ライフサイエンスコーパス: myofibrillar

1 By contrast myofibrillar actin genes unique to the adult stage were

2 D1 myopathy with sarcomeric disorganization, myofibrillar aggregates, and marked swimming defect.

3 s myofibrillar vacuolization and plaque-like myofibrillar aggregation.

4 Regulatory proteins, metabolic enzymes, some myofibrillar and blood plasma proteins were identified,

5 wo protease extracts appeared to target meat myofibrillar and collagen proteins differently, suggesti

6 as found to be more effective at hydrolysing myofibrillar and collagen proteins than the asparagus pr

7 ions using fluorescent-labelled casein, meat myofibrillar and connective tissue extracts to explore t

8 indicate that HT protease hydrolysis of meat myofibrillar and connective tissue protein extracts prod

9 valuated for their ability to hydrolyse meat myofibrillar and connective tissue protein extracts to p

10 ime course hydrolysis over 120 and 60 min of myofibrillar and connective tissue proteins, respectivel

11 g of multiple genes including those encoding myofibrillar and cytoskeletal proteins, and proteins tha

12 alone, and this was accompanied by elevated myofibrillar and cytosolic protein as well as DNA synthe

13 Massage enhances protein synthesis of the myofibrillar and cytosolic, but not the mitochondrial fr

14 nd water molecules, and distribution between myofibrillar and extra-myofibrillar compartments.

15 le biopsy samples were obtained to determine myofibrillar and mitochondrial MPS and the phosphorylati

16 We hypothesized that rates of myofibrillar and patellar tendon collagen synthesis woul

17 uce a decrease in protein solubility in both myofibrillar and sarcoplasmic fractions.

18 The basal myofibrillar and sarcoplasmic protein fractional synthet

19 To investigate this, we assessed myofibrillar and sarcoplasmic protein synthesis (MPS, SP

20 HFS significantly increased myofibrillar and sarcoplasmic protein synthesis 3 h afte

21 monstrate that several peptides derived from myofibrillar and sarcoplasmic proteins are sufficiently

22 Considerable differences in abundance of myofibrillar and sarcoplasmic proteins were observed bet

23 nificant correlation with higher contents of myofibrillar and sarcoplasmic proteins, smaller muscle f

24 egradation for a total of five non-redundant myofibrillar and sarcoplasmic proteins.

25 Thus, both myofibrillar and tendon protein synthetic rates show pro

26 s the lateral sarcomere lattice and distorts myofibrillar angular axial orientation.

27 rmediate filaments interlink the contractile myofibrillar apparatus with mitochondria, nuclei, and th

28 RNAs did not change, including those for the myofibrillar apparatus, we found a common set of genes (

29 gates and a concurrent disarrangement of the myofibrillar apparatus.

30 ly hearts for the maintenance of both normal myofibrillar architecture and cardiac physiology.

31 lying the cascade of events that destroy the myofibrillar architecture and trigger the aberrant expre

32 xhibited impaired cardiac output and altered myofibrillar architecture, and adult heart-specific inte

33 l cardiac performance, myocyte viability, or myofibrillar architecture.

34 signal that potentiates the organization of myofibrillar arrays in cardiac muscle myocytes.

35 and heterozygotes showed normal morphology, myofibrillar arrays, and contractile parameters.

36 cyte size and the organization of actin into myofibrillar arrays.

37 ha-MyHC), with the net outcome of diminished myofibrillar ATPase activity and impaired contractility.

38 Measurements of myofibrillar ATPase activity in the absence of Ca(2+) sh

39 of these mutations were determined utilizing myofibrillar ATPase measurements.

40 on to carbohydrate stimulates an increase in myofibrillar, but not mitochondrial, MPS following prolo

41 eletal muscle troponin, leading to increased myofibrillar Ca(2)(+) sensitivity in fast skeletal muscl

42 ctility that could be explained by increased myofibrillar Ca(2+) sensitivity.

43 troponin Ca(2+) affinity, thereby increasing myofibrillar Ca(2+) sensitivity.

44 measurements are normal, but an increase in myofibrillar Ca2+ sensitivity and thin filament protein

45 al effect caused the normal SL dependence of myofibrillar Ca2+ sensitivity to be reduced by 80% (mous

46 At 6 months, there is a decrease in the myofibrillar Ca2+ sensitivity, a significant increase in

47 exchange rate between them, diameter of the myofibrillar cells.

48 g human heart, offering direct evidence that myofibrillar CK energy delivery can be pharmaceutically

49 wever, ultrastructural analysis demonstrated myofibrillar collapse with abnormalities of intercalated

50 distribution between myofibrillar and extra-myofibrillar compartments.

51 blood by rapidly disassembling and reforming myofibrillar components of the sarcomere throughout cell

52 roteins in denervated muscle identified many myofibrillar components.

53 arcomere lattice, significant differences in myofibrillar connectivity were revealed between passivel

54 ss changes due to RNA interference to reduce myofibrillar content or due to aging in Drosophila myoca

55 onstrating cardiomyocyte calcium loading and myofibrillar contraction banding, with tolerance improve

56 We demonstrate that mutant desmin alters myofibrillar cytoarchitecture, markedly disrupts the lat

57 of Mef2A knock-out mice has revealed severe myofibrillar defects in cardiac muscle indicating a requ

58 Increased oxidative stress could cause myofibrillar degeneration and lipofuscin accumulation re

59 uscle isolated from bag3(-/-) mice exhibited myofibrillar degeneration and lost contractile activity

60 Electron microscopy shows progressive myofibrillar degeneration commencing at the Z-disk, accu

61 use mutant that suffers from skeletal muscle myofibrillar degeneration due to the rapid accumulation

62 phosphorylation and prevented cardiomyocyte myofibrillar degeneration in MR dogs.

63 abilizing myofibril structure and inhibiting myofibrillar degeneration in response to mechanical stre

64 LV biopsies demonstrated cardiomyocyte myofibrillar degeneration versus normal subjects (p = 0.

65 nt myopathy characterized by noninflammatory myofibrillar degeneration with apoptotic features.

66 ignificantly reduced FA protein degradation, myofibrillar degeneration, and myocyte apoptosis induced

67 termine the molecular trigger of upheld(101) myofibrillar degeneration, to evaluate contractile perfo

68 hy, characterized by protein aggregation and myofibrillar degeneration.

69 dissolution associated with accumulation of myofibrillar degradation products and ectopic expression

70 skeletal muscle Z-discs and accumulation of myofibrillar degradation products.

71 about 1 per 400 alpha-actinin) important for myofibrillar development and mechanotransduction.

72 Electron microscopy revealed myofibrillar disarray and degeneration with hyaline-like

73 had development of cardiac hypertrophy with myofibrillar disarray and fibrosis, in addition to activ

74 veloped significant cardiac hypertrophy with myofibrillar disarray and fibrosis, similar to what was

75 art examined by electron microscopy revealed myofibrillar disarray and mild fibrosis.

76 aracterized by left ventricular hypertrophy, myofibrillar disarray and sudden cardiac death.

77 ulted in preservation of titin, reduction in myofibrillar disarray, and attenuation of cardiomyocyte

78 tricular (LV) mass, contractile dysfunction, myofibrillar disarray, and fibrosis.

79 ting several cardiac abnormalities including myofibrillar disarray.

80 Myofibrillar disintegration begins at the Z-disk and res

81 cal mdx muscle is found to be a signature of myofibrillar disorder.

82 venting denervated myofibers from undergoing myofibrillar disorganization and autophagy, structural d

83 and DNAJB6b-F93L expressing mouse muscle had myofibrillar disorganization and desmin inclusions.

84 sly abnormal skeletal muscle development and myofibrillar disorganization at the microscopic level.

85 stion of whether bag3 gene knockdown induces myofibrillar disorganization caused by mechanical stress

86 thology showed abundant internalized nuclei, myofibrillar disorganization, desmin-positive inclusions

87 ults in highly diminished motor function and myofibrillar disorganization, with nemaline body formati

88 r hand, overexpression of CapZbeta1 inhibits myofibrillar disruption in bag3 knockdown cells under me

89 Myofibrillar disruption was not observed in sham-treated

90 committal term for a pathological pattern of myofibrillar dissolution associated with accumulation of

91 ankyrin repeat region a binding site for the myofibrillar elastic protein titin.

92 ons support the hypothesis that a deficit in myofibrillar energy delivery contributes to CHF pathophy

93 tease assays with connective tissue and meat myofibrillar extracts provide a more realistic evaluatio

94 t in both beef connective tissue and topside myofibrillar extracts.

95 tochondrial distribution and function; (iii) myofibrillar force generation; (iv) atrophy; and (v) aut

96 for efficient energy production, whereas the myofibrillar fraction had important contractile proteins

97 sectional area and protein synthesis of the myofibrillar fraction, but not DNA synthesis, are elevat

98 ctionation, obscurin was concentrated in the myofibrillar fraction, consistent with its identificatio

99 led a significant decrease of R448H from the myofibrillar fraction, likely due to the mutant's inabil

100 e carboxymethylation and localization to the myofibrillar fraction, of the catalytic subunit of prote

101 radicals were formed in the sarcoplasmic and myofibrillar fractions as well as in the non-soluble pro

102 efficiently fractionated to sarcoplasmic and myofibrillar fractions, prior to the identification base

103 ytron homogenizer, extraction of myosin from myofibrillar fragments by KCl/pyrophosphate to facilitat

104 concentrations (i.e. total, sarcoplasmic and myofibrillar) from the same biopsies were lower (4-9 %,

105 Oxidants depress myofibrillar function, decreasing specific force without

106 satory response to any mutation that impairs myofibrillar function.

107 of myocardin/serum response factor-regulated myofibrillar genes is extinguished, or profoundly attenu

108 tion of YY1 and transcriptional silencing of myofibrillar genes represent a new mechanism by which NF

109 B caused the pronounced induction of several myofibrillar genes, suggesting that NF-kappaB functions

110 sharp transitional boundary lies between the myofibrillar I-band and intercalated disc thin filaments

111 erozygous mice developed muscle weakness and myofibrillar instability, with formation of filamin C- a

112 ltered sarcomeric actin pattern, in affected myofibrillar integrity and in Z-band breaks, leading to

113 together, we demonstrate that CryAB ensures myofibrillar integrity in Drosophila muscles during deve

114 ruption in ordered myofibrillogenesis and/or myofibrillar integrity, and the consequent myosin aggreg

115 erated mice conditionally overexpressing the myofibrillar isoform of CK (CK-M) to test the hypothesis

116 , thick and thin filaments are arranged in a myofibrillar lattice.

117 d impaired electromechanical coupling at the myofibrillar level.

118 Myofibrillar lipid and protein oxidation increased with

119 th fluorescent antibodies to sarcolemmal and myofibrillar markers, and examined with confocal microsc

120 We speculate that the myofibrillar MARPs are regulated by stretch, and that th

121 ering calcium regulation or other aspects of myofibrillar mechanics.

122 situ cardiac systolic mechanics and in vitro myofibrillar mechanics.

123 ULLS induced a reduction of myofibrillar, metabolic (glycolytic and oxidative) and a

124 AS/HNO did not alter myofibrillar Mg-ATPase activity, supporting an effect on

125 d this led to reduced calcium sensitivity of myofibrillar MgATPase, as expected.

126 this novel line, we compiled a reference for myofibrillar microarchitecture among myocardial subtypes

127 rcise induces a gene signature that includes myofibrillar, mitochondrial and oxidative lipid metaboli

128 Myofibrillar MPS (mean +/- SD) increased (P < 0.05) abov

129 Postabsorptive rates of myofibrillar MPS and whole-body rates of phenylalanine o

130 imilarly with endurance and RE, increases in myofibrillar MPS are specific to RE, prophetic of adapta

131 These data indicate that the increase in myofibrillar MPS for C+P could, potentially, be mediated

132 ximal stimulation of postabsorptive rates of myofibrillar MPS in rested and exercised muscle of ~80-k

133 response relation of postabsorptive rates of myofibrillar MPS to increasing amounts of whey protein a

134 Myofibrillar MPS was approximately 35% greater for C+P c

135 ent study was to determine mitochondrial and myofibrillar muscle protein synthesis (MPS) when carbohy

136 Myofibrillar myopathies (MFMs) are morphologically disti

137 alignment of Z-disks, which are hallmarks of myofibrillar myopathies (MFMs).

138 tion is to provide an up-to-date overview of myofibrillar myopathies (MFMs).

139 The most important recent advance in the myofibrillar myopathies has been the discovery that muta

140 FLNC mutations have been associated with myofibrillar myopathies, and cardiac involvement has bee

141 resence of proteins typically found in human myofibrillar myopathies, suggesting that the genesis of

142 re and function at pre-symptomatic stages of myofibrillar myopathies.

143 sease genes have recently been recognized in myofibrillar myopathies.

144 tion is to provide an up-to-date overview of myofibrillar myopathies.

145 aggregates, the main pathological symptom of myofibrillar myopathies.

146 Desmin-related myofibrillar myopathy (DRM) is a cardiac and skeletal mu

147 (ACTA1), tubular aggregate myopathy (STIM1), myofibrillar myopathy (FLNC), and mutation of CHD7, usua

148 Filamin C (FLNC) mutations in humans cause myofibrillar myopathy (MFM) and cardiomyopathy, characte

149 Myofibrillar myopathy (MFM) is a morphologically distinc

150 The term myofibrillar myopathy (MFM) was proposed in 1996 as a no

151 he original patients had features resembling myofibrillar myopathy (MFM), arguing that TTN mutations

152 -girdle muscular dystrophy type 1A (LGMD1A), myofibrillar myopathy (MFM), spheroid body myopathy (SBM

153 -like motif that is mutated in zaspopathy, a myofibrillar myopathy (MFM), whereas the exon 8-11 junct

154 d "protein conformational diseases," such as myofibrillar myopathy and familial amyotrophic lateral s

155 l irritability and muscle biopsy findings of myofibrillar myopathy and mild denervation.

156 , have indicated that patients affected with myofibrillar myopathy have a more distal than proximal m

157 ese results, we suggest that p.D399Y-related myofibrillar myopathy is at least partly due to altered

158 r further research to identify therapies for myofibrillar myopathy or other degenerative diseases.

159 ) family proteins, causes cardiomyopathy and myofibrillar myopathy that is characterized by myofibril

160 R120G mutated form of HspB5 (associated with myofibrillar myopathy), or expression of the G985R and G

161 In every myofibrillar myopathy, there is abnormal accumulation of

162 tions in skeletal muscle that are typical of myofibrillar myopathy.

163 e identification of mutations in myotilin in myofibrillar myopathy.

164 alphaB-crystallin are an infrequent cause of myofibrillar myopathy; (3) alphaB-crystallin-related myo

165 ycin complex 1 (mTORC1) in the regulation of myofibrillar (MyoPS) and mitochondrial (MitoPS) protein

166 This is in contrast with the myofibrillar network, which displayed the same organizat

167 mic proteins were hydrolyzed faster than the myofibrillar ones by both human/porcine enzymes.

168 wall muscle, unc-96 mutants display reduced myofibrillar organization and characteristic birefringen

169 osin heavy chain that is required for atrial myofibrillar organization and contraction.

170 est that kettin is an important regulator of myofibrillar organization and provides mechanical stabil

171 nvestigate the effects of Erbb2 signaling on myofibrillar organization because drugs targeting ERBB2

172 in, and alpha-actinin and a complete loss of myofibrillar organization in fast-twitch muscles.

173 ltured on rigid surfaces exhibited increased myofibrillar organization, spread morphology, and reduce

174 ular matrix may be an important regulator of myofibrillar organization.

175 MFM patients, these mice develop progressive myofibrillar pathology that includes Z-disc streaming, e

176 ch-like and fast-twitch-like by PKA-mediated myofibrillar phosphorylation, which implicates a novel m

177 ependent upon protein kinase A (PKA)-induced myofibrillar phosphorylation.

178 es correlates with a significant decrease in myofibrillar PKA activity.

179 Although several myofibrillar promoters contain predicted NF-kappaB bindi

180 more, YY1 was found associated with multiple myofibrillar promoters in C2C12 myoblasts containing NF-

181 inoleic acid; liposome; emulsion) containing myofibrillar protein (MFP at 1, 8 and 20mg/mL) under hyd

182 ne required for myogenic differentiation and myofibrillar protein assembly in vertebrates.

183 Morpholino knockdown resulted in defects in myofibrillar protein assembly, particularly in slow musc

184 s as an integrator of Ca(2+) homeostasis and myofibrillar protein content during stress in the heart

185 rt failure patients due, in part, to loss of myofibrillar protein content, in particular myosin.

186 calpain activity, markedly attenuated FA and myofibrillar protein degradation induced by Cat.G.

187 in activity, which subsequently affected the myofibrillar protein degradation pattern in pork meat.

188 Cardiac troponin T (cTnT) is a myofibrillar protein essential for calcium-dependent con

189 Paramyosin, a myofibrillar protein found only in invertebrates, has be

190 During amino acid infusion, myofibrillar protein FSR increased to 3-fold, and sarcop

191 impairs contractile performance by altering myofibrillar protein function.

192 The in vitro myofibrillar protein hydrolysate showed the highest ABTS

193 ffect of the two AA isoforms on collagen and myofibrillar protein hydrolyzing activity varied dependi

194 Reduction of MbFe(IV)O by a myofibrillar protein isolate (MPI) from pork resulted in

195 uitin ligase activity, is involved in FA and myofibrillar protein stability and turnover in myocytes.

196 Whole body and leg glucose disposal, muscle myofibrillar protein synthesis (MPS) and leg protein bre

197 We investigated how myofibrillar protein synthesis (MPS) and muscle anabolic

198 ure of branched chain amino acids (BCAAs) on myofibrillar protein synthesis (MPS) at rest and after e

199 cronutrient meals on integrated 3-d rates of myofibrillar protein synthesis (MyoPS) in free-living ol

200 We have focused on pathways controlling myofibrillar protein synthesis and degradation, mitochon

201 in young men, with a stronger stimulation of myofibrillar protein synthesis during the early postpran

202 Rates of myofibrillar protein synthesis fell (P < 0.01) from 0.04

203 min after oral protein bolus, mean (+/- SEM) myofibrillar protein synthesis increased from 0.03 +/- 0

204 However, the increase in myofibrillar protein synthesis rates did not differ betw

205 lability, anabolic signaling, and subsequent myofibrillar protein synthesis rates in vivo in young me

206 Milk ingestion increased myofibrillar protein synthesis rates to a greater extent

207 +/- 0.003% to 0.10 +/- 0.01%/h; thereafter, myofibrillar protein synthesis returned to baseline rate

208 exercise resulted in greater stimulation of myofibrillar protein synthesis than did the ingestion of

209 fibre size compared to reloading alone, and myofibrillar protein synthesis, but not DNA synthesis, w

210 id transporters (LAT1, SNAT2) and CD98], and myofibrillar protein synthesis.

211 ucine kinetics, intramuscular signaling, and myofibrillar protein synthesis.Plasma appearance rates o

212 lity, anabolic signaling, and the subsequent myofibrillar protein synthetic response after the ingest

213 We compared the myofibrillar protein synthetic response and underlying n

214 and beef ingestion augment the postexercise myofibrillar protein synthetic response in young men, wi

215 ese data indicate that impaired postprandial myofibrillar protein synthetic response may be an early

216 ole-egg ingestion increased the postexercise myofibrillar protein synthetic response to a greater ext

217 There is a diminished myofibrillar protein synthetic response to the ingestion

218 However, myofibrillar protein synthetic responses (0-300 min) wer

219 Basal myofibrillar protein synthetic responses were similar be

220 Obscurin is a large myofibrillar protein that contains several interacting m

221 ctin, suggesting its likely participation in myofibrillar protein turnover, especially during muscle

222 dditives is mainly based on the induction of myofibrillar protein unfolding thus facilitating the for

223 mice caused the selective reduction of this myofibrillar protein, and this reduction correlated with

224 ion pathway occurred during the oxidation of myofibrillar proteins (MP) catalysed by a Fe(3+)/H2O2 sy

225 eins were mostly of muscle origin: including myofibrillar proteins (titin, myosin light chain 1/3, my

226 several groups of proteins among which were myofibrillar proteins and antioxidant defence systems; (

227 strate-trap) became associated with specific myofibrillar proteins and its cofactors, Ufd1 and p47, a

228 ionation step to deplete the highly abundant myofibrillar proteins and performed a second phosphoprot

229 regulation attenuated the loss of desmin and myofibrillar proteins and reduced atrophy.

230 hese data to implicate the disruption of the myofibrillar proteins and their interactions in the prop

231 meat affected the water binding sites of the myofibrillar proteins and, thereby, the interactions bet

232 During muscle atrophy, myofibrillar proteins are degraded in an ordered process

233 Several membrane and myofibrillar proteins are phosphorylated under these con

234 e distribution, protein interaction with key myofibrillar proteins as well as the conformation mallea

235 equent myofibril destruction, and over time, myofibrillar proteins become more susceptible to PAX4-in

236 phenolics on the oxidative damage caused to myofibrillar proteins by an in vitro metal-catalyzed oxi

237 Digestibility of myofibrillar proteins by pepsin was determined by in vit

238 Protein kinase A (PKA) phosphorylation of myofibrillar proteins constitutes an important pathway f

239 p97 participates to the rapid degradation of myofibrillar proteins during muscle atrophy.

240 us proteases, responsible for proteolysis of myofibrillar proteins during post-mortem storage, may be

241 ic sites as well as accumulation of degraded myofibrillar proteins forming large aggregates.

242 Myofibrillar proteins from alpha-white fibres were more

243 nvestigates the susceptibility of individual myofibrillar proteins from mackerel (Scomber scombrus) m

244 re-induced modification and functionality of myofibrillar proteins from pork meat pressurised at 200,

245 Although calcium handling and myofibrillar proteins have been implicated in maintainin

246 logy of IFN-gamma exposure and its effect on myofibrillar proteins in isolated neonatal rat ventricul

247 yme modulates the expression of myogenin and myofibrillar proteins in L6 muscle cells.

248 results predict that PKA phosphorylation of myofibrillar proteins in living myocardium contributes t

249 indicate that the phosphorylation pattern of myofibrillar proteins in PM muscle is mainly changed wit

250 A total of 656 peptides derived from major myofibrillar proteins in Protected Designation of Origin

251 zin) and an apple peel extract were added to myofibrillar proteins in three concentrations (50, 100 a

252 M) changes in protein phosphorylation of the myofibrillar proteins in three groups of pigs with diffe

253 d selective hydrolytic activity towards meat myofibrillar proteins including myosin and actin.

254 Loss of myofibrillar proteins is a hallmark of atrophying muscle

255 line, suggesting that the phosphorylation of myofibrillar proteins may be related to the meat rigor m

256 scle atrophy is the excessive degradation of myofibrillar proteins primarily by the ubiquitin proteas

257 of Frigate mackerel had greater contents of myofibrillar proteins than had catfish muscle (p<0.05).

258 t is assumed to be heated homogeneously, and myofibrillar proteins to be directly in contact with pep

259 In dry fermented sausages, myofibrillar proteins undergo intense proteolysis genera

260 roteomic approach involved the separation of myofibrillar proteins using OFFGEL electrophoresis, SDS-

261 tion factors, ion channels, and cytoskeletal/myofibrillar proteins was downregulated consequent to lo

262 The peptide HL from myofibrillar proteins was identified only in the ex vivo

263 Myofibrillar proteins were observed as the major fractio

264 iaphragm lysates and the abundance of select myofibrillar proteins were unchanged by PH.

265 At the level of the myofibrillar proteins, activation of myocardial contract

266 basic model made of an aqueous suspension of myofibrillar proteins, and a complex model, in which oxi

267 on as well as the expression of myogenin and myofibrillar proteins, and these effects were also depen

268 ture, such targets are presumed to represent myofibrillar proteins, but whether these proteins are re

269 xidant activity against protein oxidation in myofibrillar proteins, emphasizing the potential of appl

270 ler myofiber size, decreased mRNA levels for myofibrillar proteins, increased proteolytic enzyme acti

271 in carbonylation and tryptophan depletion in myofibrillar proteins, ovalbumin, beta-lactoglobulin, so

272 ediate remodeling by cleavage and release of myofibrillar proteins, targeting them for ubiquitination

273 that did not correspond to any of the major myofibrillar proteins.

274 s released during post-mortem proteolysis of myofibrillar proteins.

275 il, suggesting their interaction with surimi myofibrillar proteins.

276 has been involved in the degradation of bulk myofibrillar proteins.

277 ntifications were present on highly abundant myofibrillar proteins.

278 onths), focusing on those derived from major myofibrillar proteins.

279 ed an increased expression of genes encoding myofibrillar proteins.

280 th a negative impact on the digestibility of myofibrillar proteins.

281 The initial step in myofibrillar proteolysis is unknown because this proteol

282 The pattern of stimulation of myofibrillar, sarcoplasmic and mitochondrial protein was

283 alysing distinct subcellular fractions (e.g. myofibrillar, sarcoplasmic, mitochondrial) may provide a

284 The compartment model corresponds to the myofibrillar space (MS) and a calcium store, the sarcopl

285 ise in calcium (Ca(2+)) concentration in the myofibrillar space.

286 These results suggest that myofibrillar-space calcium causes crossbridges to move a

287 stretch, and that this links titin-N2A-based myofibrillar stress/strain signals to a MARP-based regul

288 We observed a progressive decline in myofibrillar structural integrity (underpinning meat ten

289 lidation, we found that two fragments of the myofibrillar structural protein myomesin-3 (MYOM3) are a

290 tion that can adversely affect cardiomyocyte myofibrillar structure and function.

291 The mechanism by which myofibrillar structure is maintained under mechanical st

292 rsal vessels characterized by a disorganized myofibrillar structure, reduced systolic and diastolic d

293 f contractility may arise from alteration of myofibrillar structure.

294 Because PKA has multiple myofibrillar substrates including titin, myosin-binding

295 d in physiological Ca(2+) handling of the SR-myofibrillar system.

296 Notably, Ca(2)(+)-sensitivity and passive myofibrillar tension were decreased in heterozygous fibe

297 brosis and abnormal mitochondrial but normal myofibrillar ultrastructure.

298 ology that includes Z-disc streaming, excess myofibrillar vacuolization and plaque-like myofibrillar

299 and diffusion coefficient of intra and extra myofibrillar water populations, exchange rate between th

300 lamin influences the mechanical stability of myofibrillar Z-discs, explaining the muscle weakness in