ライフサイエンスコーパス: myoblast

1 and cytoplasmic Qk6, are regulated in mouse myoblasts.

2 fibroblasts, and in primary mouse and human myoblasts.

3 le on the cell membranes of rapsyn-deficient myoblasts.

4 trol over antioxidant fluxes in H9c2 cardiac myoblasts.

5 ellular antigen-1-positive granules in C2C12 myoblasts.

6 o stress-inducing conditions in H9c2 cardiac myoblasts.

7 e week after initiating differentiation from myoblasts.

8 ring myogenic progression in mouse and human myoblasts.

9 murine myoblasts and in FSHD patient-derived myoblasts.

10 tes in the inhibition of SG formation in DM1 myoblasts.

11 cation between NG2(+) interstitial cells and myoblasts.

12 cavities before the migration of the somitic myoblasts.

13 tant versions of myomaker were mixed with WT myoblasts.

14 partner gene Tcap was validated in cultured myoblasts.

15 ve and active mechanical properties of C2C12 myoblasts.

16 ut also tracheal epithelial cells, and C2C12 myoblasts.

17 ng negatively regulates Dl expression in the myoblasts.

18 ted by TPE-OLD-dependent variegation in FSHD myoblasts.

19 EBPbeta turnover is a major role for Mdm2 in myoblasts.

20 re than 10-fold in myotubes versus levels in myoblasts.

21 ake by L6 myotubes and neonatal rat skeletal myoblasts.

22 by hypoxia in satellite cell-derived primary myoblasts.

23 ed by RNA-sequencing on FSHD patient-derived myoblasts.

24 gnaling and for a signal relay system in the myoblasts.

25 esistant rats and TNF-alpha exposed cultured myoblasts.

26 ssed the myogenic capacity of human skeletal myoblasts.

27 a serine/threonine kinase, in proliferating myoblasts.

28 d GFPT1 expression levels in patient-derived myoblasts.

29 ribute to cellular ATP production in control myoblasts.

30 ion by depleting individual MEF2 proteins in myoblasts.

31 iated lamellipodia, spreading, and fusion of myoblasts.

32 hatidylserine receptors to promote fusion of myoblasts.

33 ng factors, followed by differentiation into myoblasts.

34 provide evidence that p.D399Y stiffens mouse myoblasts.

35 hanges are still incomplete when compared to myoblasts.

36 e determination of these indices using C2C12 myoblasts.

37 erentiated cells compared to fibroblasts and myoblasts.

38 We conclude that ICAM-1 augments myoblast adhesion and fusion through its ability to self

39 ICAM-1 mediated myoblast adhesion and fusion were quantified using novel

40 We report that ICAM-1 augments myoblast adhesion to myoblasts and myotubes through homo

41 und that while the transcriptome profiles of myoblast and myotube nuclei are relatively homogeneous,

42 ction of all the known and candidate KDMs in myoblast and osteoblast differentiation using the C2C12

43 L-6) stimulation in HepG2 hepatocytes, C2C12 myoblasts and 3T3-L1 adipocytes and casein injection in

44 In vitro, PDGF-BB attracted myoblasts and activated their proliferation.

45 We used cultured mammalian myoblasts and an RNA interference library targeting 571

46 ween quiescent/proliferating/differentiating myoblasts and by maintaining the differentiation process

47 ly released by differentiating human primary myoblasts and C2C12 cultures, chemical induction of apop

48 e to impede differentiation in proliferating myoblasts and carried out mechanistic studies to show th

49 cell type-specific manner in fibroblasts and myoblasts and conferred an additional 28 +/- 1.5 and 3.4

50 ch do not constitutively express ICAM-1, and myoblasts and fibroblasts forced to express full length

51 t mAgrin enhances laminin binding to primary myoblasts and fibroblasts from an FKRP mutant mouse mode

52 Hypotheses were tested using cultured myoblasts and fibroblasts, which do not constitutively e

53 to be necessary for the survival of skeletal myoblasts and for the efficient formation of intact myot

54 tify target genes, we over-expressed DUX4 in myoblasts and found that the receptor tyrosine kinase Re

55 roliferation and differentiation of cultured myoblasts and impairs the regeneration of injured muscle

56 fferentiation in both DUX4-expressing murine myoblasts and in FSHD patient-derived myoblasts.

57 yoblast proliferation, expanding the pool of myoblasts and leading to increased myoblast fusion.

58 rt that ICAM-1 augments myoblast adhesion to myoblasts and myotubes through homophilic trans-interact

59 s are stored in macrophages and delivered to myoblasts and newly formed myotubes.

60 enters macrophages, actively differentiating myoblasts and newly forming myotubes.

61 age commitment to a differentiating state in myoblasts and offer a useful resource for others studyin

62 ith our previous study of STK25 knockdown in myoblasts and reciprocal to the metabolic phenotype of S

63 ncRNAs were identified that are expressed in myoblasts and regulated during differentiation.

64 NC that is induced during differentiation of myoblasts and whose knockdown decreases differentiation,

65 ty was solely activated in Mb-overexpressing myoblasts, and complex IV activity was decreased in the

66 yotubes differentiated from C2C12 or primary myoblasts, and conversely, its inhibition attenuates atr

67 in myoblasts, doxycycline-inducible DUX4 in myoblasts, and differentiated human FSHD myocytes expres

68 y or late stages of differentiation on C2C12 myoblasts, and primary satellite cells from mouse and hu

69 We hypothesized that DMD myoblasts are less sensitive to cues in the extracellula

70 Myoblasts are precursor skeletal muscle cells that diffe

71 tellite cells and activated satellite cells (myoblasts) are poorly understood.

72 levels of active Rac in adherent and fusing myoblasts, as well as triggered lamellipodia, spreading,

73 We then compared snRNA-seq of myoblasts before and after differentiation.

74 and indicate elastase-mediated regulation of myoblast behaviour as a potential mechanism underlying l

75 Abl2 acts in myoblasts, but as a consequence of expansion of the diap

76 n vivo proteins present only in transplanted myoblasts, but not in host tissue, and proteins exclusiv

77 aker in fibroblasts drives their fusion with myoblasts, but not with other myomaker-expressing fibrob

78 A.Z in the growth and differentiation of the myoblast C2C12 cell line.

79 Low RS concentration (10 muM) stimulated myoblast cell cycle arrest, migration and sprouting, whi

80 along with phenotypic data on adipocyte and myoblast cell differentiation assays.

81 We generated a myoblast cell line expressing a dual tdTomato:GFP constr

82 tream of MET and acts as a potent inducer of myoblast cell migration.

83 rinted platform is tested using C2C12 murine myoblasts cell line.

84 roliferation and inhibits differentiation of myoblast cells by attenuating function of miR-30c.

85 nd that GFPT1 protein levels were reduced in myoblast cells of the patients carrying this variant.

86 ilar range of motion within the cytoplasm of myoblast cells regardless of size.

87 proliferation and inhibit differentiation of myoblast cells, whereas miR-30c targets the 3'-UTR of Tn

88 ratus and organization of F-actin bundles in myoblast cells.

89 ouring differentiated cells through a draper-myoblast city-Rac1-basket (also known as JNK)-dependent

90 Myoblast clones with CRISPR/Cas9-mediated knockout of C3

91 roenvironment compared with unconditioned or myoblast containing matrices.

92 extravasation rates of cancer cells into the myoblast-containing matrices compared with untreated cel

93 ly 60% of myotubes formed from Stac3-deleted myoblasts contracted (P = 0.05).

94 ne, over 90% of myotubes formed from control myoblasts contracted, but only 60% of myotubes formed fr

95 We use human primary myoblast culture and in vivo murine models to establish

96 ide generation rates captured from monolayer myoblast cultures containing about 4x10(4) cells, varied

97 Wg) from the disc, and Delta (Dl)-containing myoblast cytonemes contribute to Notch activation in the

98 Frizzled (Fz)-containing myoblast cytonemes take up Wingless (Wg) from the disc,

99 Ascl2 knockout in embryonic myoblasts decreases both the number of Pax7(+) cells and

100 crest (CNC) cells are in direct contact with myoblasts derived from the pharyngeal mesoderm, and Dlx5

101 , highlighting the requirement of additional myoblast-derived factors for fusion.

102 ow that co-culture of these cells with human myoblast-derived skeletal muscle builds a functional all

103 3 complex specifically functions by blocking myoblast determination protein 1 (MYOD1)-mediated activa

104 in activity was also crucial during terminal myoblast differentiation and aggregation of acetylcholin

105 n-1 mutants in C2C12 cells caused defects in myoblast differentiation and fusion associated with dysr

106 We show that bexarotene promotes myoblast differentiation and fusion through the activati

107 It has been shown to regulate myoblast differentiation and has also been implicated in

108 Applying TASIC to in vitro myoblast differentiation and in-vivo lung development da

109 Myomixer expression coincides with myoblast differentiation and is essential for fusion and

110 lated and translocated to the nucleus during myoblast differentiation and plays a key role in myogene

111 The nuclear receptor REV-ERB suppresses myoblast differentiation and recently we have demonstrat

112 mall interfering RNA (siRNA) of MUNC reduced myoblast differentiation and specifically reduced the as

113 ed differences in FSHD by protecting against myoblast differentiation impairments in this disease.

114 cise-induced myoinjury, and concomitant with myoblast differentiation in culture.

115 ify Pak1 and Pak2 as redundant regulators of myoblast differentiation in vitro and in vivo and as com

116 , inhibition of MSTN activity, and increased myoblast differentiation in vitro Unexpectedly, a marked

117 , MYF5 is implicated in the initial steps of myoblast differentiation into myotubes.

118 that 4.1R expression increases during C2C12 myoblast differentiation into myotubes.

119 enome-wide DNA methylation status in a human myoblast differentiation model, where myoblasts were cul

120 nued expression of this protein inhibits the myoblast differentiation program.

121 ion of the Nup210 nucleoporin to NPCs during myoblast differentiation results in assembly of an Mef2C

122 110beta overexpression was unable to promote myoblast differentiation under conditions of p110alpha i

123 ng of BRD4 to the Myog promoter during C2C12 myoblast differentiation, co-incident with increased lev

124 entified 55 kinases whose knockdown promoted myoblast differentiation, either independently or in con

125 Our findings suggest that, during myoblast differentiation, Pask stimulates the conversion

126 ID subunits and TBP are downregulated during myoblast differentiation, reduced amounts of these prote

127 During myoblast differentiation, we observed that the levels an

128 transmit bexarotene action in the context of myoblast differentiation.

129 selective signaling to promote and to retain myoblast differentiation.

130 2A.Z-Ac-mut) resulted in a complete block of myoblast differentiation.

131 and the expression of myogenic genes during myoblast differentiation.

132 ene and is directly activated by MyoD during myoblast differentiation.

133 e PyV ST, it also has the ability to inhibit myoblast differentiation.

134 Pak1 and Pak2 are activated during mammalian myoblast differentiation.

135 DM1 myoblasts display increased expression and sequestration

136 of FSHD-lentiviral-based DUX4 expression in myoblasts, doxycycline-inducible DUX4 in myoblasts, and

137 tal muscle fibers form through the fusion of myoblasts during development and regeneration.

138 ced muscle repair due to a reduced number of myoblasts during regeneration.

139 dish models by inducing both mouse and human myoblast durotaxis to stripes where they aligned, differ

140 Following gene editing in DMD patient myoblasts, dystrophin expression is restored in vitro.

141 f Nur77 on IGF1 was recapitulated in primary myoblasts, establishing this as a cell-autonomous effect

142 yofibers confirmed that HIF1alpha/2alpha dKO myoblasts exhibit reduced self-renewal but more pronounc

143 croscopy, we studied the elasticity of mouse myoblasts expressing a mutant form of the gene encoding

144 Primary myoblasts expressing the shMdm2 construct were unable to

145 Moreover, we discovered that DM1 myoblasts fail to properly form SGs in response to arsen

146 nal behavior, as engineered tongues from DMD myoblasts failed to achieve the same contractile strengt

147 bes differentiated from C2C12 mouse skeletal myoblasts for three weeks by utilizing micromolded (mumo

148 d nanonet platform for measuring C2C12 mouse myoblast forces attached to fibers of three diameters (2

149 On this platform, DMD myoblasts formed fewer and smaller myotubes and exhibite

150 etic regulatory cascades selectively specify myoblasts from a pool of naive mesodermal progenitors.

151 Myoblasts from Megf10-/- mice and Megf10-/-/mdx double k

152 ession of this gene is altered by TPE-OLD in myoblasts from patients affected with the age-associated

153 ired proliferation and migration compared to myoblasts from wild type and mdx mice, whereas the dko m

154 Megf10 regulation of myoblast function appears to be mediated at least in par

155 During skeletal muscle development, myoblasts fuse to form multinucleated myofibers.

156 es to the plasma membrane, where it promotes myoblast fusion and associates with Myomaker, a fusogeni

157 lular components and mechanisms that control myoblast fusion and muscle formation.

158 ss-of-function screen for genes required for myoblast fusion and myogenesis, we discovered an 84-amin

159 uscle-specific protein that is essential for myoblast fusion and sufficient to promote fusion of fibr

160 Our study shows that MyD88 modulates myoblast fusion and suggests that augmenting its levels

161 alized isoform of USP19 (USP19-ER) modulated myoblast fusion as well as the expression of myogenin an

162 apsigargin was able to reverse the defect in myoblast fusion caused by the overexpression of USP19-ER

163 usly expressed and specifically required for myoblast fusion in Drosophila We report that both Pak1 a

164 cytoskeleton and actin-based protrusions for myoblast fusion in mammals and its requirement to achiev

165 ixer using CRISPR/Cas9 mutagenesis abolishes myoblast fusion in vivo.

166 Myoblast fusion is an indispensable step for skeletal mu

167 cardiotoxin injury and suffer from defective myoblast fusion necessary for the proper repair and rege

168 ikely to represent general principles of the myoblast fusion process.

169 findings identify myomerger as a fundamental myoblast fusion protein and establish a system that begi

170 These data reveal that myoblast fusion requires myomaker activity at the plasma

171 ibition of WNT/beta-catenin signaling blocks myoblast fusion through the inhibition of the Fermitin f

172 nserved plasma membrane protein required for myoblast fusion to form multinucleated myotubes in mouse

173 uring zebrafish embryogenesis coincides with myoblast fusion, and genetic deletion of myomixer using

174 of myogenesis, including cell proliferation, myoblast fusion, and homeostasis, by targeting step-spec

175 scle specific membrane protein essential for myoblast fusion, is activated mainly in muscle progenito

176 specific transmembrane protein necessary for myoblast fusion, is sufficient to fuse 10T 1/2 fibroblas

177 ogenesis, such as myoblast specification and myoblast fusion, the molecules that regulate myotube elo

178 provide insights into the molecular basis of myoblast fusion.

179 utonomous role of MyD88 in the regulation of myoblast fusion.

180 attributed to deficient SC proliferation and myoblast fusion.

181 c) is a muscle-specific protein required for myoblast fusion.

182 additional sarcomeric RNAs, and by promoting myoblast fusion.

183 tein X), which promotes and is necessary for myoblast fusion.

184 e pool of myoblasts and leading to increased myoblast fusion.

185 I hinders myogenic development by repressing myoblast fusion.

186 low for the induction of factors crucial for myoblast fusion.

187 ration were also impaired due to a defect of myoblast fusion.

188 fibroblast-fibroblast fusion and fibroblast-myoblast fusion.

189 er and myomixer cooperate to drive mammalian myoblast fusion.

190 f elastase on satellite cell-derived primary myoblast growth and differentiation is substrate-indepen

191 Indeed, TrxR1 depletion reduces myoblasts growth by inducing an early myogenesis -relate

192 However, Myf5 is not restricted to committed myoblasts in embryos but is also expressed in multipoten

193 ased engraftment and differentiation of FSHD myoblasts in regenerating mouse muscle.

194 liferation and suppresses differentiation of myoblasts in skeletal muscle development by attenuating

195 nly NDRG2 accumulated in skeletal muscle and myoblasts in the absence of TRIM32.

196 ress muscle differentiation in proliferating myoblasts in the presence or absence of a sensitizing ag

197 is sufficient to fuse 10T 1/2 fibroblasts to myoblasts in vitro.

198 and complex IV activity was decreased in the myoblasts in which Mb expression was suppressed by Mb-si

199 In cultured myoblasts (in which AChRs are absent), myristoylated WT

200 receptors were localised in the cytoplasm in myoblasts, in the nucleus in myotubes, in the extracellu

201 egulation of complex IV activity in cultured myoblasts; in contrast, suppression of Mb expression ind

202 mRNA encoding TERT to human fibroblasts and myoblasts increases telomerase activity transiently (24-

203 bility of PAX3 to promote migration of C2C12 myoblasts indicating that BRAF directly activates PAX3.

204 Overexpressing hsp60 in cultured myoblasts induced only the expression of PGC1 1alpha, su

205 he expression of this mutant desmin in C2C12 myoblasts induces desmin network disorganization, desmin

206 Brg1 with a phosphomimetic mutant in primary myoblasts inhibits myogenesis, whereas replacement with

207 The differentiation and fusion of myoblasts into mature myotubes are complex processes res

208 uscle fibers, which arise from the fusion of myoblasts into multinucleated myotubes during myogenesis

209 proliferation as well as differentiation of myoblasts into myotubes.

210 rs differentiation of both primary and C2C12 myoblasts into myotubes.

211 ic lesions, and second, fusion of PMO-loaded myoblasts into repairing myofibers.

212 ents to understand the effects of PDGF-BB on myoblasts involved in the pathophysiology of muscular dy

213 nses similar to primary differentiated human myoblasts, IR-Mut myotubes demonstrated severe impairmen

214 rentiation are suppressed in a proliferating myoblast is much less clear.

215 EZH2 premature degradation in proliferating myoblasts is prevented by low levels of PJA1, its cytopl

216 Here, we have utilized myoblasts isolated from FSHD patients (FSHD myoblasts) t

217 Finally, myoblasts isolated from Kcne3(-/-) mice exhibit faster-i

218 inhibited myogenic differentiation in C2C12 myoblasts; (+)-JQ1, PFI-1, and Bromosporine.

219 Although cultured myoblasts lacking LAP1 demonstrated defective terminal d

220 ers the traction forces generation of single myoblasts lacking organized sarcomeres.

221 Furthermore, primary myoblasts lacking Pak1 and Pak2 display delayed expressi

222 were notoriously absent in fusion-defective myoblasts lacking Srf.

223 NDRG2 overexpression in myoblasts led to reduced cell proliferation and delayed

224 ervical carcinoma HeLa cells and mouse C2C12 myoblasts led to two surprising discoveries: (i) many ex

225 A patient myoblast line showed a severe reduction in complex I, as

226 While cells of the myoblast lineage secrete exosomes, it is not known wheth

227 ion has been added since then to resolve how myoblasts migrate to the ends of fibers.

228 elopment of newborn muscles to ensure proper myoblast migration for fiber growth.

229 NF-kappaB in NG2(+) cells promotes myoblast migration to the tips of myofibers through cell

230 rder, somite chevron morphology and hypaxial myoblast migration.

231 ng protein which associated with a subset of myoblast mRNAs.

232 Human skeletal muscle myoblasts, muscle progenitor cells and adipose-derived s

233 We find that IFM myoblast-myotube fusion proceeds in a stepwise fashion a

234 asts did not augment their fusion to ICAM-1+ myoblasts/myotubes.

235 Immunoblotting from fibroblasts and myoblasts of an affected Scottish patient showed normal

236 Here we have developed a myoblast optical reporter system with the purpose of ide

237 In cultured H9c2 myoblasts, pharmacological inhibition of cathepsin K, or

238 In fibroblasts and myoblasts polarizing for migration, retrograde actin flo

239 ld myoblasts, SMAD4 levels increased in this myoblast population.

240 cle growth results from nuclear accretion of myoblasts preferentially at the tips of myofibers.

241 tin-remodeling enzymes, is required for both myoblast proliferation and differentiation, and the cont

242 le-specific microRNAs (miRNAs) that regulate myoblast proliferation and differentiation.

243 ling in Smad7(-/-) muscle results in reduced myoblast proliferation and differentiation.

244 eletal muscle, multiple pathways involved in myoblast proliferation and fusion into myotubes are misr

245 2 and TRIM72, due to their putative roles in myoblast proliferation and myogenesis.

246 2-mediated phosphorylation of Brg1 regulates myoblast proliferation and provides insight into one mec

247 CND1 expression while silencing MYF5 reduced myoblast proliferation as well as differentiation of myo

248 reased myofiber length is caused by enhanced myoblast proliferation, expanding the pool of myoblasts

249 knockdown of CD82 in myogenic cells reduces myoblast proliferation, suggesting it is functionally in

250 n of a key transcription factor required for myoblast proliferation, was in an inaccessible chromatin

251 expression of either RET9 or RET51 increased myoblast proliferation, whereas siRNA-mediated knockdown

252 pharmacological inhibition of CK2 increased myoblast proliferation.

253 myoblasts with long telomeres or in healthy myoblasts regardless of telomere length.

254 RS-doses augmented the H2O2-induced impaired myoblast regeneration and mitochondrial dehydrogenase ac

255 rect lineage conversion from chondrocytes to myoblast represents a novel non-viral Method to convert

256 portance, down-regulation of Staufen1 in DM1 myoblasts rescues SG formation.

257 y expressed in pre- and post-differentiation myoblasts, respectively.

258 cilitating reprogramming of fibroblasts into myoblasts, respectively.

259 rated with the MyoD(Cre) system in embryonic myoblasts resulted in apparently normal muscle developme

260 Silencing MYF5 expression in proliferating myoblasts revealed that MYF5 promoted CCND1 translation

261 , and gamma-actin isoforms in SPARC knockout myoblasts reveals a changed expression pattern with domi

262 eeping with the low levels of miR-431 in old myoblasts, SMAD4 levels increased in this myoblast popul

263 e well-studied events of myogenesis, such as myoblast specification and myoblast fusion, the molecule

264 ote the proliferation and differentiation of myoblast stem cells.

265 in dystrophic (mdx(4cv)) muscle and impairs myoblast survival in culture.

266 epatocarcinoma Huh7 cells and to C2C12 mouse myoblasts that differentiated into myotubes.

267 Although BRG1-deleted myoblasts that ectopically express the SA-Brg1 mutant pr

268 ining 78+/-3% could be achieved in the C2C12 myoblasts that had undergone transposition.

269 ubpopulation of Pax7(+) MyoD(+) progenitors (myoblasts) that become Pax7(+) MyoD(-) satellite cells p

270 rubicin-induced premature senescence in H9C2 myoblasts, the effect was ablated by MIF replenishment.

271 localize to the plasma membrane in cultured myoblasts, the protein also resides in the Golgi and pos

272 erentiation in C2C12 cells and primary human myoblasts through an Akt-dependent mechanism, while expr

273 gered lamellipodia, spreading, and fusion of myoblasts through the signaling function of the cytoplas

274 ng conversions, from B cells to macrophages, myoblasts to adipocytes, and human fibroblasts to neuron

275 action partners are required for adhesion of myoblasts to extracellular matrix, and for the formation

276 al muscle formation occurs through fusion of myoblasts to form multinucleated myofibers.

277 e formation requires fusion of mononucleated myoblasts to form multinucleated myofibers.

278 overexpression promotes fusion of exogenous myoblasts to injured myofibers.

279 ortalized heterozygous R349P desmin knock-in myoblasts to magnetic tweezer experiments that revealed

280 myoblasts isolated from FSHD patients (FSHD myoblasts) to investigate the effect of estrogens on mus

281 itochondrial respiration was up-regulated in myoblasts transiently overexpressing Mb; complex IV acti

282 owever, we found that, in quiescent (G0) rat myoblasts transiting to the G1 phase, cyclin D1 (Ccnd1)

283 esult, both inhibitors rescued myogenesis in myoblasts treated with GDF8.

284 In C2C12 myoblasts, two of them improved mitochondrial density an

285 Using immortalized human myoblasts, we performed RNA-seq analysis of single cells

286 Using C2C12 myoblasts, we show that over-expression of NKX2-5 or mut

287 human myoblast differentiation model, where myoblasts were cultured in low-serum medium to stimulate

288 Myoblasts were differentiated for 8 d, with or without t

289 or by restoring dystrophin expression in DMD myoblasts, where dystrophin was expressed at the sarcole

290 d promotes myogenic induction of C2C12 mouse myoblasts, whereas depletion of RanBP3L expression enhan

291 liferation and restrained differentiation of myoblasts; whereas inhibition of AK017368 had completely

292 pound 53 improves delayed myogenesis in CDM1 myoblasts, while compounds 1 and 53 have neuroprotective

293 iR-431 improved the myogenic capacity of old myoblasts, while inhibiting endogenous miR-431 lowered m

294 Using immortalized human myoblasts with a titratable DUX4 transgene, we identify

295 hort telomeres, while not detectable in FSHD myoblasts with long telomeres or in healthy myoblasts re

296 Co-incubation of differentiating myoblasts with rIL-15 and rTNFalpha, limited the reducti

297 SORBS2 is expressed in FSHD myoblasts with short telomeres, while not detectable in

298 eract the differentiation impairment of FSHD myoblasts without affecting cell proliferation or surviv

299 Deletion of MyD88 impairs fusion of myoblasts without affecting their survival, proliferatio

300 g microdystrophins were transfected in C2C12 myoblasts, yielding 65+/-2% MD1 and 66+/-2% MD2 expressi