ライフサイエンスコーパス: myoblast

1 g C2C12 myotubes but not in undifferentiated myoblasts.

2 Myf5 transcriptional activation in committed myoblasts.

3 tein was not detected in lactacystin-treated myoblasts.

4 on of p53 promotes survival of the Plk1-null myoblasts.

5 ous defect in the proliferative expansion of myoblasts.

6 ed hypotrophic myotubes to form from control myoblasts.

7 g PtdSer on sperm and BAI1/3, ELMO2, RAC1 in myoblasts.

8 d skeletal muscle differentiation from C2C12 myoblasts.

9 sed during myotube formation of murine C2C12 myoblasts.

10 n skeletal muscle cells and primary cultured myoblasts.

11 e the fusion of mouse fibroblasts with C2C12 myoblasts.

12 s odontoblasts, osteoblasts, adipocytes, and myoblasts.

13 lecular signature similar to embryonic/fetal myoblasts.

14 les, isolated myofibers and DMD immortalized myoblasts.

15 d mouse (HSA(LR)) models and patient-derived myoblasts.

16 r cells from among the broader population of myoblasts.

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

18 a serine/threonine kinase, in proliferating myoblasts.

19 iated lamellipodia, spreading, and fusion of myoblasts.

20 provide evidence that p.D399Y stiffens mouse myoblasts.

21 lncRNA that is enriched in the proliferating myoblasts.

22 hanges are still incomplete when compared to myoblasts.

23 e determination of these indices using C2C12 myoblasts.

24 erentiated cells compared to fibroblasts and myoblasts.

25 ith the Fbxl2 core promoter in proliferating myoblasts.

26 lator of optimal differentiation of skeletal myoblasts.

27 ins showing altered expression in Zbed6(-/-) myoblasts.

28 ar the tracheal air sac primordium (ASP) and myoblasts.

29 cluding mouse embryonic stem cells and mouse myoblasts.

30 r proliferation patterns in Megf10-deficient myoblasts.

31 higher expression of alpha5beta1 integrin in myoblasts.

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

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

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

35 unique trajectory of differentiation of each myoblast along the myogenic lineage complicates teasing

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

37 delicate cell cycle regulation of embryonic myoblasts and adult muscle satellite cells (MuSCs).

38 We demonstrate that skeletal muscle myoblasts and brain choroid plexus epithelial cells are

39 (R)-ginsenoside Rh(2) increased viability in myoblasts and cardiomyocytes, but not fibroblasts or dis

40 90 in Mb maturation in C2C12 skeletal muscle myoblasts and cell lines.

41 of syncytial muscle cells into mononucleate myoblasts and depends on Org-1 (Drosophila Tbx1).

42 dependent gene expression in differentiating myoblasts and determined that Cn is broadly required for

43 es skeletal muscle differentiation in normal myoblasts and ERMS.

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

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

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

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

48 ysfunction to the ISR in proliferating mouse myoblasts and in differentiated myotubes.

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

50 expressed by a population of satellite cells/myoblasts and myofibers.

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

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

53 e induced during differentiation of skeletal myoblasts and promote myogenesis in vitro.

54 Here, we use gene editing in mouse C2C12 myoblasts and show that ZBED6 regulates Igf2 exclusively

55 w here that cell fusion between immortalized myoblasts and transformed fibroblasts, through genomic i

56 n, suppressed Fbxl2 mRNA expression in C2C12 myoblasts and triggered significant alterations in cell

57 thway in both Zbed6(-/-) and Igf2(DeltaGGCT) myoblasts, and a significant enrichment of mitochondrial

58 terior compartment of the wing disc, ASP and myoblasts, and activates genes in each tissue.

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

60 tor or maintain quiescence of the nearby sex myoblasts, and developmental progression in daf-18(0) do

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

62 e have impaired muscle function and Dock3 KO myoblasts are defective for myogenic differentiation.

63 is understood in much greater detail, where myoblasts are divided into two distinct pools, founder c

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

65 Upon initiation of myogenesis from primary myoblasts, both MTF1 expression and nuclear localization

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

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

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

69 erol-mediated signalling in lipin1 deficient myoblasts by phorbol 12-myristate 13-acetate transiently

70 st identified in fibroblast (C3H/10T1/2) and myoblast (C2C12) cell lines.

71 ic flux of [U-(13)C]glucose in a mouse C2C12 myoblast cell line, TAZ-KO, which is CL-deficient becaus

72 cytosolic sensing of this nucleic acid in a myoblast cell line.

73 myodifferentiation of LHCN-M2 human skeletal myoblast cell line.

74 that hypomorphic mtFAS mutant mouse skeletal myoblast cell lines display a severe loss of electron tr

75 increased in human and mouse skeletal muscle myoblast cell lines using a single-guide RNA (sgRNA).

76 5 (12i) displayed an EC(50) of 4.3 muM in L6 myoblast cells and excellent oral bioavailability and li

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

78 ossibility by using Dox-treated H9c2 cardiac myoblast cells expressing either the mitochondria-target

79 In C2C12 mouse myoblast cells, P3 had no effect on BMP9-induced osteoge

80 In primary myoblast cells, stimulation of AMPK and AKT was observed

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

82 ound 10b had an EC(50) value of 190 nM in L6 myoblast cells.

83 ulating enhancer activity in skeletal muscle myoblasts cells, further confirming the regulation of WB

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

85 d control healthy myotubes compared to their myoblast counterparts, so is higher in myogenic differen

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

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

88 Although proliferative, SOD1 myoblasts demonstrated delayed and reduced fusion effici

89 s observed in Zbed6(-/-) and Igf2(DeltaGGCT) myoblasts demonstrates that ZBED6 affects mitochondrial

90 were performed on primary screen hits using myoblasts derived from Megf10-/- mice, induced pluripote

91 control cell proliferation, we established a myoblast-derived cell line with inducible silencing of C

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

93 AUF1 include Twist1, decay of which promotes myoblast development; CyclinD1, decay of which blocks my

94 in embryonic myoblasts leads to depletion of myoblasts, developmental failure and prenatal lethality.

95 ubation of ID1 protein with proteasomes from myoblasts did not show differentiation stage-associated

96 OIP5-AS1 in myogenesis, the process whereby myoblasts differentiate into myotubes during muscle deve

97 he distribution of nuclear pore complexes in myoblasts differentiated on a soft hydrogel surface.

98 expression increased robustly in mouse C2C12 myoblasts differentiating into myotubes.

99 romatin state of precursors of muscle cells (myoblasts) differentiating into specialized myotubes.

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

101 er demonstrate its utility for understanding myoblast differentiation and disentangling known heterog

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

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

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

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

106 e nuclear envelope, such that C2C12 skeletal myoblast differentiation and neonatal rat ventricular my

107 teasomal activity is up-regulated to further myoblast differentiation and that the increased proteaso

108 to determine whether the proteasome promotes myoblast differentiation by degrading ID1 protein.

109 Inhibition of PKCmu activity suppresses myoblast differentiation by inhibiting MyoD and MEF2c ex

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

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

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

113 w here that P-TEFb surprisingly inhibits the myoblast differentiation into myotubes, and that P-TEFb

114 Skeletal muscle myoblast differentiation involves elaborate signaling ne

115 the increased proteasomal activity improves myoblast differentiation partly by inhibiting the synthe

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

117 Here we used myoblast differentiation to identify the E3 ligase CUL2(

118 tor of DNA binding 1 (ID1) protein inhibited myoblast differentiation too.

119 nt myoblasts suggested that lipin1 regulates myoblast differentiation via the protein kinase Cmu (PKC

120 rther understand the mechanism that controls myoblast differentiation, a key step in skeletal muscle

121 uscle stem cell proliferation, self-renewal, myoblast differentiation, and ultimately formation of mu

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

123 ation), VRAC inhibition no longer suppressed myoblast differentiation, suggesting that VRAC acts upst

124 e results of this study suggest that, during myoblast differentiation, the proteasomal activity is up

125 During myoblast differentiation, we observed that the levels an

126 protein and mRNA expression decreased during myoblast differentiation.

127 asome-specific inhibitor lactacystin impeded myoblast differentiation.

128 nscriptional activity, which in turn affects myoblast differentiation.

129 egulated anion channel (VRAC) promotes mouse myoblast differentiation.

130 Pak1 and Pak2 are activated during mammalian myoblast differentiation.

131 reduced mitochondrial activities, and ceased myoblast differentiation.

132 me and inhibitor of DNA binding 1 protein in myoblast differentiation.

133 n-proteasome system were up-regulated during myoblast differentiation.

134 Cu and MTF1 regulate gene expression during myoblast differentiation.

135 Canonical Wnts promote myoblast differentiation; however, the role of beta-cate

136 the disease including mouse myoblast, human myoblast, Drosophila and zebrafish models.

137 us internalization reached over 30% in human myoblasts due to a higher percentage of infected myoblas

138 1as) transcript that are decreased in the WT myoblasts due to SUN1 inhibition of Drosha.

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

140 show that Plk1's expression closely mirrors myoblast dynamics during embryonic and postnatal myogene

141 for the rise of myogenin-positive committed myoblasts (early stage of myogenesis), whereas mTORC1-S6

142 differentiation, and epigenetic directive in myoblasts, elucidating why the developmental potential o

143 Myoblasts embedded in extracellular matrix self-organize

144 Here we report that in the absence of Mll1, myoblasts exhibit reduced H3K4me3 at both Pax7 and Myf5

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

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

147 fic small molecule inhibitor of DUSP6, while myoblasts expressing the canonical DUSP6 displayed enhan

148 Mll1-deficient myoblasts fail to proliferate but retain their different

149 ols, founder cells (FC) and fusion competent myoblasts (fcm).

150 However, compared with fetal myoblasts, following transplantation they show superior

151 e expression of myogenic markers in cultured myoblasts from both species.

152 mice, induced pluripotent stem cell-derived myoblasts from MEGF10 myopathy patients, mutant Drosophi

153 Their trophic effects extend to myoblasts from non-hibernating species (including C. ele

154 macrophage behavior and influence on primary myoblasts from older individuals.

155 way but also reduces the mutant DMPK mRNA in myoblasts from patients with adult DM1 and congenital DM

156 We found that myoblasts from the D2 background were insensitive to a s

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

158 Fewer myoblasts fuse into regenerating muscle in vivo after co

159 whereas mTORC1-S6K signaling is required for myoblast fusion (later stage of myogenesis).

160 hagy flux is upregulated specifically during myoblast fusion and declines in myotubes.

161 eview, we revisit key findings in Drosophila myoblast fusion and highlight the critical roles of cell

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

163 oblast proliferation and cell-cycle exit, to myoblast fusion and myotubes maturation.

164 on of new myofibers in vertebrates occurs by myoblast fusion and requires fusogenic activity of the m

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

166 In the past two decades, Drosophila myoblast fusion has been used as a powerful genetic mode

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

168 ry that orchestrates the discrete process of myoblast fusion in mammals is poorly understood and unex

169 o emphasize recent discoveries in vertebrate myoblast fusion in skeletal muscle, which is composed of

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

171 pelling invasive membrane protrusions during myoblast fusion in vivo.

172 Myoblast fusion is an indispensable step for skeletal mu

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

174 s myoferlin's activity is maximal during the myoblast fusion stage of early skeletal muscle cell deve

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

176 transcription factor myogenin and suppressed myoblast fusion while not affecting myoblast proliferati

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

178 1/2, mTOR signaling, muscle differentiation, myoblast fusion, cellular oxygen consumption, and glycol

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

180 atenin and thus prevent precocious/excessive myoblast fusion.

181 I hinders myogenic development by repressing myoblast fusion.

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

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

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

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

186 fibroblast-fibroblast fusion and fibroblast-myoblast fusion.

187 er and myomixer cooperate to drive mammalian myoblast fusion.

188 yoblasts promoted muscle differentiation and myoblasts fusion.

189 We report that tKO C2C12 myoblasts generated using CRISPR/Cas9 method differentia

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

191 lasts due to a higher percentage of infected myoblasts (>11%) as compared to keratinocytes (<3%).

192 FSHD patient myoblasts have defective myogenic differentiation, formi

193 ltiple models of the disease including mouse myoblast, human myoblast, Drosophila and zebrafish model

194 Affinity purification of Zfp423 in myoblasts identified Satb2 as a nuclear partner of Zfp42

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

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

197 roliferation but promotes differentiation of myoblasts in vitro, and blocks muscle regeneration in vi

198 rment blocks the differentiation of skeletal myoblasts in vitro.

199 by beta-catenin and defined novel targets in myoblasts, including the fusogenic genes myomaker and my

200 cases differentiation, of old primary human myoblasts increase as much as 30% when exposed to a youn

201 slow muscles, and Mettl21c overexpression in myoblasts increased Hspa8 trimethylation and protein lev

202 Subsequent in vitro study in FSHD patient myoblasts indicated that berberine treatment reduced DUX

203 Surprisingly, forced expression of Zfp423 in myoblasts induces differentiation into adipocytes and ar

204 fp423, shRNA-mediated knockdown of Zfp423 in myoblasts inhibits differentiation.

205 3) During differentiation of C2C12 myoblasts into myotubes, the apo-Mb-hsp90 complex associ

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

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

208 fect of MyHC-emb on myogenic progenitors and myoblasts is mediated by the fibroblast growth factor (F

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

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

211 scriptomes of thousands of MuSCs and primary myoblasts isolated from homeostatic or regenerating musc

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

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

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

215 Consistent with this finding, primary myoblasts lacking Rev-erbalpha display significantly enh

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

217 Cell-specific deletion of Plk1 in embryonic myoblasts leads to depletion of myoblasts, developmental

218 In contrast, ZBED6-overexpression in myoblasts led to cell apoptosis, cell cycle arrest, redu

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

220 genic differentiation of transdifferentiated myoblast-like cells.

221 s an aggressive pediatric cancer composed of myoblast-like cells.

222 represents a high-grade neoplasm of skeletal myoblast-like cells.

223 sed the differentiated human skeletal muscle myoblast line, LHCN-M2, which expresses typical muscle p

224 ces in understanding fusion between gametes, myoblasts, macrophages, trophoblasts, epithelial, cancer

225 initiates after this stage (concomitant with myoblast migration into the LPM) and is therefore unlike

226 EMT) in the lateral plate mesoderm (LPM) and myoblast migration into the LPM, occur at equivalent sta

227 rder, somite chevron morphology and hypaxial myoblast migration.

228 deficiency on iron homeostasis in the mouse myoblast model of BTHS tafazzin knockout (TAZ-KO) cells.

229 Lymphoblast score is unaltered between FSHD myoblasts/myotubes and their controls however, implying

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

231 PCAF)-epigenetic cascades, whereas depriving myoblasts of ambient magnetic fields slowed myogenesis,

232 Higher cytotoxicity for myoblasts of NSTI-SA as compared to BSI-SA was attribute

233 In human myoblasts, OIP5-AS1 levels increased robustly early in m

234 Similarly, murine myoblasts overexpressing a catalytically inactive TRIM32

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

236 e) differentiation, resulting in myotube and myoblast phenotypes, respectively.

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

238 progenitor cell pool and an increase in the myoblast pool, whereas fetal myogenesis-specific deletio

239 he depletion of both myogenic progenitor and myoblast pools.

240 e steps of skeletal muscle development, from myoblast proliferation and cell-cycle exit, to myoblast

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

242 development; CyclinD1, decay of which blocks myoblast proliferation and initiates differentiation; an

243 2-mediated phosphorylation of Brg1 regulates myoblast proliferation and provides insight into one mec

244 onversely, knockdown of Phospho1 accelerates myoblast proliferation but impairs myotube formation.

245 Overexpression of Phospho1 inhibits myoblast proliferation but promotes their differentiatio

246 ung, but not old, bone marrow cells promoted myoblast proliferation in vitro, and we found that facto

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

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

249 ppressed myoblast fusion while not affecting myoblast proliferation.

250 Overexpression of SMYD3 in myoblasts promoted muscle differentiation and myoblasts

251 variants in human and mouse skeletal muscle myoblasts promoted myotube differentiation and prevented

252 ly, mammalian sperm could fuse with skeletal myoblasts, requiring PtdSer on sperm and BAI1/3, ELMO2,

253 Re-expression of PAX7 in committed Mll1 cKO myoblasts restored H3K4me3 enrichment at the Myf5 promot

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

255 Gene silencing of Fbxl2 in skeletal myoblasts resulted in increased proliferative responses

256 RNA sequencing of primary bovine myoblasts revealed many genes encoding the ubiquitin-pro

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

258 Similarly, C2C12 myoblasts show a reduced oxygen consumption rate mediate

259 Both Zbed6(-/-) and Igf2(DeltaGGCT) myoblasts showed a faster growth rate and developed myot

260 Our results from lipin1-deficient myoblasts suggested that lipin1 regulates myoblast diffe

261 internalization into human keratinocytes and myoblasts than NSTI-GAS or CNS.

262 individual cell analysis of differentiating myoblasts that characterizes autophagy flux (i.e., autop

263 is is recapitulated in the tissue culture of myoblasts that differentiate by fusion and then by the f

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

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

266 We confirmed in myoblasts that EIF4G2 is a direct target of miR-379, and

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

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

269 However, in myoblasts, the statin-mediated decrease in insulin sensi

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

271 A lone 10 min exposure of myoblasts to 1.5 mT amplitude supplemental pulsed magnet

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

273 Moreover, exposure of GLUT4-Myc-labeled L6 myoblasts to compound A increased GLUT4 trafficking.

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

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

276 overexpression promotes fusion of exogenous myoblasts to injured myofibers.

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

278 ted myocytes promotes commitment of adjacent myoblasts to terminal differentiation.

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

280 of proliferating skeletal muscle precursors (myoblasts) to terminally-differentiated myocytes is a cr

281 und Fer1l6 expression was independent of the myoblast-to-myotube transition.

282 llular basis of high internalization rate in myoblasts was attributed to higher expression of alpha5b

283 In myoblasts, we find that impaired NADH oxidation upon ele

284 erated beta-catenin-null primary adult mouse myoblasts, we found that beta-catenin was essential for

285 ient-derived TXNIP-deficient fibroblasts and myoblasts, we show that oxidative phosphorylation is imp

286 isingly, this reversal was not observed when myoblasts were also treated with the mRNA translation in

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

288 Using this approach, myoblasts were phenotypically identified by their positi

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

290 transduction are common to the disc, ASP and myoblasts, whereas others are tissue-specific.

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 However, treating myoblasts with lactacystin reversed the decrease in ID1

294 A) in muscle and treatment of differentiated myoblasts with NEAA is sufficient to induce hypertrophy.

295 on of distinct clusters of MuSCs and primary myoblasts with partially overlapping but distinct transc

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

297 Treating myoblasts with the proteasome-specific inhibitor lactacy

298 enome-wide transcriptomic analysis of murine myoblasts, with silenced or overexpressed SMYD3, reveale

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

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