ライフサイエンスコーパス: myotube

1 Ms proceeds until tracheal branches fill the myotube.

2 even spacing of nuclei within the developing myotube.

3 l distributions of nuclear proteins within a myotube.

4 (myoblasts) differentiating into specialized myotubes.

5 dehydrogenases were expressed and active in myotubes.

6 r antagonists and GPR55 gene silencing in L6 myotubes.

7 esis than ammonia treatment in ethanol-naive myotubes.

8 R mutant that did not form clusters in C2C12 myotubes.

9 ibition of PERK leads to atrophy in cultured myotubes.

10 ely MYOD1, MYOG, and MYF5 in differentiating myotubes.

11 calises with mDia1 in cytoplasmic punctae in myotubes.

12 notably in high glucose- and insulin-treated myotubes.

13 A-mediated clock disruption in human primary myotubes.

14 ) and impaired ability to differentiate into myotubes.

15 differentiating myoblasts and newly forming myotubes.

16 ot augment their fusion to ICAM-1+ myoblasts/myotubes.

17 cleation from the NE on nuclear spreading in myotubes.

18 C12 mouse myoblasts that differentiated into myotubes.

19 IGF-1-mediated hypertrophy of human primary myotubes.

20 ed in HSALR muscle and in cultured human DM1 myotubes.

21 associated splicing abnormalities in patient myotubes.

22 n mouse C2C12 myoblasts differentiating into myotubes.

23 growth factor-beta1-induced atrophy in C2C12 myotubes.

24 h compounds disrupted the function of intact myotubes.

25 esprin-1alpha is increased in differentiated myotubes.

26 /- 2% vs. IGF-1; P < 0.001) in IGF-1-treated myotubes.

27 4 inhibitor, increased FAO rates in MEFs and myotubes.

28 and delivered to myoblasts and newly formed myotubes.

29 ed, differentiated, and fused into patterned myotubes.

30 ion of UPR causes severe atrophy in cultured myotubes.

31 ed this using both tsA201 cells and Stac3 KO myotubes.

32 ificantly following ASO treatment in patient myotubes.

33 and analyzed separately from multi-nucleated myotubes.

34 mRNA expression in both mouse SkM and C2C12 myotubes.

35 itial steps of myoblast differentiation into myotubes.

36 s during C2C12 myoblast differentiation into myotubes.

37 on and promotes mitochondrial maintenance in myotubes.

38 muprinted PDMS precluded robust detection of myotubes.

39 uced contractile force and synchrony in SOD1 myotubes.

40 er repair and regeneration of multinucleated myotubes.

41 ing very large, multinucleated cells such as myotubes.

42 n were observed in Stac3-deleted and control myotubes.

43 mitochondrial oxidative function in cultured myotubes.

44 as well as differentiation of myoblasts into myotubes.

45 sion of the full-length human DYS protein in myotubes.

46 ed Ca(2+) entry (SOCE) mechanism in skeletal myotubes.

47 ts and for the efficient formation of intact myotubes.

48 ion of both primary and C2C12 myoblasts into myotubes.

49 ion, proliferation, and differentiation into myotubes.

50 hat differentiate into fused, multinucleated myotubes.

51 rmal control (wild-type and/or heterozygous) myotubes.

52 etabolic plasticity in the SOD1-iPSC derived myotubes.

53 ficient skeletal muscle and cultivated C2C12 myotubes.

54 tiate by fusion and then by the formation of myotubes.

55 roteins from patient-derived fibroblasts and myotubes.

56 cally during myoblast fusion and declines in myotubes.

57 rating mouse myoblasts and in differentiated myotubes.

58 tive form of XBP1 caused atrophy in cultured myotubes.

59 genic differentiation results in hypotrophic myotubes.

60 insic FUS toxicity in both motor neurons and myotubes.

61 oduction were increased in ABA-treated human myotubes.

62 me activity prevented atrophy of Mettl21e KD myotubes.

63 er poles of nuclear chains in human skeletal myotubes.

64 ) pathway-mediated differentiation of mature myotubes.

65 bility of MyoD to drive differentiation into myotubes.

66 d TCAP expression in LGMD2G iPS cell-derived myotubes.

67 nonuclear progenitors to form multinucleated myotubes, a critical but poorly understood process.

68 In human myotubes, ACSL6 overexpression reduced palmitate oxidati

69 ession in a fraction of dystrophin-deficient myotubes after fusion in vitro.

70 ystrophin was expressed at the sarcolemma of myotubes after myogenic differentiation.

71 d roscovitine) differentiation, resulting in myotube and myoblast phenotypes, respectively.

72 ) and cleaves it in both DM1 patient-derived myotubes and a DM1 mouse model, leaving short repeats of

73 Desmin amyloids were cytotoxic to myotubes and disrupted their myofibril organization comp

74 s the activity of Rho/Rac GTPases in nascent myotubes and effects changes in the actin cytoskeleton.

75 form, DMD myoblasts formed fewer and smaller myotubes and exhibited impaired polarization of the cell

76 auses severe positioning defects in immature myotubes and fully differentiated myofibers, where it fo

77 ed muscle catabolism and wasting in cultured myotubes and in mice.

78 n sensitivity and insulin secretion in C2C12 myotubes and INS-1 832/13 pancreatic beta-cells.

79 LC3-II, and loss of muscle proteins both in myotubes and mouse muscle.

80 C5/irisin and beta-aminoisobutyric acid from myotubes and muscle in rats and humans.

81 expressed in mouse primary or C2C12 skeletal myotubes and the functional properties of the myotubes w

82 st score is unaltered between FSHD myoblasts/myotubes and their controls however, implying a non-myog

83 expression and activity in mouse muscle and myotubes and ureagenesis in hepatocytes were quantified.

84 EGFR blockade promotes the ST phenotype in myotubes and zebrafish embryos.

85 TRPC4, and calmodulin 1 are increased in the myotubes, and MG53 directly binds to TRPC3, which sugges

86 rentiate normally but fail to form syncytial myotubes, and Minion-deficient mice die perinatally and

87 (KD) of Mettl21e led to atrophy of cultured myotubes, and targeted mutation of Mettl21e in mice redu

88 omparable between muscle tissue and cultured myotubes, and temporal lipid profiles correlated with tr

89 y inhibits the myoblast differentiation into myotubes, and that P-TEFb and its two positive complexes

90 chimeras were expressed in triadin knockout myotubes, and their mobility was compared with the mobil

91 ntiation and fusion of myoblasts into mature myotubes are complex processes responding to multiple si

92 ed in myoblast proliferation and fusion into myotubes are misregulated in LOS fetuses.

93 Mutant myotubes are unable to buffer the increase in membrane t

94 fdfl/Y mice led to a complete loss of normal myotube arrangement and hypoglossia.

95 f cultured myotubes to CKD serum resulted in myotube atrophy and elevated oxidative stress, which wer

96 In contrast, knockdown of XBP1 inhibits myotube atrophy in response to LLC or C26 adenocarcinoma

97 nd autophagy-lysosome pathways, resulting in myotube atrophy.

98 kdown of T-cadherin in differentiating C2C12 myotubes attenuated both adiponectin-accumulation and ad

99 differentiation, nuclear movements along the myotube axis might represent the event required for the

100 LRRC8A over-expression in Lrrc8a KO myotubes boosts PI3K-AKT-mTOR signaling to supra-normal

101 d exosome secretion in differentiating C2C12 myotubes but not in undifferentiated myoblasts.

102 eased glucose uptake in differentiated C2C12 myotubes by stimulating glucose transporter-4 (GLUT-4) m

103 ted in congenital muscular dystrophy patient myotubes carrying a nonsense mutation within the SYNE1 g

104 e effect of beta-agonist stimulation in SBMA myotube cells derived from mice and patients, and in kno

105 the brain, spleen, or cultured N2a or C2C12 myotube cells.

106 Myotubes, characterized by myofibril development and bot

107 naemic portacaval anastomosis rat, and C2C12 myotubes compared to appropriate controls.

108 rate of DMD transcription in patient-derived myotubes compared to healthy controls, suggesting a tran

109 ker was elevated in FSHD and control healthy myotubes compared to their myoblast counterparts, so is

110 ptor binding subunit, IL-15ralpha in elderly myotubes confirmed that autocrine concentrations of IL-1

111 skeletal muscle in vivo and in primary human myotubes cultured in vitro.

112 Viral-mediated PDK4 overexpression in myotube cultures was sufficient to promote myofiber shri

113 ACSL6 genic inhibition in rat primary myotubes decreased lipid accumulation, as well as activa

114 ation with the remarkable ability to promote myotube dedifferentiation in vitro.

115 skeletal muscle has been challenging due to myotube delamination from synthetic culture substrates a

116 imary differentiated human myoblasts, IR-Mut myotubes demonstrated severe impairment in insulin signa

117 roperties of these model nuclear proteins in myotubes depended on molecular weight and nuclear import

118 S)-induced contractile activity upon primary myotubes derived from lean and severely obese (BMI >= 40

119 IGF-1-mediated increases in myotube diameter (1.27 +/- 0.09-fold, P < 0.05 vs. contr

120 amic ribosomal biogenesis response to IGF-1, myotube diameter and protein accretion were sustained.

121 reased autophagy with a consequent decreased myotube diameter to a greater extent than either treatme

122 We observed reduced myotube diameter, impaired protein synthesis, and increa

123 Myotube diameter, protein synthesis, and molecular respo

124 Myotube diameter, total protein, and RNA and DNA levels

125 d creatine kinase activity, fusion index and myotube diameter; likewise, the myosin heavy chain (MyHC

126 However, the CaV1.1 remaining in Stac3 KO myotubes did not generate appreciable Ca(2+) currents or

127 miR-29b promotes atrophy of myotubes differentiated from C2C12 or primary myoblasts,

128 and mouse skeletal muscle myoblasts promoted myotube differentiation and prevented dexamethasone-indu

129 time in motion, speed, and alignment during myotube differentiation and temporal interference of cyt

130 ng bone marrow cells were more supportive of myotube differentiation in vitro.

131 w TCA cycle intermediates and ATP content in myotubes during hyperammonaemia.

132 process whereby myoblasts differentiate into myotubes during muscle development and muscle regenerati

133 the fusion of myoblasts into multinucleated myotubes during myogenesis.

134 In C2C12 myotubes, EGFR inhibition/silencing increased ST, includ

135 ansformation during myogenesis, in which the myotubes elongate over several cell diameters and are di

136 ntiation of pluripotent stem (PS) cells into myotubes enables in vitro disease modeling of skeletal m

137 In dysgenic myotubes, energy transfer was observed from an N-termina

138 osition, show little resemblance to cultured myotube enhancers, and identify glycolytic and oxidative

139 ost importantly, whereas control iPS-derived myotubes exhibited in vitro responses similar to primary

140 Additionally, SOD1 myotubes exhibited significantly reduced length and cros

141 C2C12 myotubes exposed to excess free fatty acids with or with

142 ch in irisin and the conditioned medium from myotubes exposed to palmitate for 4 h significantly redu

143 ted by elevated oxidative stress in cultured myotubes exposed to palmitate in the presence of a beta-

144 We show that treatment of myotubes expressing polyglutamine-expanded AR with the b

145 chains were the only significant proteins in myotube extracts pulled down by nesprin-1-alpha2, but no

146 keletal muscle stem cell differentiation and myotube formation during regeneration in mice.

147 Moreover, cell proliferation and myotube formation improved without compromising each oth

148 ts of heteromeric VRAC were expressed during myotube formation of murine C2C12 myoblasts.

149 show up-regulation of myosin heavy chain and myotube formation when grown in differentiation medium.

150 yogenesis (cell cycling, differentiation and myotube formation).

151 gnaling, particularly at later timepoints of myotube formation, corresponding with reduced morphologi

152 divisions generating myocytes and subsequent myotube formation, inefficient skeletal muscle regenerat

153 ation of skeletal muscle differentiation and myotube formation, partially via the myogenin transcript

154 usion-based strategy to decouple mitosis and myotube formation, we demonstrate that the cell-specific

155 dation of mitochondria) is also active after myotube formation.

156 nd thus generate functional Mb during muscle myotube formation.

157 ing to supra-normal levels and fully rescues myotube formation.

158 sion of myogenic differentiation markers and myotube formation.

159 reduced expression of myogenin and impaired myotube formation.

160 celerates myoblast proliferation but impairs myotube formation.

161 n response to 4-CMC or caffeine, over 90% of myotubes formed from control myoblasts contracted, but o

162 ontrol myoblasts contracted, but only 60% of myotubes formed from Stac3-deleted myoblasts contracted

163 ture-dependent increase in resting Ca(2+) in myotubes from an RYR1-RM mouse model.

164 Thus, iPS-derived myotubes from individuals with genetically determined in

165 EPS improved insulin signal transduction in myotubes from lean but not severely obese subjects and E

166 EPS improved insulin signal transduction in myotubes from lean but not severely obese subjects and i

167 roximately 80%) relative to that observed in myotubes from normal control (wild-type and/or heterozyg

168 We show here that myotubes from patients bearing the CAV3 P28L and R26Q mu

169 ripotent stem cell-derived motor neurons and myotubes from patients with FUS-ALS revealed endplate ma

170 ntraction, insulin action was compromised in myotubes from the severely obese as was evident from red

171 ) phosphorylation, but to a lesser degree in myotubes from the severely obese.

172 ) phosphorylation, but to a lesser degree in myotubes from the severely obese.

173 Expression of WT Stac3 in Stac3 KO myotubes fully restored Ca(2+) currents and EC coupling

174 or mTORC1 substrate, p70S6K, is required for myotube fusion and hypertrophy, an mTORC1 effector for t

175 ed by the induction of myogenin expression), myotube fusion, and, ultimately, hypertrophy (later stag

176 quate for neuromuscular diagnostics, whereas myotubes generated by transdifferentiation from an indiv

177 ss (htl), or its ligands, caused significant myotube guidance defects.

178 Although this process of myotube guidance is essential to pattern the musculoskel

179 skeletal system, the mechanisms that control myotube guidance remain poorly understood.

180 FGF signals are thus essential regulators of myotube guidance that act through cytoskeletal regulator

181 Also, SOD1 myotubes had loosely arranged myosin heavy chain and red

182 pectively) in hyperammonemic murine skeletal myotubes, HEK cells, and skeletal muscle from hyperammon

183 L-type current in myotubes homozygous for RyR1-E4242G was substantially re

184 In myotubes, however, impaired NADH oxidation following ETC

185 mal RNA (rRNA) production and IGF-1-mediated myotube hypertrophy in vitro Primary skeletal myotubes w

186 ppear to be a prerequisite for IGF-1-induced myotube hypertrophy in vitro.

187 ts showed a faster growth rate and developed myotube hypertrophy.

188 iRNA profiles between wildtype and SUN1 null myotubes identified a cluster of miRNAs encoded by a non

189 In cultured myotubes, IL-6 promoted muscle degradation via JAK/STAT,

190 (EPS; 24 h) of primary human skeletal muscle myotubes improved insulin action in tissue from both lea

191 vels in both patient fibroblasts and patient myotubes in a concentration dependent fashion.

192 ) signaling pathway were enriched in nascent myotubes in Drosophila embryos.

193 d for myoblast fusion to form multinucleated myotubes in mouse, chick, and zebrafish.

194 Myotubes in the tissues are connected in parallel and in

195 ward type I and IIa fibers in rat muscle and myotubes in vitro.

196 d prevented dexamethasone-induced atrophy in myotubes in vitro.

197 d and transduced cells remained able to form myotubes in vitro.

198 proteins that interact with TBC1D1 in C2C12 myotubes including VPS13A and VPS13C, the Rab binding pr

199 ACSL6 overexpression in human primary myotubes increased phospholipid species and decreased ox

200 t increase in pSTAT3 levels compared with WT myotubes, indicating that alpha7beta1 can act as a negat

201 erent responses on lipid metabolism in human myotubes, indicating that the two enzymes play distinct

202 ost-differentiation myocytes and post-fusion myotubes, is unknown.

203 Interestingly, myotubes lacking integrin alpha7beta1, a laminin-recepto

204 with FN, myogenic index, myotube width, and myotube length on mumolded gelatin hydrogels was similar

205 arge number of clusters, proportional to the myotube length, with a small average number of nuclei pe

206 ent and differentiation, myocyte fusion, and myotube maturation.

207 and cell-cycle exit, to myoblast fusion and myotubes maturation.

208 ucose modulating effect of CO-EtOAc using L6 myotubes model.

209 Treatment with mdivi-1 did not alter myotube morphology, but did increase the mitochondrial t

210 brid muscle is similar to that of the single myotube movement, but has faster relaxation kinetics bec

211 the present study show that at the level of myotubes MTM1 mutations do not dramatically affect calci

212 subjects, rIL-15 increased the thickness of myotubes (MTT) from both age groups to a similar extent.

213 e the transcriptome profiles of myoblast and myotube nuclei are relatively homogeneous, MNC nuclei ex

214 ts pericentriolar material to the surface of myotube nuclei, where it nucleates microtubules to ensur

215 umbers were not altered in Mb-overexpressing myotubes, O2 consumption was greater in these myotubes t

216 moval of a duplication of DMD exons 18-30 in myotubes of an individual affected by DMD produced full-

217 on, PGC1alpha content, and insulin action in myotubes of both the lean and severely obese subjects.

218 These data reveal that myotubes of severely obese individuals enhance insulin a

219 Silencing p300 in myotubes or overexpressing a dominant negative p300 muta

220 Interestingly, skeletal myotubes over-expressing MG53 or PRY-SPRY display a redu

221 In myotubes, over-expression of mDia1DeltaN3, a RhoA-indepe

222 0 provoked rapid acetylation of C/EBPbeta in myotubes, particularly at its Lys39 residue.

223 genistein, each rescued the hypotrophic FSHD myotube phenotype.

224 L is demonstrated in both single-channel and myotube preparations.

225 y reduced and forced GBE expression in C2C12 myotubes promoted glucose uptake.

226 us abnormalities in cultured HACD1-deficient myotubes provide additional evidence that these defects

227 erestingly, inhibition of ER stress in C2C12 myotubes reduces food deprivation-induced expression of

228 Hyperammonaemia in C2C12 myotubes resulted in impaired intact cell respiration, r

229 Knocking down DAPIT in skeletal myotubes resulted in reduced ATP synthesis and myogenic

230 nd demonstrate that Notch1 activity improves myotube's function as a stem cell niche.

231 two smaller clusters to spreading along the myotube's length.

232 This, coupled with our observation that myotubes secrete IL-15 in response to TNFalpha stimulati

233 In cultured human myotubes, siRNA inhibition of FN14 increased expression

234 ryanodine receptor 1, though they do affect myotube size and nuclear content.

235 , blockade of PDK4 was sufficient to restore myotube size in C2C12 cultures exposed to tumor media.

236 tivation of the Akt pathway and increases in myotube size, in type IIb fiber hypertrophy, and ultimat

237 Differentiated murine C2C12 myotubes, skeletal muscle from pair-fed or ethanol-treat

238 termined that alphaLNNd expression increased myotube surface accumulation of polymerization-deficient

239 and regeneration were evaluated based on the myotube surface area as well as gene and cytokine profil

240 yotubes, O2 consumption was greater in these myotubes than that in mock cells (Mock vs. Mb-Flag::GFP:

241 model of nuclear protein transport within a myotube that recapitulates the results of our in vitro e

242 e used a mosaic transfection model to create myotubes that contained exactly one myonucleus expressin

243 ring differentiation of C2C12 myoblasts into myotubes, the apo-Mb-hsp90 complex associates with 5 cel

244 In Stac3 KO myotubes, there was reduced, but still substantial CaV1.

245 Like the cultured myotubes, these tissues accumulated ceramides but not SM

246 have been shown to promote ATP release from myotubes through an unknown mechanism.

247 dynamics and signaling in embryonic skeletal myotubes through fluorescent Ca(2+) imaging and measurem

248 augments myoblast adhesion to myoblasts and myotubes through homophilic trans-interactions.

249 TG storage and mitochondrial maintenance in myotubes through inhibition of the cAMP pathway by activ

250 Exposure of myotubes to chronically elevated IL-6 further increased

251 Exposure of cultured myotubes to CKD serum resulted in myotube atrophy and el

252 died on RYR1 single-channel currents and HET myotubes to define molecular mechanisms of gene-by-envir

253 PGC1alpha knock-down caused hypotrophic myotubes to form from control myoblasts.

254 Acute exposure of myotubes to IL-6 increased the mitochondrial reactive ox

255 ffectively transmits the forces generated by myotubes to the load.

256 was tested as a signaling molecule in C2C12 myotubes to understand the mechanism.

257 sis, and molecular responses in C2C12 murine myotubes to withdrawal of ammonium acetate following 24-

258 xpression was independent of the myoblast-to-myotube transition.

259 tasis in atrophying myotubes, whereas normal myotubes treated with AMD3100 showed time- and dose-depe

260 Similarly, atrophying myotubes treated with either SDF1alpha or SDF1beta had g

261 ATP synthase inhibition in myotubes triggers the ISR via a distinct mechanism relat

262 myogenic differentiation in vitro, resulting myotubes typically display an embryonic identity.

263 Nascent myotubes undergo a dramatic morphological transformation

264 cell-conditioned medium (LCM)-treated C2C12 myotubes underwent a rapid catabolic response in a TLR4-

265 Mechanistically, Notch1 activation in myotubes upregulates the expression of Notch ligands, wh

266 as successfully conducted in C57BL/6 primary myotubes using phosphorodiamidate morpholino oligomer or

267 se obesity-induced effects in cultured C2C12 myotubes, using BSA-conjugated palmitate to increase syn

268 In myotubes, UT attenuated the ability of FFAs to induce in

269 ological agents reverted cancer cell-induced myotube wasting in culture conditions and mouse models.

270 In cultured myotubes, we determined that alphaLNNd expression increa

271 Using mouse myotubes, we found that either pharmacological inhibitio

272 Although myotubes were 19% thinner in cultures derived from elder

273 , additional studies in differentiated C2C12 myotubes were conducted after subjecting to media contai

274 yotubes and the functional properties of the myotubes were examined using cell physiological and bioc

275 INS-1 pancreatic beta-cells, or C2C12 mouse myotubes were incubated in standard tissue culture media

276 Robust contractions were observed when mouse myotubes were stimulated by ACh, with twitch duration an

277 yotube hypertrophy in vitro Primary skeletal myotubes were treated with IGF-1 (50 ng/ml) with or with

278 C2C12 myotubes were treated with the PKC/D1 activator phorbol

279 eted by tumor cells accelerates autophagy in myotubes when complexed with soluble IL-6 receptor (tran

280 Fused myotubes, when cocultured with MNs, were able to form ev

281 la, this pattern is established in embryonic myotubes, where myonuclei move via microtubules (MTs) an

282 not affect protein homeostasis in atrophying myotubes, whereas normal myotubes treated with AMD3100 s

283 re obtained following ACSL6 knockdown in rat myotubes, which was associated with a decreased accumula

284 d of PDMS muprinted with FN, myogenic index, myotube width, and myotube length on mumolded gelatin hy

285 eight and nuclear import rate, as well as on myotube width.

286 Treatment of myotubes with 0.5 mmol/L palmitate for 4 h, but not with

287 The model predicts that, in longer mammalian myotubes with a large number of nuclei, the spreading st

288 Treatment of C2C12 myotubes with ADMA impaired protein synthesis and reduce

289 ST markers were quantified in C2C12 myotubes with EGF-neutralizing antibody, EGFR inhibitor

290 en whose combinatorial treatment resulted in myotubes with enhanced maturation, as shown by the expre

291 ndrial physiology, we treated differentiated myotubes with exogenous IL-6 to evaluate the dose- and d

292 e recapitulated in vitro by incubating C2C12 myotubes with high-Pi media.

293 such coculture models have randomly oriented myotubes with immature synapses that contract asynchrono

294 Permeabilized C2C12 myotubes with knocked-down ANT1 exhibited higher calcium

295 artial or complete lack of ANT1 and in C2C12 myotubes with knocked-down ANT1 expression.

296 Short-term treatments of myotubes with palmitate, a ceramide precursor, or direct

297 onal regulation was also perturbed in IR-Mut myotubes with reduced insulin-stimulated expression of m

298 ve myogenic differentiation, forming smaller myotubes with reduced myosin content.

299 ssed genes in Zbed6(-/-) and Igf2(DeltaGGCT) myotubes, with an enrichment of upregulated genes involv

300 er cell-induced muscle protein loss in C2C12 myotubes without suppressing p38alpha MAPK-dependent myo