ライフサイエンスコーパス: myofilament

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

2 actile function directly at the level of the myofilament.

3 elaxation has been proposed to reside in the myofilament.

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

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

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

7 talytic subunit content in the cytoplasm and myofilaments.

8 hostatin A, enhances contractile activity of myofilaments.

9 rdiomyocytes, allowing an in vivo imaging of myofilaments.

10 resembled that found previously in mammalian myofilaments.

11 omyosin ATPase activity and contractility of myofilaments.

12 ns, indicating cross-bridge association with myofilaments.

13 mic inclusions, and focal disorganization of myofilaments.

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

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

16 hostatin A, enhances contractile activity of myofilaments.

17 functions to modulate activation of cardiac myofilaments.

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

19 attributable to changes at the level of the myofilaments.

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

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

22 n-contraction coupling coupled to a model of myofilament activation and force development.

23 cantly our ability to understand its role in myofilament activation and the molecular mechanism of mu

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

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

26 contributes to several properties of cardiac myofilament activation.

27 he regulation of myocyte calcium cycling and myofilament activity.

28 Myofilament ADP sensitivity was higher in IDCM and HCM c

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

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

31 runcated ssTnT is unable to incorporate into myofilament and is degraded in muscle cells.

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

33 ted decrease of phosphorylation in important myofilament and Z-disk proteins with a linear correlatio

34 C10 mutant MyBP-C failed to incorporate into myofilaments and degradation rates were accelerated by ~

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

36 ant TNNT1 gene is unable to incorporate into myofilaments and is degraded in muscle cells.

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

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

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

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

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

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

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

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

51 Myofilament Ca sensitization increases cytosolic Ca bind

52 n intrafusal nuclear bag fibres may increase myofilament Ca(2+) -sensitivity and tension, impairing s

53 iac TnT in nuclear bag fibres would increase myofilament Ca(2+) -sensitivity and tension, thus affect

54 minal extension of insect TnT functions as a myofilament Ca(2+) buffer/reservoir and is potentially c

55 Myofilament Ca(2+) desensitization with blebbistatin pre

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

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

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

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

64 Results show that loss of gammaC0C7 reduced myofilament Ca(2+) sensitivity and increased cross-bridg

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

101 r bundles revealed a significant decrease in myofilament Ca(2+)-responsiveness (pCa(50)=6.15+/-0.11 [

102 7.2+/-2.3 kN/m(2), respectively), and higher myofilament Ca(2+)-sensitivity (EC(50)=2.5+/-0.2, 2.4+/-

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

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

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

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

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

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

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

110 that modulation of S1PR results in decreased myofilament-Ca(2+)-responsiveness and improved diastolic

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

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

113 raction, both of which paralleled changes in myofilament calcium affinity.

114 ected calcium reporter to monitor changes in myofilament calcium affinity.

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

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

117 on in combination with better maintenance of myofilament calcium sensitivity and sarcoplasmic reticul

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

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

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

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

122 technique and observed reduced function and myofilament calcium sensitivity.

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

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

125 translocation of PKA and phosphatases to the myofilament compartment as shown by fractionation, immun

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

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

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

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

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

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

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

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

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

135 mutation in eight genes commonly mutated in myofilament disease.

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

137 n complex regulates the Ca(2+) activation of myofilaments during striated muscle contraction and rela

138 incorporates a biophysical representation of myofilament dynamics.

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

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

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

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

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

144 Myofilament force-calcium relationships were measured in

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

146 f kinase and phosphatase activity within the myofilament fraction of cardiac myocytes after exposure

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

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

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

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

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

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

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

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

155 ivator complex to AMPK would uniquely impact myofilament function.

156 ansients, suggesting targeted improvement of myofilament function.

157 s multiple sarcomeric substrates to regulate myofilament function.

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

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

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

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

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

163 comparison between the two proposed rates of myofilament inactivation.

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

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

166 so cause loss of function through failure of myofilament incorporation and rapid degradation.

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

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

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

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

171 dysregulation of protein phosphorylation on myofilaments is not clear.

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

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

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

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

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

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

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

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

180 Myofilament lattice spacing from TEM was significantly g

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

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

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

184 embryogenesis and display disruption of the myofilament lattice.

185 ly followed by progressive disruption of the myofilament lattice.

186 tructural support and radial rigidity to the myofilament lattice.

187 rayed myofibrils with some disruption of the myofilament lattice.

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

189 situ in the native environment of the muscle myofilament lattice.

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

191 laments that correlate with titin strain and myofilament LDA.

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

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

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

195 Myofilament length-dependent activation is a universal p

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

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

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

199 Myofilament length-tension relationships were considerab

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

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

202 ssense variants falling in enriched domains, myofilament localization and degradation rates were meas

203 Examination of myofilament longitudinal stiffness under rigor condition

204 dependent changes in calcium affinity to the myofilament may promote arrhythmogenic intracellular cal

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

206 iples to derive a coarse-graining multiscale myofilament model that can describe the thin-filament ac

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

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

209 ivo and normal stoichiometry of total TnT in myofilaments of heterozygous female flies.

210 laments to monitor structural changes in the myofilaments of intact heart muscle cells associated wit

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

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

213 The alteration in myofilament organization was associated with decreased e

214 rements and dependent on lattice spacing and myofilament overlap.

215 were unaffected, implying that CRT enhances myofilament phosphorylation.

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

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

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

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

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

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

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

223 diomyocyte intracellular Ca(2+) and aberrant myofilament protein composition.

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

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

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

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

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

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

230 Enhanced myofilament protein phosphorylation detected after hRFRP

231 heart during identical infusions to measure myofilament protein phosphorylation.

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

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

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

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

236 contribution of the extracellular matrix or myofilament proteins at larger excursions.

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

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

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

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

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

242 ges with decreased oxidative modification of myofilament proteins via downregulation of NOX2.

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

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

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

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

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

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

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

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

251 ol mice aiming to examine the composition of myofilament proteins, we found that, in contrast to extr

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

253 or post-translational modifications of major myofilament proteins.

254 ression of cardiac transcription factors and myofilament proteins.

255 ated PKA activity and PKA phosphorylation of myofilament proteins.

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

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

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

259 irectly affects thin filament activation and myofilament relaxation kinetics.

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

261 ionship between cardiomyocyte morphology and myofilament relaxation, and suggest that functional dive

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

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

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

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

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

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

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

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

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

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

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

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

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

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

276 d troponin behavior is altered, and that the myofilament spacing is increased.

277 cMyBP-C alters myofilament structure and contractile properties in a pr

278 Without inducing cell death and damage to myofilament structure, CCBs elicited line-specific inhib

279 old adult flies, prior to degradation of IFM myofilament structure, which started at 2 days old and i

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

281 ac isoform alters contractile properties and myofilament structure.

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

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

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

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

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

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

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

289 dge kinetics, the increase in sensitivity of myofilaments to calcium was significantly blunted by hum

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

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

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

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

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

295 -1 impaired myocyte shortening indicated the myofilament was its primary downstream target.

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

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

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

299 trastructural change was at the level of the myofilaments, which regularly extended into the papillae

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