ライフサイエンスコーパス: myotube

1 even spacing of nuclei within the developing myotube.

2 itial steps of myoblast differentiation into myotubes.

3 s during C2C12 myoblast differentiation into myotubes.

4 on and promotes mitochondrial maintenance in myotubes.

5 muprinted PDMS precluded robust detection of myotubes.

6 er repair and regeneration of multinucleated myotubes.

7 ing very large, multinucleated cells such as myotubes.

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

9 mitochondrial oxidative function in cultured myotubes.

10 as well as differentiation of myoblasts into myotubes.

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

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

13 ts and for the efficient formation of intact myotubes.

14 ion of both primary and C2C12 myoblasts into myotubes.

15 ion, proliferation, and differentiation into myotubes.

16 hat differentiate into fused, multinucleated myotubes.

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

18 in mononucleated myocytes and multinucleated myotubes.

19 localized in the plasma membrane of skeletal myotubes.

20 expression in differentiated multinucleated myotubes.

21 e T241 is correlated with differentiation to myotubes.

22 te nuclei throughout the length of syncytial myotubes.

23 for STAT reporter activation and atrophy in myotubes.

24 ation, STAT3 phosphorylation, and atrophy in myotubes.

25 in how kinesin-1 functions to move nuclei in myotubes.

26 differentiating myoblasts and newly forming myotubes.

27 K and stimulated lipid oxidation in cultured myotubes.

28 r (AChR) clusters on the surface of cultured myotubes.

29 ial for Tm2 protein expression in developing myotubes.

30 sufficient to activate the STAT reporter in myotubes.

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

32 pport for the polarisation and elongation of myotubes.

33 cleation from the NE on nuclear spreading in myotubes.

34 myogenic differentiation into multinucleated myotubes.

35 tion of the C2C12 cells and the formation of myotubes.

36 blasts to within a minimal distance from the myotubes.

37 cells but not in 3T3-L1 adipocytes or C2C12 myotubes.

38 WEAK induced atrophy in C2C12 differentiated myotubes.

39 of alpha-actinin at the PM of differentiated myotubes.

40 kinase inhibitor, were decreased in affected myotubes.

41 liferation but inhibits differentiation into myotubes.

42 pathways to trigger glucose uptake in C2C12 myotubes.

43 by respiratory chain inhibition in cultured myotubes.

44 cycle markers were induced in Abeta-bearing myotubes.

45 sured in muscle tissue as well as in primary myotubes.

46 ermeabilized myofibers as well as in primary myotubes.

47 localization of OGT in C2C12 skeletal muscle myotubes.

48 n vivo differences would be preserved in the myotubes.

49 t agrin-induced clusters in C2C12 or primary myotubes.

50 C12 mouse myoblasts that differentiated into myotubes.

51 tal muscular dystrophy type 1A myoblasts and myotubes.

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

53 ation were studied in cultured human primary myotubes.

54 ins and acetylation of Lys-9 on histone 3 in myotubes.

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

56 associated splicing abnormalities in patient myotubes.

57 A-mediated clock disruption in human primary myotubes.

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

59 h compounds disrupted the function of intact myotubes.

60 esprin-1alpha is increased in differentiated myotubes.

61 /- 2% vs. IGF-1; P < 0.001) in IGF-1-treated myotubes.

62 4 inhibitor, increased FAO rates in MEFs and myotubes.

63 ) and impaired ability to differentiate into myotubes.

64 and delivered to myoblasts and newly formed myotubes.

65 ed, differentiated, and fused into patterned myotubes.

66 ion of UPR causes severe atrophy in cultured myotubes.

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

68 ificantly following ASO treatment in patient myotubes.

69 and analyzed separately from multi-nucleated myotubes.

70 mRNA expression in both mouse SkM and C2C12 myotubes.

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

72 In human myotubes, ACSL6 overexpression reduced palmitate oxidati

73 e administration of nitrite to human primary myotubes acutely inhibited respiration.

74 nuclei after 5 days and formed similar-sized myotubes after 7 days.

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

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

77 ramides antagonize insulin signaling in both myotubes and adipocytes, whereas glucosyceramides are on

78 he insulin receptor (IR-Mut) into functional myotubes and characterizing their response to insulin in

79 nuclear factor-kappaB (NF-kappaB) pathway in myotubes and elevated cytokine expression, but the monoc

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

81 GDNF content in myotubes and GDNF in conditioned culture medium were qua

82 active oxygen species production in cultured myotubes and improved insulin-stimulated glucose uptake

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

84 a dominant negative Stat3Cbeta-EGFP gene in myotubes and in mouse muscle blocked the atrophy caused

85 us AChR beta-subunit transcripts in cultured myotubes and in vivo, and this binding is increased in d

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

87 dramatically up-regulated in differentiating myotubes and is essential for myotube formation.

88 her MTX promotes AMPK activation in cultured myotubes and isolated skeletal muscle.

89 tures, we investigated the crosstalk between myotubes and monocytes exposed to physiological levels o

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

91 ated insulin stimulated glucose uptake by L6 myotubes and neonatal rat skeletal myoblasts.

92 ate that the nucleus is a kinesin-1 cargo in myotubes and that nesprins function as nuclear cargo ada

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

94 Using a three-dimensional coculture of human myotubes and VAT adipocytes, we showed the decreased exp

95 The myofiber precursor is the nascent myotube, and during myogenesis the myotube completes gui

96 cation in the unique shared cytoplasm of the myotube, and FSHD cell death that depends on its activat

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

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

99 activity and nuclear localization of OGT in myotubes, and phospho-mimetic T444E-OGT exhibits altered

100 saturated fatty acid-induced inflammation in myotubes, and point to nucleotides as possible mediators

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

102 d by extensive cytopathic damage with marked myotube apoptosis (widespread microscopic blebs, caspase

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

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

105 severely deficient in their ability to form myotubes as compared with myogenic progenitor cells from

106 pathological phenotypes in plectin-deficient myotubes as well as in plectin-deficient mice.

107 orter activation, STAT3 phosphorylation, and myotube atrophy but blocking antibodies to IL-6 or OSM d

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

109 ading to an increase in MuRF1 expression and myotube atrophy.

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

111 tor Egr3 is induced in Ia-afferent contacted myotubes by Neuregulin1 (Nrg1)/ErbB receptor signaling a

112 Formation of multinucleate myotubes by SMN-deficient muscle cells is inhibited at a

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

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

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

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

117 Myotubes, characterized by myofibril development and bot

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

119 e nascent myotube, and during myogenesis the myotube completes guided elongation to reach its target

120 Further studies in C2C12 myotubes confirmed a direct effect of acipimox on NAD(+)

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

122 lin action were recapitulated in Parkin-null myotubes, confirming a role for the HSP72-Parkin axis in

123 ed the expression of contractile proteins in myotubes, consequently inducing atrophy.

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

125 To examine this, we used myotubes cultured on agrin patches that induce AChR clus

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

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

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

129 Cardiomyocytes and skeletal muscle myotubes derived from reframed hiPSC clonal lines had re

130 Plectin-deficient myotubes, derived from myoblasts, were fully functional

131 CaV1.1 is quantitatively similar to that in myotubes, despite the absence of RyR1.

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

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

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

135 Myotube diameter, protein synthesis, and molecular respo

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

137 STAT signaling inhibition in LLC-treated myotubes did not attenuate the induction of p38 or AMPK

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

139 acetylcholine receptors (AChRs) in cultured myotubes differentiated ex vivo from immortalized plecti

140 we successfully maintained aligned skeletal myotubes differentiated from C2C12 mouse skeletal myobla

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

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

143 tylcholine receptor (AChR) clustering during myotube differentiation.

144 uring myogenesis induces TBP degradation and myotube differentiation.

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

146 the fusion of myoblasts into multinucleated myotubes during myogenesis.

147 potent than VAT adipocytes in inducing these myotube dysfunctions.

148 ryos are largely paralytic due to defects in myotube elongation and sarcomeric protein expression.

149 myoblast fusion, the molecules that regulate myotube elongation are largely unknown.

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

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

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

153 Cultured myotubes exposed to high CO2 had reduced fiber diameter,

154 (AMPK), a metabolic sensor, was activated in myotubes exposed to high CO2, and loss-of-function studi

155 expression and p38 phosphorylation in C2C12 myotubes exposed to LLC-treated medium was attenuated by

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

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

158 es are only efficacious in adipocytes: 1) In myotubes exposed to saturated fats, inhibitors of enzyme

159 Upon differentiation, both FSHD and healthy myotubes express SORBS2, suggesting that SORBS2 is norma

160 Both chicken and duck myotubes expressed avian and human sialic acid receptors

161 Conversely, myotubes expressing a phosphomimetic form of CLASP2 (CLA

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

163 nt study, GDNF production by skeletal muscle myotubes following treatment with acetylcholine was exam

164 FAM65B is known to be involved in myotube formation and in regulation of cell adhesion, po

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

166 ist arachidonoyl-2-chloroethylamide, prevent myotube formation in a manner antagonized by CB1 knockdo

167 oylglycerol (2-AG) are decreased both during myotube formation in vitro from murine C2C12 myoblasts a

168 ndings are consistent with a role for SMN in myotube formation through effects on muscle differentiat

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

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

171 combined knockdown almost completely blocks myotube formation.

172 ifferentiating myotubes and is essential for myotube formation.

173 sion of myogenic differentiation markers and myotube formation.

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

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

176 Using cultured skeletal myotubes from both humans and mice, we found that tomati

177 ls of GLUT4 ( approximately 50%) in cultured myotubes from C57BL6 mice.

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

179 ndifferentiated myoblasts and differentiated myotubes from mouse and human skeletal muscle cultures.

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

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

182 We find that IFM myoblast-myotube fusion proceeds in a stepwise fashion and is gov

183 In palmitate-treated C2C12 skeletal myotubes, GLP-1(32-36)amide activated AMPK and inhibited

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

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 Forced expression of GPR56 results in myotube hypertrophy through the expression of insulin-li

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

189 development, nuclei move dynamically through myotubes in a microtubule-dependent manner, driven by th

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

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

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

193 this protein in the formation/maturation of myotubes in vivo.

194 normal myotubes, unlike dyspedic (RyR1 null) myotubes in which the L-type currents have markedly acce

195 he cytoplasm in myoblasts, in the nucleus in myotubes, in the extracellular matrix, in satellite cell

196 ition, chronic NP treatment in human primary myotubes increased lipid oxidation in a PGC1alpha-depend

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

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

199 Depletion of CHC in myotubes induced a loss of actin and alpha-actinin sarco

200 idence of reentry and DNA synthesis in C2C12 myotubes induced to express beta-amyloid (Abeta42).

201 erexpression of glucosylceramide synthase in myotubes induces glucosylceramide but enhances insulin s

202 Additionally, in chicken myotubes infected with H5N1 viruses, the induction of in

203 In cultured myotubes, inhibition of ERK, but not Jun NH2-terminal ki

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

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

206 enotype by promoting F-actin assembly at the myotube leading edge, by restoring the expression of add

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

208 In cultured C2C12 myotubes, MGF increased glucose and pyruvate oxidation a

209 DOCK3 overexpression in human myotubes modulated PTEN/AKT signaling, which regulates m

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

211 pigenome profiles from human myoblasts (Mb), myotubes (Mt), muscle and diverse non-muscle samples to

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

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

214 hus, in muscles in vivo, but not in cultured myotubes, neural agrin promotes the recycling of AChRs a

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

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

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

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

219 Infected myotubes of both avian species displayed rapid virus acc

220 port activity were strongly suppressed in L6 myotubes or HeLa cells preincubated with LOA.

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

222 retained for palmitate oxidation in primary myotubes (P = 0.38); however, incorporation of FAs into

223 gated RS dose-response on C2C12 myoblast and myotube plasticity 1. in the presence and 2. absence of

224 Infected chicken myotubes produced significantly higher levels of proinfl

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 orporation between muscle tissue and primary myotubes (r = 0.848, P = 0.008).

228 current properties in dysgenic (CaV1.1-null) myotubes reconstituted with either CaV1.1a or CaV1.1e.

229 siRNA knockdown of NCX3 in MHS myotubes reduced [Ca(2+)]r and the Ca(2+) transient area

230 inetics of the L-type current in RyR1-E4242G myotubes resembled those of normal myotubes, unlike dysp

231 cs, marked upregulation of HSPs, and reduced myotube resilience following mechanical stretch.

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

233 ated throughout myocyte differentiation into myotubes, RNP immunoprecipitation (RIP) analysis indicat

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

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

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

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

238 By contrast, myotube-specific Notch1 activation improves the regenera

239 treated rats reproduced this effect in C2C12 myotubes, suggesting that toxic lung mediators were resp

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

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

242 In C2C12 myotubes, TGF-beta suppresses FNDC5 and PGC-1alpha mRNA

243 exon-skipping data, with higher activity in myotubes than in myoblasts or cardiomyocytes.

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

245 d increases AChR cluster size, compared with myotubes that express similar levels of wild type CLASP2

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

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

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

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

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

251 pression in M-ERRalphaWT muscle and in C2C12 myotubes through induction of the Esrra promoter, indica

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

253 Exposure of C2C12 cultured myotubes to either high glucose concentration, palmitate

254 used primary chicken and duck multinucleated myotubes to examine their susceptibility and innate immu

255 (Ia-afferent) innervation induces contacted myotubes to transform into intrafusal muscle fibers that

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

259 C2C12 myotubes treated with conditioned medium from C26 cancer

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

261 e expression analysis was conducted on human myotubes treated with MR agonist (aldosterone; EC50 1.3

262 Media from L6 myotubes treated with palmitate-but not palmitoleate-ind

263 ce subjected to an exercise regime and C2C12 myotubes treated with TGF-beta, a TGF-beta receptor 1 ph

264 In myotubes, UnAG consistently lowered mitochondrial ROS pr

265 lar and extracellular S1P and failed to form myotubes under conditions that normally stimulate myogen

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

267 R1-E4242G myotubes resembled those of normal myotubes, unlike dyspedic (RyR1 null) myotubes in which

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

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

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

271 As that are upregulated more than 10-fold in myotubes versus levels in myoblasts.

272 bolic insulin response and glucose uptake in myotubes via its GEF function.

273 y at agrin-induced AChR clusters in cultured myotubes via PI3 kinase acting through GSK3beta.

274 and matrix (M) gene RNA in chicken and duck myotubes was accompanied by extensive cytopathic damage

275 Increased glucose uptake in L6 myotubes was attributed to GLUT 4 translocation, the mos

276 In cultured myotubes, we determined that alphaLNNd expression increa

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

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

279 We show here that cultured chicken and duck myotubes were highly susceptible to infection with both

280 Acetylcholine receptors on myotubes were identified with labeled alpha-bungarotoxin

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

282 nd that Ia-afferent contacted Egr3-deficient myotubes were induced in normal numbers, but their devel

283 ssion and activity of pannexin-3 channels in myotubes were mediated by TLR4-NF-kappaB, and TLR4-NF-ka

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

285 fferentiated C2C12, primary mouse, and human myotubes were treated with acylcarnitines (C4:0, C14:0,

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

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

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

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

290 us ceramides antagonize insulin signaling in myotubes, whereas ganglioside precursors do not.

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

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

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

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

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

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

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

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

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

300 d nicotinic acetylcholine receptors in C2C12 myotubes with significantly higher frequency than wild t