte shortening indicated the myofilament was its primary downstream target.

297 ts regulatory subunit MYPT2 bound tightly to myofilaments was constitutively phosphorylated in beatin

298 length-dependent activation (LDA) of cardiac myofilaments, we tested the influence of OM on this fund

299 rect effect on the Ca(2+) sensitivity of the myofilament, which may alter Ca(2+) handling and contrib

300 MN-1 acts in muscle, where it colocalizes at myofilaments with ARX-2, a component of the Arp2/3 actin