ライフサイエンスコーパス: muscle fiber

1 with microscopic core-like structures in the muscle fiber.

2 wed by Mg(2+) in the context of an activated muscle fiber.

3 s phagocytose nerve terminals contacting the muscle fiber.

4 ant populations, which fuse with the injured muscle fiber.

5 y impaired myogenic capacity in regenerating muscle fibers.

6 d the expression of the NOTCH ligand JAG2 in muscle fibers.

7 including blood vessels, motor neurons, and muscle fibers.

8 mechanics of either fully active or resting muscle fibers.

9 trophic factors, controls the properties of muscle fibers.

10 actomyosin crossbridge formation in skeletal muscle fibers.

11 levels of nuclear factors in differentiated muscle fibers.

12 cise-mediated glucose uptake in nonoxidative muscle fibers.

13 macrophages are likely involved in damaging muscle fibers.

14 shold MNs innervating fatigue resistant slow muscle fibers.

15 ptic motor neuron and multiple post-synaptic muscle fibers.

16 nza A viruses to replicate in avian skeletal muscle fibers.

17 to repair damaged muscle fibers or form new muscle fibers.

18 find unexpected roles for distinct planarian muscle fibers.

19 thelial tumors by wrapping around vessels or muscle fibers.

20 cle cells frequently locate in the middle of muscle fibers.

21 (+)]e and increased its rate of decay in MHS muscle fibers.

22 ate excitation-contraction coupling in adult muscle fibers.

23 eased and accumulated in highly atrophic DM2 muscle fibers.

24 nsemble average measurements in solution and muscle fibers.

25 the myosin motor domain in relaxed skeletal muscle fibers.

26 rvation with subsequent reinnervation of the muscle fibers.

27 nd the halothane-triggered MH episode in MHS muscle fibers.

28 nt model of Ca(2+) dynamics in frog skeletal muscle fibers.

29 eased the peak Ca(2+) release flux by 49% in muscle fibers.

30 to disperse unnecessary receptor clusters on muscle fibers.

31 dependent calcium signaling in frog skeletal muscle fibers.

32 ult patients with storage of polyglucosan in muscle fibers.

33 tional behavior of N-cTnC in skinned cardiac muscle fibers.

34 nd in atrophy especially in the case of slow muscle fibers.

35 n events to share matrix content in skeletal muscle fibers.

36 y required for embryonic development of slow muscle fibers.

37 lin during membrane repair in adult skeletal muscle fibers.

38 surface and in close proximity to the mature muscle fibers.

39 by activating the Akt/mTOR growth pathway in muscle fibers.

40 excitation contraction coupling in skeletal muscle fibers.

41 rvation with subsequent reinnervation of the muscle fibers.

42 blast proliferation and differentiation into muscle fibers.

43 sory structures typical of striated skeletal muscle fibers.

44 AGFP) exchanged into permeabilized papillary muscle fibers.

45 in the t-tubule membrane of mature skeletal muscle fibers.

46 cellular excitability in sensory neurons and muscle fibers.

47 ), which form the connection between MNs and muscle fibers.

48 on, and mitochondrial structure in diaphragm muscle fibers.

49 aments, similar to what has been observed in muscle fibers.

50 at 199 miRNAs identified in the two types of muscle fibers.

51 located parts, and efferents also innervate muscle fibers.

52 mportant to ensure the cell/matrix anchor of muscle fibers.

53 anes, causing disorganization of regenerated muscle fibers.

54 nce training increased its content in type I muscle fibers.

55 anical phenotype but fully restored type IIa muscle fiber (9.19% vs 9.13% SR; P > 0.05 vs 15.9% UR; P

56 eveal that the Kbtbd5 null mice have smaller muscle fibers, a disorganized sarcomeric structure, incr

57 d restoration in the architecture of cardiac muscle fibers and a reduction in the extent of fibrosis

58 membrane resealing was defective in ML1-null muscle fibers and also upon acute and pharmacological in

59 Caveolae accumulate in dystrophic muscle fibers and caveolin and cavin mutations cause mus

60 mode NCX3 blocker, reduces [Ca(2+)]r in MHS muscle fibers and decreases the amplitude of [Ca(2+)]r r

61 CU showed a predominance of type I oxidative muscle fibers and higher capillary density, enhanced exp

62 ing methodology to study IL-6 in fixed mouse muscle fibers and in live animals in vivo.

63 scues the Ca(2+) release defects in isolated muscle fibers and increases the lifespan and mobility of

64 , and coursed in apposition with, bundles of muscle fibers and interstitial cells of Cajal.

65 performed by many other groups using single muscle fibers and isolated myofibrils.

66 reconcile previous contradictory reports in muscle fibers and isolated RyRs, where Mg(2+) is present

67 elevates [Ca(2+)]r in both MHN and MHS swine muscle fibers and it is prevented by removal of extracel

68 Additionally, fungal cells invaded host muscle fibers and joined together to form networks that

69 ng of mAgrin to hypoglycosylated alpha-DG on muscle fibers and possibly abrogation of binding from mo

70 eurons when changing their target innervated muscle fibers and sensory feedback.

71 depends upon interactions between developing muscle fibers and the extracellular matrix (ECM) that an

72 s contributed to the regeneration of damaged muscle fibers and the satellite cell compartment.

73 e microimaging techniques to visualize mouse muscle fibers and their nuclei.

74 has been applied to differentiate PSCs into muscle fibers and their progenitors in vitro.

75 Excitability differs among muscle fibers and undergoes continuous changes during de

76 ich is involved in the cellular structure of muscle fibers and, along with DMD, forms part of the dys

77 hole cell lysates of mouse brain, liver, red muscle fibers, and CaCo-2 cells using the TAPEG FASP app

78 nied by reduced inflammation, more oxidative muscle fibers, and improved strength of the weak diaphra

79 a synapse between motor neurons and skeletal muscle fibers, and is critical for control of muscle con

80 or of vesicle-mediated membrane resealing in muscle fibers, and localizes to muscle fiber wounds foll

81 icles from CB1 knockout embryos contain more muscle fibers, and postnatal mice show muscle fibers of

82 D) is characterized by a progressive loss of muscle fibers, and their substitution by fibrotic and ad

83 Our findings highlight that avian skeletal muscle fibers are capable of productive influenza virus

84 Specifically, fewer muscle fibers are degenerating, fiber size varies less,

85 art Muscle (muHM) arrays, in which elongated muscle fibers are formed in an easily fabricated templat

86 Muscle fibers are particularly susceptible to injury, an

87 Studies on isolated cells and muscle fibers as well as intact animals have shown that

88 es insights into the contractile strength of muscle fibers as well as the length of the thin filament

89 factors onto permeabilized rat gastrocnemius muscle fibers, as well as isolated mitochondrial subpopu

90 gm of FgfrL1 knockout animals lacks any slow muscle fibers at E18.5 as indicated by the absence of sl

91 a(2+)]r in both swine and murine MHN and MHS muscle fibers at rest and decreased the magnitude of the

92 d reduced (appendicular) muscle mass (-10%), muscle fiber atrophy (-27%), and decreased quadriceps st

93 n vitro, anti-SRP and anti-HMGCR Abs induced muscle fiber atrophy and increased the transcription of

94 which is both sufficient to induce skeletal muscle fiber atrophy and required for Gadd45a-mediated s

95 n-26 (C-26) cancer cachexia causes diaphragm muscle fiber atrophy and weakness and compromises ventil

96 tically ill patients have manifest diaphragm muscle fiber atrophy and weakness in the absence of mito

97 s treatment failed to rescue the age-related muscle fiber atrophy associated with muscle atrophy and

98 Skeletal muscle fiber atrophy develops in response to severe seps

99 redox environment is not a key regulator of muscle fiber atrophy during sarcopenia but may play a ke

100 resulted in reduced contractile function and muscle fiber atrophy for longer duration of MV.

101 Sepsis triggers more severe and sustained muscle fiber atrophy in limb muscles when compared with

102 In addition, the muscle fiber atrophy was associated with high levels of

103 y and required for Gadd45a-mediated skeletal muscle fiber atrophy.

104 ich is necessary and sufficient for skeletal muscle fiber atrophy.

105 lation rescued exercise endurance and type I muscle fiber atrophy; it also prolonged survival.

106 impair its ability to polymerize within the muscle fiber BM.

107 ompound increased the number of newly formed muscle fibers but delayed their terminal differentiation

108 ns, which encompasses injury not only to the muscle fibers, but also to the surrounding tissue compon

109 -1 reduced inflammatory cell infiltration of muscle fibers, but only early in disease progression.

110 network (SSTN) has been detected in skeletal muscle fibers by confocal imaging after the removal of t

111 XPHOS capacity was measured in permeabilized muscle fibers by high-resolution respirometry in a cross

112 ctive subjects, and the resulting changes in muscle fiber Ca(2+)-handling trigger muscular adaptation

113 y the presence of two distinct categories of muscle fibers called type I "red" slow twitch and type I

114 The growth of muscle fibers can be negatively regulated by bovine myos

115 ks actin filaments to the plasma membrane of muscle fiber cells (sarcolemma).

116 rf2-null mice displayed smaller, immature TA muscle fibers compared with WT counterparts on d 15 afte

117 b)orders, possibly due to specializations in muscle fiber composition and musculoskeletal systems.

118 Single-muscle fiber contractility testing showed near normal co

119 Muscle samples were used to measure single-muscle fiber contractility.

120 29, and 51% with corresponding reductions in muscle fiber cross-sectional area of 18, 42, and 69% aft

121 that fld mice exhibited smaller regenerated muscle fiber cross-sectional areas compared with wild-ty

122 ult from a defect in the linkage between the muscle fiber cytoskeleton and the basement membrane (BM)

123 Defects in this BM lead to muscle fiber damage from the force of contraction.

124 ve for muscle atrophy, dysphagia, pronounced muscle fiber damage, and vasculitis.

125 tor muscle neovascularization, and decreased muscle fiber damage.

126 Muscular diseases lead to muscle fiber degeneration, impairment of mobility, and i

127 n, fatty replacement of skeletal muscle, and muscle fiber degeneration.

128 d intestinal motilities along with thickened muscle fibers, demonstrating a critical role of mst in t

129 rnal-zygotic tmem2 mutants (MZtmem2) exhibit muscle fiber detachment, in association with impaired la

130 Leg muscle fiber diameter remained subnormal at 14 days with

131 rrelated with increases in muscle weight and muscle fiber diameter, resulting in long-term improvemen

132 al muscle dysfunction as by judged decreased muscle fiber diameter.

133 e expression that promotes normal intrafusal muscle fiber differentiation and fusimotor innervation h

134 We also measured diaphragm muscle fiber dimensions from stained cross sections, and

135 Muscle fibers do not normally express major histocompati

136 inhibiting nuclear factor-kappaB only within muscle fibers during acute endotoxemia.

137 nged intracellular recording from individual muscle fibers during induction of warmup in a mouse mode

138 x-ray diffraction pattern of rabbit skeletal muscle fibers during ramp stretch compared to those duri

139 n important role in fuel delivery in Mb-rich muscle fibers (e.g. type I fibers and cardiomyocytes), a

140 n which proliferative muscle progenitors and muscle fibers establish the skeletal musculature.

141 We conclude that Arg1457His compromises muscle fiber excitability.

142 Surprisingly, a few muscle fibers express strong F-alpha-DG.

143 oneurons that innervate the fast-contracting muscle fibers (F-type motoneurons) are vulnerable and de

144 Muscle fibers form as a result of myoblast fusion, yet t

145 Multinucleated skeletal muscle fibers form through the fusion of myoblasts durin

146 s a biomarker of the quantity and quality of muscle fiber formation.

147 We obtained muscle fiber fragments from skeletal muscle biopsy speci

148 Transplantation of human muscle fiber fragments into irradiated muscle of immunod

149 her, we determined that subjecting the human muscle fiber fragments to hypothermic treatment successf

150 well as the length of the thin filaments, in muscle fibers from 51 patients with thin filament myopat

151 by those obtained ex vivo on adult skeletal muscle fibers from a biopsy from a pseudomyotonia-affect

152 Diaphragm muscle fibers from critically ill patients displayed sig

153 arcolemmal integrity and protecting skeletal muscle fibers from damage.

154 tect laminin alpha2 chain-deficient skeletal muscle fibers from degeneration.

155 Permeabilized muscle fibers from HFD-fed SIRT3 knockout (KO) mice show

156 ns of single membrane-permeabilized skeletal muscle fibers from mice lacking Tmod1.

157 Muscle fibers from MTM1-deficient mice present defects i

158 alcium entry (SOCE) in fast- and slow-twitch muscle fibers from normotensive Wistar-Kyoto rats and sp

159 Lower force generation was observed in muscle fibers from patients of all genotypes.

160 Furthermore, muscle fibers from r-irisin-injected mice displayed enha

161 McTnT(1-44Delta) and McTnT(45-74Delta), into muscle fibers from Tm(H276N).

162 tem cells within their endogenous niche, and muscle fiber fusion at single-cell resolution.

163 by forming a complex with MEKK4 in skeletal muscle fibers, Gadd45a increases MEKK4 protein kinase ac

164 llular matrix remnants from injured skeletal muscle fibers, "ghost fibers," govern muscle stem/progen

165 pression profile properties in fast and slow muscle fibers had been investigated at the mRNA levels,

166 Cultured Fnip1-null muscle fibers had higher oxidative capacity, and isolate

167 Synaptic pathology and denervation of target muscle fibers has been reported prior to the appearance

168 ear factor-kappaB signaling within diaphragm muscle fibers has complex effects on caspase-3 activatio

169 owever, the subcellular location for SOCE in muscle fibers has not been unequivocally identified.

170 xpression of DGKzeta is sufficient to induce muscle fiber hypertrophy through an mTOR-dependent mecha

171 matergic motor neurons synapsing on the same muscle fiber in Drosophila larvae.

172 We hypothesized that weakness of diaphragm muscle fibers in critically ill patients is accompanied

173 e exploration of both correct and off-target muscle fibers in Drosophila embryos.

174 We observed that regenerating and necrotic muscle fibers in muscle biopsy samples from DMD patients

175 skinned guinea pig (Cavia porcellus) cardiac muscle fibers in the absence and presence of 0.3 and 3.0

176 Yet no gene targeting of Erk1/2 in muscle fibers in vivo has been reported to date.

177 d45a as it induces atrophy in mouse skeletal muscle fibers in vivo We found that Gadd45a interacts wi

178 el, in plane, or perpendicular to paraspinal muscle fibers; in kidney tissue, in the cortex or adjace

179 interacts with multiple proteins in skeletal muscle fibers, including, most prominently, MEKK4, a mit

180 trate multiple degenerating and regenerating muscle fibers, increased central nuclei, elevated creati

181 s in relaxed permeabilized porcine papillary muscle fibers indicated slightly differently oriented le

182 There was significantly less muscle fiber injury in the PJ34-treated group than in th

183 Normally quiescent, following muscle fiber injury, we show that these cells express Zf

184 the activity of individual motor units (the muscle fibers innervated by a single motor neuron) and m

185 cytolinker protein plectin is essential for muscle fiber integrity and myofiber cytoarchitecture.

186 encoding dystrophin, a protein required for muscle fiber integrity.

187 In normal adult muscle, each muscle fiber is innervated by a single axon, but at birt

188 At birth, each mammalian skeletal muscle fiber is innervated by multiple motor neurons, bu

189 In consequence, each agonist muscle fiber is stimulated by an agonist neuron, while a

190 ed by an agonist neuron, while an antagonist muscle fiber is unstimulated by a pause and step from th

191 lear factor-kappaB signaling within skeletal muscle fibers is a key pathway leading to diaphragmatic

192 Dye influx into muscle fibers lacking both dysferlin and the related pro

193 of Tmod1 from either wild-type or Tmod4(-/-) muscle fibers leads to thin filament elongation by appro

194 Muscle fiber length is nearly uniform within a muscle bu

195 ise tolerance, mitochondrial biogenesis, and muscle fiber maintenance in miR-133a-deficient mice.

196 Cardiac muscle fiber mechanic studies demonstrate cross-bridge a

197 bers (SIF) and multiply innervated nontwitch muscle fibers (MIF).

198 P5K orthologs in zebrafish embryos disrupted muscle fiber morphology and resulted in abnormal eye dev

199 In single muscle fibers (myofibers) harvested and grown ex vivo fo

200 e exosomes, it is not known whether skeletal muscle fibers (myofibers) release exosomes.

201 rons in the midbrain is presented to drive a muscle fiber oculomotor plant during horizontal monkey s

202 olated from flexor digitorum brevis skeletal muscle fibers of adult mice.

203 more muscle fibers, and postnatal mice show muscle fibers of an increased diameter relative to wild-

204 sion pattern, with focal accumulation in the muscle fibers of autoantibody-positive patients compared

205 Our results indicate that avian skeletal muscle fibers of chicken and duck could be significant c

206 These findings show that diaphragm muscle fibers of critically ill patients display atrophy

207 Both slow- and fast-twitch diaphragm muscle fibers of critically ill patients had approximate

208 iber size and increased fibrosis in skeletal muscle fibers of D2-mdx mice compared with B10-mdx and c

209 We hypothesized that diaphragm muscle fibers of mechanically ventilated critically ill

210 s in baseline Na(+) and Ca(2+) in dystrophic muscle fibers of the hind-limb musculature predicts a ne

211 croscopy confirmed shorter thin filaments in muscle fibers of these patients.

212 fusion of engrafted wild-type myoblasts with muscle fibers; on the other hand, very few or no red mus

213 d myogenic cells then fuse to repair damaged muscle fibers or form new muscle fibers.

214 on filopodia repeatedly contacted off-target muscle fibers over several hours during late embryogenes

215 ncreased oxidative capacity in permeabilized muscle fibers (P-time x treatment < 0.05, P-EGCG+RES < 0

216 y applied tubular system markers in skeletal muscle fiber preparations with a combination of three im

217 Importantly, in skinned muscle fiber preparations, we found markedly impaired le

218 YAP forced-activity in muscle fibers prevents the decrease of JAG2 expression a

219 myostatin loss attenuated the activation of muscle fiber proteolytic pathways by inhibiting the expr

220 Intracellular muscle fiber recordings and tension measurements show th

221 rescues macrophage homeostasis and skeletal muscle fiber regeneration, showing that Tregs can direct

222 ngiogenesis in both glycolytic and oxidative muscle fiber regions at day 7.

223 These findings demonstrate that skeletal muscle fibers release exosomes which can exert biologica

224 uptake in normal and insulin-resistant adult muscle fibers, resembling the reported effect of exercis

225 t E12.5, a time when phrenic nerves approach muscle fibers, resulted in smaller and fewer nerve-induc

226 cal microscopy of uninjured adult dysf-pHGFP muscle fibers revealed that dysferlin is highly enriched

227 ink between the extracellular matrix and the muscle fiber sarcolemma, and proper glycosylation is cri

228 We show that muscle fibers secrete and concentrate the fibroblast gro

229 Here, we show that muscle fibers secrete and concentrate the fibroblast gro

230 igh-threshold MNs innervating fast fatigable muscle fibers selectively degenerate compared with low-t

231 Caveola-deficient cavin-1(-/-) muscle fibers showed a striking loss of sarcolemmal orga

232 tra of BSL-myosin bound to actin in oriented muscle fibers showed sharp three-line spectra, indicatin

233 lar muscles contain singly innervated twitch muscle fibers (SIF) and multiply innervated nontwitch mu

234 in a significant decrease in both diaphragm muscle fiber size and diaphragm-specific force productio

235 of the gastrocnemius, revealing a decreased muscle fiber size and increased fibrosis in skeletal mus

236 lts, muscle regeneration was stimulated, and muscle fiber size decreased markedly.

237 In addition, electrocardiogram and muscle fiber size distribution were also normal.

238 Muscle fiber size is activity-dependent and clinically i

239 he motor neurons of SMA model mice increases muscle fiber size, enhances the post-synaptic NMJ area,

240 hypertrophy and abnormal distribution of the muscle fiber size.

241 lic proteins were obtained from rabbit psoas muscle fibers skinned in oil and transferred to physiolo

242 n in the motor column related to the type of muscle fibers (slow, intermediate, fast) they innervate.

243 iptional and splicing regulatory network for muscle fiber specification.

244 elease and Ca(2+) currents in adult skeletal muscle fibers subjected to voltage-clamp and on RyR1 cha

245 Inhibition of NOTCH ligand activity in muscle fibers suffices to reduce the progenitor pool.

246 owever, centrally aligned nuclei observed in muscle fibers suggest for muscle regeneration in these s

247 on membrane repair is abolished in mg53(-/-) muscle fibers, suggesting that MG53 functions as a poten

248 proper nuclear position is not restricted to muscle fibers, suggesting that the nesprin-dependent rec

249 scle force and intracellular organization of muscle fibers, supporting BIN1 as a negative regulator o

250 side-VI is expressed in muscle fibers targeted by the ISNb nerve, as well as at

251 SIF motoneurons, paralleling their different muscle fiber targets.

252 yield energy, a shift to increased type IIa muscle fibers than SR (15.9% vs 9.13%; P < 0.001), and s

253 method to isolate nuclei from adult skeletal muscle fibers that are suitable for electrophysiological

254 Lightweight artificial muscle fibers that can match the large tensile stroke of

255 tacted myotubes to transform into intrafusal muscle fibers that form the stretch receptor core.

256 apse formed between motoneurons and skeletal muscle fibers that is covered by Schwann cells (SCs).

257 We also engineered muscle fibers that mimic the native myofiber of the MuSC

258 sed of anatomically segregated fast and slow muscle fibers that possess different metabolic and contr

259 ell theory, the structure and development of muscle fibers, the inner ear, leukaemia, and scarlet fev

260 used as a model system because of its large muscle fibers, there are two troponin-C isoforms, called

261 ce thick-to-thin filament spacing in skinned muscle fibers, thereby increasing force production at lo

262 urons, reduces muscle degeneration, improves muscle fiber thickness and muscle growth, improves motor

263 1C)AEDANS-DDPM was incorporated into skinned muscle fibers to monitor N-cTnC opening.

264 This allowed muscle fibers to operate at a shorter sarcomere length a

265 le where it physically links the interior of muscle fibers to the extracellular matrix.

266 fficiently produce striated, millimeter-long muscle fibers together with satellite-like cells from hu

267 esults indicate that Fnip1 controls skeletal muscle fiber type specification and warrant further stud

268 sm, intramuscular fatty acid deposition, and muscle fiber type which attribute to pork quality (TG, F

269 Our findings indicate that muscle-, fiber type-, and mutation-specific factors affe

270 as likely secondary to alterations in tongue muscle fiber-type or secondary to chronic denervation.

271 coordinates the exercise-stimulated skeletal muscle fiber-type switch from glycolytic fast-twitch (ty

272 the development and performance of different muscle fiber types in Chinese perch.

273 There are two muscle fiber types in extraocular muscles: those receivi

274 structural determinants controlling the two muscle fiber types.

275 cing differences between the flight and jump muscle fiber types.

276 embrane stress in vitro, dysferlin-deficient muscle fibers undergo extensive functional and structura

277 ally greater than control or individual null muscle fibers, underscoring the importance of shoulder-l

278 physiology, and dynamic imaging of zebrafish muscle fibers, we find significantly reduced DHPR levels

279 o visualize endogenous IL-6 protein in fixed muscle fibers, we found IL-6 in small vesicle structures

280 d 2 (ERK1/2) in slow-twitch, type 1 skeletal muscle fibers, we studied the soleus muscle in mice gene

281 T2- and RcT1-RfsT2-reconstituted rat cardiac muscle fibers were captured by fitting the recruitment-d

282 ibers; on the other hand, very few or no red muscle fibers were observed, indicating the absence of m

283 A number of green fluorescent muscle fibers were observed, showing the fusion of engra

284 projected axons to denervated gastrocnemius muscle fibers, where they formed functional NMJs, restor

285 axonal dieback occurs first from fast-twitch muscle fibers, whereas slow-twitch fibers remain innerva

286 ucleated and contractile structures known as muscle fibers, which arise from the fusion of myoblasts

287 esults in a decreased calcium sensitivity of muscle fibers, which could in turn plays a role in muscl

288 tion, where YAP activates JAG2 expression in muscle fibers, which in turn regulates the pool of fetal

289 ated respiration was higher in permeabilized muscle fibers, which may contribute to the increased rel

290 enabling the 3D reconstruction of individual muscle fibers, which was previously impossible using any

291 proportion of type IIa fast-twitch oxidative muscle fibers, which was verified using immunofluorescen

292 is characterized pathologically by necrotic muscle fibers with absent or minimal inflammation.

293 mTOR signaling is elevated and the number of muscle fibers with centrally located nuclei is increased

294 ches for restoration of F-alpha-DG in mature muscle fibers with defects in FKRP functions.

295 al respiration was measured in permeabilized muscle fibers with high-resolution respirometry.

296 ed numerous nitric oxide synthase 2-positive muscle fibers with sarcoplasmic colocalization of marker

297 heterogeneous within myotubularin-deficient muscle fibers, with focally defective areas recapitulati

298 les had significant numbers of smaller-sized muscle fibers, without signs of regeneration.

299 esis that muscles rich in type I vs. type II muscle fibers would exhibit similar changes in intramyoc

300 resealing in muscle fibers, and localizes to muscle fiber wounds following sarcolemma damage.