ライフサイエンスコーパス: myogenin

1 h as (DBP, c-ETS1-68), (DBP, USF2) and (DBP, MYOGENIN).

2 e encoding the myogenic transcription factor Myogenin.

3 on of the late myogenic transcription factor myogenin.

4 to recapitulate MyoD-dependent activation of Myogenin.

5 ogenesis in MSCs by transactivating MyoD and myogenin.

6 ownregulated genes were selective targets of myogenin.

7 expression of the myogenic regulatory factor myogenin.

8 fferentiation encodes the myogenic regulator myogenin.

9 late a restricted subset of genes, including myogenin.

10 coding for the early differentiation marker, Myogenin.

11 ranscription of the muscle regulatory factor myogenin.

12 yosin heavy chain (MHC), myostatin, myoD and myogenin.

13 on prior to the transcriptional induction of myogenin.

14 to another Rho-induced differentiation gene, myogenin.

15 the myogenic transcription factors MyoD and myogenin.

16 skeletal myogenesis up to the activation of myogenin.

17 lation of the myogenic transcription factor, myogenin.

18 myosin, alpha-actin, integrin alpha(7), and myogenin.

19 low cell density Myf5 inhibits induction of myogenin.

20 estabilization of labile transcripts such as myogenin.

21 gene expression, including up-regulation of myogenin.

22 including the transcription factors MyoD and myogenin.

23 ll self-renewal, and downregulating MyoD and myogenin.

24 n atrogene induction occurs independently of myogenin.

25 cell proliferation or expression of MyoD or myogenin.

26 -329, and miR-96) were predicted to bind the myogenin 3'-untranslated region (UTR).

27 e role microRNAs (miRNAs) play in regulating myogenin, a bioinformatics approach was used and six miR

28 ker of activated macrophages as well as with myogenin, a marker of activated muscle precursor cells.

29 2C12 differentiation and decreased levels of myogenin, a member of the MyoD family of myogenic regula

30 Myod-driven Myogenin activity alone is sufficient for lateral fast s

31 Myogenin activity is a significant contributor to fast f

32 ct innervation-dependent mechanisms restrain myogenin activity: an inactivation mechanism mediated by

33 Here, we demonstrate that myogenin also binds to its own promoter during the late

34 Induction of myogenin, an earlier marker of muscle differentiation, i

35 not interact with or remodel the promoter of myogenin, an essential early gene.

36 We show that myogenin, an essential regulator of muscle development,

37 Ectopic expression of myogenin and a specific Mef2 isoform induced myogenic di

38 sion of myogenic regulatory factors MyoD and myogenin and also induced the degradation of MyoD protei

39 and 5 in skeletal muscle fail to upregulate myogenin and also preserve muscle mass following denerva

40 and in developing embryonic tissue, whereas myogenin and Brg1 are critical for the expression of the

41 However, in mature myofibers, myogenin and Brg1 are preferentially co-localized to the

42 of transfected reporter genes, including the myogenin and creatine kinase promoters, and by complete

43 ion of Cugbp1 gene in muscle is regulated by myogenin and E proteins and suggest that the co-operatio

44 expression of the regeneration markers MyoD, myogenin and embryonic myosin (myosin heavy chain 3, MYH

45 2112 infusion potentiated CTX injury-induced myogenin and embryonic myosin heavy chain expression and

46 ed expression of alpha7beta1 integrin, Pax7, myogenin and embryonic myosin heavy chain, indicating a

47 sion of the myoblast differentiation markers myogenin and embryonic myosin heavy chain.

48 enhances the myogenic potential of MyoD and myogenin and establishes direct interactions with MyoD,

49 patient muscle in association with increased myogenin and histone deacetylase-4 (HDAC4) expression.

50 ass II transactivator, CIITA, which binds to myogenin and inhibits its activity.

51 inhibitor p27) and differentiation markers (myogenin and integrin alpha7A isoform).

52 bers is probably linked to the expression of myogenin and is a unique attribute of the EOM allotype.

53 MEF2 site, and muscle transcription factors myogenin and MEF2C stimulate RGMc promoter function in n

54 entified in many muscle promoters, including Myogenin and MEF2C, and one motif was shown to be critic

55 Hey1 is recruited to the promoter regions of myogenin and Mef2C, two genes whose induction is critica

56 present study, TGF-beta was shown to inhibit myogenin and MEF2D expression and myotube formation in C

57 ther demonstrated that ectopic expression of myogenin and Mef2D, in the absence of MyoD, was sufficie

58 al myogenic transcription factors, including myogenin and MEF2D.

59 e of myogenic regulators (MRFs), Myf5, MyoD, Myogenin and MRF4 in the regulation of muscle specific m

60 The transcription of MyoD-target genes myogenin and muscle creatine kinase were suppressed by P

61 lated gene expression pattern which includes myogenin and Myf5 up-regulation and Cyclin D1 decrease.

62 s, by negatively affecting the expression of Myogenin and MyHC.

63 is, we demonstrate that the myogenic factors Myogenin and MyoD bind to regions upstream of these micr

64 Salmon Stac3 mRNA was highly correlated with myogenin and myoD1a expression during differentiation of

65 itinating enzyme modulates the expression of myogenin and myofibrillar proteins in L6 muscle cells.

66 myoblast fusion as well as the expression of myogenin and myofibrillar proteins, and these effects we

67 acterized by a decrease in the expression of myogenin and myosin heavy chain (MHC) proteins, whereas

68 ifferentiation and terminal differentiation (myogenin and myosin heavy chain 2) were increased on d 2

69 m terminally differentiating as shown by low myogenin and myosin heavy chain expression, and lack of

70 se 4 (HDAC4) can mediate denervation-induced myogenin and nicotinic acetylcholine receptor gene expre

71 of myogenic factors such as MyoD, Myf5, and myogenin and of one of their targets, the developmental

72 cilitates effective association of KSRP with myogenin and other labile transcripts, and we propose th

73 promotes myogenesis by stabilizing the MyoD, myogenin and p21 mRNAs during the fusion of muscle cells

74 alpha2 subunit resulted in downregulation of myogenin and reduced myogenesis.

75 The results identify new target genes for myogenin and show that myogenin's target gene selectivit

76 a silent differentiation signal muscle gene myogenin and that Suv39h1 presence correlated with H3-K9

77 and HDAC1 are both occupying the promoter of myogenin and that this gene is in a region of repressed

78 y sequences but prevents the binding of both myogenin and the Brg1 ATPase that catalyzes SWI/SNF-depe

79 e skeletal muscle phenotype is maintained by myogenin and the continuous activity of Brg1-based SWI/S

80 iated with myogenic gene activation, such as myogenin and the SWI/SNF chromatin remodelling enzyme AT

81 r, several inferred TFAs like those of MyoD, myogenin and YY1 are well supported by biological experi

82 as to compare embryonic skeletal muscle from myogenin(+/+) and myogenin(-/-) mice to identify genes w

83 tivity of myogenic regulatory factors (MyoD, myogenin) and effectors (p21).

84 MYC/MAX heterodimer), (DBP, USF2) and (DBP, MYOGENIN); and down-regulated ERalpha target genes signi

85 ent of the developmental regulators MyoD and myogenin, and activation of miR-214 transcription.

86 proliferation/differentiation markers (MyoD, myogenin, and active-Notch) after cardiotoxin-induced mu

87 xpression of differentiation markers such as myogenin, and began to differentiate into multinucleated

88 o DNA of the c-Fos, c-Jun, E2F1, E2F4, MyoD, myogenin, and c-Myc transcription factors.

89 containing muscle reporter genes by MyoD or myogenin, and did not inhibit the expression or function

90 ee energy of dissociation (DeltaG) for MyoD, Myogenin, and E12 as homo- and heterodimers to the well-

91 ions downstream of or in parallel with MyoD, myogenin, and MEF2 in muscle development to govern the l

92 sion of myogenic transcription factors MyoD, myogenin, and Myf-5.

93 rologous promoter increased endogenous MyoD, Myogenin, and Myh3 (myosin heavy chain, [MHC] gene) mRNA

94 d the tumor cells to be positive for desmin, myogenin, and myogenic differentiation 1 (MyoD1).

95 he up-regulation of Pax-7, MyoD, Myf5, Myf6, myogenin, and myosin heavy chain (MHC) in obestatin-infu

96 The expression of myogenic regulators, MyoD, myogenin, and p21WAF1/CIP1, was severely decreased in NF

97 (HGF); the myogenic regulatory factors MyoD, myogenin, and Pax7; and a marker for nuclei in all proli

98 tine kinase, myosin heavy chain-fast twitch, myogenin, and the formation of multinucleated myotubes.

99 ession of the myogenic transcription factor, myogenin, and the subsequent development of more mature

100 ression (endogenous p21, myosin heavy chain, myogenin, and Tmod) but did not affect endogenous glycer

101 This E-box binds myogenin, and we showed that myogenin is necessary for n

102 ise to pleomorphic rhabdomyosarcomas (MyoD-, Myogenin- and Desmin-positive), whereas introduction of

103 myogenic regulatory factors (MRFs)--MyoD and myogenin--and Myocyte Enhancer Factor 2 (MEF2).

104 The myogenic regulatory factors MyoD and myogenin are crucial for skeletal muscle development.

105 MyoD and Myogenin are dominant myogenic regulatory factors (MRFs)

106 expression of the transcriptional regulator, myogenin, as ectopic expression of myogenin eliminates P

107 The recruitment is dependent on myogenin, as knockdowns of myogenin show no recruitment

108 he expression and inhibiting the activity of myogenin at different stages of myogenesis.

109 We find that phosphorylation of myogenin at T87 is dispensable for skeletal muscle devel

110 ion mechanism mediated by phosphorylation of myogenin at T87, and a second, novel regulatory mechanis

111 ed in mutant mice lacking phosphorylation of myogenin at T87.

112 Furthermore, the expression of myogenin at the protein, but not mRNA, level is drastica

113 rical activity stimulates phosphorylation of myogenin at threonine 87 (T87) in vivo and that calmodul

114 ranscription factors of myogenesis (MyoD and Myogenin) at extragenic enhancer regions coinciding with

115 s (Human beta-cardiac myosin heavy chain and myogenin) became localized to the periphery of an SC-35

116 Removing myogenin before embryonic muscle development resulted in

117 myogenic regulatory factors, MyoD, Myf5 and Myogenin, bind to the E-box, while a lymphoid transcript

118 ogenin but not MyoD and to determine whether myogenin-binding sites could be found within regulatory

119 Myogenin bound within conserved regulatory regions of se

120 expression was dependent on the presence of myogenin but not MyoD and to determine whether myogenin-

121 /-) mice was downregulated in the absence of myogenin, but in the presence of MyoD.

122 recombinant adenoviruses expressing MyoD or myogenin, but it was reversibly impaired by the PI3-kina

123 of the myogenic regulatory factors MyoD and Myogenin, but not Myf5, which suggests that Six1 acts on

124 ed fiber type distribution at the expense of myogenin-containing (slow-twitch) fibers.

125 ance of one of these domains, which contains Myogenin, correlates with reduced transcriptional variab

126 nd MyoD increased, while later stage protein myogenin decreased.

127 luence myogenesis by preventing VHL-mediated myogenin degradation.

128 These results indicate that myogenin-dependent atrogene induction is amenable to pha

129 could be found within regulatory regions of myogenin-dependent genes independent of MyoD.

130 ervation-induced muscle atrophy via an HDAC4-myogenin-dependent process, whereas increased BMP-Smad1/

131 results show that the FACT complex promotes myogenin-dependent transcription and suggest that FACT p

132 Conversely, myogenin directly affects Pax7 expression and may be cri

133 control mice, suggesting that the absence of myogenin disrupted general body growth.

134 ring myogenic differentiation, expression of myogenin does not seem to be altered.

135 ntiated myotubes this element is occupied by myogenin, E12 and p300.

136 , we found expression upregulation of Pax-7, myogenin, E2-ubiquitin ligase UBE2Q1 and acetylcholine r

137 egulator, myogenin, as ectopic expression of myogenin eliminates Prmt5 dependency.

138 Moreover, myogenin+ ERMS cells can enter the vasculature, whereas

139 tumor only after seeding by highly migratory myogenin+ ERMS cells.

140 5b expression results in severe reduction of myogenin expression and consequent lack of myoblast fusi

141 ing protein 2), underlying FAK regulation of myogenin expression and muscle differentiation.

142 chromatin remodelling that is important for myogenin expression and muscle-terminal differentiation,

143 Myogenin expression and myogenesis were nearly abolished

144 PAX3/FOXO1A or PAX7/FOXO1A inhibited myogenin expression and prevented terminal differentiati

145 evidence for a novel pathway that regulates myogenin expression and skeletal muscle differentiation.

146 Further analyses show that Pax-7 and myogenin expression are mutually exclusive during differ

147 an inhibitor of MAPK kinase (MEK), restored myogenin expression but did not reinstate the myogenic p

148 s myogenin expression, whereas TAL1 inhibits myogenin expression by decreasing MyoD binding to and ac

149 , and that PAX3-FKHR is directly involved in myogenin expression in aRMS cells.

150 In addition, there was decreased MyoD and myogenin expression in regenerating muscle in CXCL16KO m

151 We demonstrate that PAX3-FKHR could induce myogenin expression in undifferentiated myoblasts by a M

152 ever, IL-10 mutation significantly increased myogenin expression in vivo during the acute and the reg

153 Furthermore, myogenin expression increased in IL-10 mutant muscle at

154 TGF-beta signaling through Smad3 represses myogenin expression independently of E-boxes, and preven

155 ssion of myogenin itself, while in myotubes, myogenin expression is unaffected.

156 mycin, a kinase-inactive mTOR fully supports myogenin expression, but causes a delay in contractile p

157 bx1, which cooperates with MyoD to stimulate myogenin expression, is constitutively bound to the myog

158 last proliferation without affecting MyoD or myogenin expression, showing that M2 macrophages promote

159 ion of injured muscle and decreased MyoD and myogenin expression, suggesting that CKD impairs prolife

160 Sirt1 to the myogenin promoter and represses myogenin expression, whereas TAL1 inhibits myogenin expr

161 d protein activity, permitting it to promote Myogenin expression.

162 ite in the myogenin promoter, thus, inducing myogenin expression.

163 promoter chromatin structure and facilitate myogenin expression.

164 last differentiation, protein synthesis, and myogenin expression.

165 gh cell density, Myf5 is a potent inducer of myogenin expression.

166 ion of markers of differentiation, including myogenin, fast twitch troponin T, and muscle myosin heav

167 Deletion of myogenin from adult mice diminishes expression of MuRF1

168 Here, we identify myogenin gene as a direct target of PD-dependent PAX3-FK

169 nhibition of transcription of the endogenous myogenin gene but had no effect on MyoD protein levels,

170 entiation and enables MEF2 to transcribe the myogenin gene by decreasing the nuclear accumulation of

171 xpression of Dach2 and MITR that function as myogenin gene corepressors.

172 ox, suggesting a mechanism for inhibition of myogenin gene expression.

173 ffects of muscle depolarization on nAChR and myogenin gene expression.

174 ated during muscle differentiation, when the myogenin gene is expressed at high levels.

175 tones surrounding a MEF2-binding site in the myogenin gene promoter are highly methylated in undiffer

176 ified novel regulatory elements flanking the myogenin gene that function as a key differentiation-dep

177 at MyoD binds to noncanonical E boxes in the myogenin gene, a critical locus required for myogenesis,

178 by initial inhibition of the myoD, E2A, and myogenin genes followed by resumption of their expressio

179 Additionally, after the rescue of MNs in myogenin glial cell line-derived neurotrophic factor (My

180 nic basic helix-loop-helix regulatory factor myogenin has in postnatal muscle growth and adult muscle

181 l embryonic skeletal muscle, indicating that myogenin has separate functions during postnatal life.

182 ltaG = 19.6 kcal/mol) in comparison with the Myogenin homodimer-MCK interaction (DeltaG = 16.6 kcal/m

183 tes functional interactions between MyoD and myogenin in co-activation of muscle-specific gene expres

184 termining the role of the myogenic regulator myogenin in postnatal life.

185 led to reduced body size implying a role for myogenin in regulating body homeostasis.

186 Conversely, forced expression of myogenin in skeletal muscle of HDAC mutant mice restores

187 The relevance of myogenin in the continued expression from its own promot

188 entages of satellite cells were positive for myogenin in the orbital layer, but the global layer had

189 an unsuspected non-cell autonomous role for myogenin in the regulation of tissue growth.

190 iR-206 and the myogenic transcription factor myogenin in the tibialis anterior muscle were found to p

191 demonstrated in culture, where we show that myogenin, in the absence of MyoD, is capable of maintain

192 the Cugbp1 promoter since overexpression of myogenin increases the activity of the Cugbp1 promoter;

193 ssion by its miRNA in C2C12 cells attenuates myogenin induction and/or impairs muscle-terminal differ

194 ssion of Pax-7 down-regulates MyoD, prevents myogenin induction, and blocks MyoD-induced myogenic con

195 y myoblasts down-regulates MyoD and prevents myogenin induction, inhibiting myogenesis.

196 We have discovered that myogenin interacts with the FACT complex.

197 Our data show that myogenin is a key regulator of the Cugbp1 promoter since

198 We found that myogenin is absolutely required for skeletal muscle deve

199 Transfection of FACT subunits with myogenin is highly stimulatory for endogenous muscle gen

200 his E-box binds myogenin, and we showed that myogenin is necessary for not only MuSK but also nAChR g

201 Myogenin is required not for the initiation of myogenesi

202 Myogenin is upregulated in skeletal muscle following den

203 le-specific genes includes the expression of myogenin itself, while in myotubes, myogenin expression

204 he initiation of chromatin remodeling at the myogenin locus, together regulate a restricted subset of

205 ion of EGLN3, suggesting that its binding to myogenin may prevent VHL-mediated degradation.

206 ery, p < 0.05), consistent with the S6K1 and myogenin measurements.

207 y members, we examined MyoD, Myf5, MRF4, and myogenin-mediated induction of muscle differentiation in

208 on and fusion indices and decreases in MyoD, myogenin, MEF2A, and MEF2C, independently of Staufen-med

209 on of differentiation-specific genes such as myogenin, MEF2C, and myosin heavy chain is impaired by S

210 ow that cell fate-determining factors [MyoD, myogenin (Mgn), Runx2, C/EBPbeta] occupy rDNA loci and s

211 -helix muscle-specific transcription factor, myogenin (Mgn).

212 yonic skeletal muscle from myogenin(+/+) and myogenin(-/-) mice to identify genes whose expression wa

213 ose expression in embryonic tongue muscle of myogenin(-/-) mice was downregulated in the absence of m

214 e ankyrin repeat protein (MARP) genes (myoD, myogenin, MLP and CARP) depended both on peak muscle str

215 e expression of certain genes (such as myoD, myogenin, MLP and CARP) is sensitive to muscle stress wh

216 ption factors including Pax3, Paraxis, Myf5, myogenin, Mrf4 and MyoD.

217 rget whose decay promotes myogenesis whereas myogenin mRNA is a classical NMD target encoding a prote

218 RP dismissal from H19 and, as a consequence, myogenin mRNA is stabilized while KSRP is repurposed to

219 clei (7 +/- 2% and 13 +/- 2%), less myoD and myogenin mRNA, and fewer (P < 0.05) proliferating myobla

220 We show, however, that the decrease in myogenin (myg) expression following innervation is delay

221 entiation, including increased expression of Myogenin (MYOG) and Myosin Light Chain (MYL1) in RMS cel

222 was likely because of the failure to induce myogenin (Myog) and p21 despite normal expression of Myo

223 ix-loop-helix transcription factors MyoD and myogenin (Myog) direct the development of skeletal muscl

224 Dyrk1b is required for myogenin (myog) expression in differentiating mouse C2C1

225 on the promoter of the differentiation gene myogenin (Myog) via Wdr5 phosphorylation.

226 This gene subset included myogenin (MyoG), Hdac4, Ampd3, Trim63 (MuRF1), and acety

227 of a subset of Myod target genes, including myogenin (Myog); thus, Pbx proteins might modulate the p

228 xpression levels of differentiation markers (myogenin, myosin heavy chain, troponinT-1, and Pax3) and

229 A could not recapitulate the selectivity for myogenin observed in vivo.

230 cle specification, a transition from MyoD to myogenin occurred at late gene loci, concomitant with lo

231 red myoblasts and fibroblasts overexpressing myogenin or MyoD, indicating that expression from exogen

232 MRFs), Myf5, MyoD, Myf6, and myogenin, where myogenin plays a critical role in the regulation of the

233 Thus, myogenin plays a dual role as both a regulator of muscle

234 Finally, we discovered an HDAC4/myogenin positive feedback loop that coordinates gene in

235 obal layer had few satellite cells that were myogenin positive.

236 y a dramatic drop in the number of Pax7- and myogenin-positive cells relative to WT muscles, suggesti

237 ax7 mRNA but lower (P < 0.05) percentages of myogenin-positive nuclei (7 +/- 2% and 13 +/- 2%), less

238 control myoblasts had similar percentages of myogenin-positive nuclei after 5 days and formed similar

239 ost entirely of rhabdomyoblasts (desmin- and myogenin-positive) was discovered along with rare cluste

240 deleted adult muscle stem cells, the loss of myogenin profoundly altered the pattern of gene expressi

241 MyoD initially interacts indirectly with the myogenin promoter and attracts chromatin-remodeling enzy

242 MyoD to bind to noncanonical E boxes in the myogenin promoter and for the formation of a tetrameric

243 nteracts with Sirt1 and targets Sirt1 to the myogenin promoter and represses myogenin expression, whe

244 association of MyoD to the DRR enhancer and myogenin promoter but not to another MyoD-dependent enha

245 O1A or PAX7/FOXO1A reduced occupation of the myogenin promoter by RNA polymerase II and decreased ace

246 not MyoD or Myf5, enhanced activation of the myogenin promoter in a Mirk kinase-dependent manner.

247 n expression, is constitutively bound to the myogenin promoter in a SWI/SNF-independent manner, sugge

248 ethylated H3R8 were also associated with the myogenin promoter in activated satellite cells isolated

249 (histone 3 arginine 8) are localized at the myogenin promoter in differentiating cells.

250 cells, and the recruitment of GRIP-1 to the myogenin promoter in differentiating myoblasts.

251 myogenesis, MyoD and Brg1 co-localize to the myogenin promoter in primary adult muscle satellite cell

252 Thus, the myogenin promoter is occupied by different myogenic fact

253 Chromatin immunoprecipitation on the myogenin promoter showed that PAX3/FOXO1A or PAX7/FOXO1A

254 essary for the stable binding of MyoD to the myogenin promoter through an interaction with an adjacen

255 to bind to target DNA sites at the proximal myogenin promoter, as assessed by chromatin immunoprecip

256 scle regulatory proteins did not bind to the myogenin promoter, thereby providing evidence for SWI/SN

257 tylase complex 1) and methyl CpG site in the myogenin promoter, thus, inducing myogenin expression.

258 in directing transcription initiation at the Myogenin promoter.

259 as well as sustained methylation of H3-K9 on myogenin promoter.

260 Brg1 are preferentially co-localized to the myogenin promoter.

261 ha-mediated NFkappaB activation fused to the myogenin promoter.

262 chromatin immunoprecipitations analyzing the myogenin promoter.

263 ylation of Ser-10 can now be observed at the myogenin promoter.

264 l of an approximately 1.6-kb fragment of the myogenin promoter.

265 histone H4, but did not directly bind to the myogenin promoter.

266 easing MyoD binding to and activation of the myogenin promoter.

267 its ability to transcriptionally repress the myogenin promoter.

268 required for the continued production of the myogenin protein in newborn skeletal muscle tissue.

269 ort that EGLN3 interacts with and stabilizes myogenin protein, whereas VHL associates with and destab

270 ivates the expression of endogenous MyoD and myogenin proteins in transduced NIH3T3 fibroblasts, it i

271 the Cugbp1 promoter; while the inhibition of myogenin reduces activity of the Cugbp1 promoter.

272 new target genes for myogenin and show that myogenin's target gene selectivity is not based solely o

273 t is dependent on myogenin, as knockdowns of myogenin show no recruitment of the FACT complex.

274 Thus, a HDAC-Dach2-myogenin signaling pathway has been identified to decode

275 These results indicate that myogenin specifies the muscle phenotype by cooperating w

276 The effect of VHL on myogenin stability and ubiquitination can be reversed, a

277 as assayed by myosin heavy chain (MyHC) and Myogenin staining.

278 er NRF-1 (brown fat and developing brain) or myogenin (striated muscle).

279 The binding of myogenin to the Cugbp1 promoter correlates with activati

280 ediated by the additive effect of binding of myogenin to three critical E boxes within this region.

281 ing of these bHLH proteins, notably MyoD and myogenin, to E-boxes in their own regulatory regions is

282 endent transcription by regulating the Dach2-myogenin transcriptional cascade where inhibition of the

283 enuates reporter gene expression in MyoD- or myogenin-transfected HEK cells.

284 of muscle differentiation-specific proteins (myogenin, troponin T, or myosin heavy chain), did not bl

285 ranscript levels for K(v)7.4, as well as for myogenin, troponinT-1, and Pax3, were reduced by REST ov

286 pression of the cell cycle inhibitor p21 and myogenin, two markers of differentiation, and inhibited

287 s with VHL and, when overexpressed, reverses myogenin ubiquitination and stability.

288 vels of myogenic regulatory factors MyoD and myogenin upon induction of differentiation.

289 Lindau (VHL) protein is known to destabilize myogenin via the ubiquitin-proteasome pathway.

290 whereas VHL associates with and destabilizes myogenin via the ubiquitin-proteasome system.

291 ion pattern of the myogenic factors MyoD and myogenin was similar for both types of mice, while NCAM,

292 enic factor 5, myoblast determination 1, and myogenin-were higher in muscles from patients with SMA c

293 latory factors (MRFs), Myf5, MyoD, Myf6, and myogenin, where myogenin plays a critical role in the re

294 mulated myoblasts to express MyoD, Myf5, and myogenin, which are myogenic transcription factors that

295 ts the induction of the transcription factor myogenin, which in turn activates synaptic gene expressi

296 d for expression of the transcription factor myogenin, which in turn drives differentiation of muscle

297 ing acute denervation, they are activated by myogenin, which is in turn regulated by histone deacetyl

298 in the promoter of the transcription factor myogenin, which regulates myogenic differentiation.

299 eriments, we find that heterodimerization of myogenin with E12 occurs prior to DNA-binding.

300 muscle development factors, such as MyoD and myogenin, with differentiation of SMN-deficient cells.