ライフサイエンスコーパス: MEF2

1 of the myocyte-enhancer family of proteins (Mef2).

2 cting through the myocyte enhancer factor 2 (MEF2).

3 nase-1 (Pdk1) and myocyte enhancer factor-2 (Mef2).

4 This loss is attenuated by expression of MEF2.

5 the exclusively nuclear transcription factor Mef2.

6 ession is the conserved transcription factor Mef2.

7 or of the master muscle transcription factor MEF2.

8 ulatory circuit that fine-tunes the level of Mef2.

9 o show that these compounds directly bind to MEF2.

10 and MEF2, and for IL1Ra, included NRF-1 and MEF2.

11 lates MuRF1 through the transcription factor MEF2.

12 on of the core cardiac transcription factor, MEF2.

13 er under control of the transcription factor MEF2.

14 quent activation of the transcription factor MEF2.

15 by Six1, not on the binding site of MyoD or MEF2.

16 the activity-regulated transcription factor MEF2.

17 at overlap significantly with the targets of MEF2.

18 a significantly different fashion than Notch-Mef2.

19 trolled by the transcription factors SRF and MEF2.

20 nsistent response in HCM, from heterogeneous Mef2 activation and reexpression of a fetal gene program

21 n MHC(403/+) and MHC(403/403) hearts defines Mef2 activation as a molecular signature of stressed HCM

22 apse density, implicating activity-dependent MEF2 activation as critical for MHCI signaling.

23 Here, we demonstrate that MEF2 activation fails to eliminate functional or structu

24 How MEF2 activation results in PSD-95 degradation and why th

25 Upon MEF2 activation, PSD-95 is ubiquitinated by the ubiquiti

26 nuclear localized basally, and unaffected by MEF2 activation, which our data suggest due to an enhanc

27 sponses to cocaine and suggest that reducing MEF2 activity (and increasing spine density) in NAc may

28 DAC5, act as signal-responsive repressors of MEF2 activity in cardiac myocytes and their nuclear expo

29 rget salt-inducible kinase 1 (SIK1) promotes MEF2 activity in myocytes via phosphorylation of class I

30 We show that reducing MEF2 activity in the NAc in vivo is required for the coc

31 Thus, a normal level of Mef2 activity is required in clock neurons to maintain r

32 ver, increasing dihydrosphingosine activates Mef2 activity through PDK1 in mammalian neuronal cell li

33 he inactivation of Nur77, induced by loss of MEF2 activity, plays a critical role in nigrostriatal de

34 the MLCP in VSMCs, as a potent repressor of MEF2 activity.

35 ting a pivotal role for CPI-17 in regulating MEF2 activity.

36 induced a significantly greater increase in MEF2 activity.

37 e RhoA/ROCK signaling cascade might regulate MEF2 activity.

38 tabilizing a repressor complex that controls MEF2 activity.

39 Manipulating MEF2 alone alters synaptic strength and GluA1 content, b

40 We previously reported that Notch-Mef2 also activates JNK, indicating that there are commo

41 on mediated by ERalpha and its regulation by MEF2 and class II HDACs.

42 hese compounds can be used as tools to study MEF2 and class IIa HDACs in vivo and as leads for drug d

43 MEF2 and FMRP cooperatively regulate the expression of P

44 Our results reveal that active MEF2 and FMRP function together in an acute, cell-autono

45 atal MyoD enhancer through associations with MEF2 and members of the Myocardin family.

46 r regulating cellular programs controlled by MEF2 and other transcription factors.

47 fic microRNA, miR-92b, which is activated by Mef2 and subsequently downregulates Mef2 through binding

48 on represses the transcriptional activity of MEF2 and that forced expression of MEF2-VP16 can restore

49 Our analyses showed that Brg1 interacts with MEF2 and that MEF2 is required for Brg1 recruitment to t

50 tion of HDAC5 and myocyte enhancer factor-2 (MEF2) and enhanced MEF2 transcriptional activity, which

51 nscription factor myocyte enhancer factor 2 (MEF2) and that Brg1 regulates the activity-induced expre

52 lear respiratory factor (NRF)-2 (Gabpa), and MEF2, and for IL1Ra, included NRF-1 and MEF2.

53 nSOD enzyme through the transcription factor Mef2, and predictably, perturbations in MnSOD modify p38

54 of collagen X-luciferase by exogenous Runx2, MEF2, and Smad1 in transfected chondrocytes.

55 e involved in cardiac myocyte growth through MEF2- and GATA4-dependent transcription.

56 We found that CREB, SRF, and MEF2 are all required for ODP, but have differential eff

57 for both Dc-ODP and Pc-ODP, whereas SRF and MEF2 are only needed for Dc-ODP.

58 Together, our findings implicate MEF2 as a key regulator of structural synapse plasticity

59 molecules that can modulate the function of MEF2 as research tools and therapeutic leads.

60 ty-regulated factors, such as CREB, Crest or Mef2, as well as activity-regulated immediate-early gene

61 In this study we investigated the role of MEF2 at different stages of adult skeletal muscle format

62 gonizes muscle differentiation by disrupting Mef2 beta-exon splicing.

63 e identify calcium-response element 1 as the MEF2 binding site in promoter IV of the Bdnf gene and de

64 RX, which recruits MEF2D away from canonical MEF2 binding sites and redirects it to retina-specific e

65 lanking region contains two highly conserved Mef2 binding sites and that Mef2c is able to bind to the

66 1, and a subsequent recruitment of P-TEFb to MEF2 binding sites in the promoter region of MEF2 target

67 at is synergistically activated by homotypic MEF2 binding sites.

68 Unlike ETS-mediated regulation, MEF2-binding motifs are not ubiquitous to all endothelia

69 a-specific enhancers that lack the consensus MEF2-binding sequence.

70 servations, we generated a homology model of MEF2 bound to a myocardin family protein, MASTR, that ac

71 nscription factor myocyte enhancer factor 2 (Mef2) by promoting exclusion of the alternatively splice

72 Myocyte enhancer factor 2 (MEF2) C, a member of the MEF2 family of transcription fa

73 ocytes at promoter modules containing Nkx2.5/Mef2, C/EBp, and a cis regulatory module.

74 n via RNAi or expressing a repressor form of Mef2 caused flies to lose circadian behavioral rhythms.

75 phosphorylation is lost, and the activity of MEF2 changes--MEF2 now associates with the TATA binding

76 A core component of the MEF2 complex is the MEF2D subunit.

77 ion via phosphorylation of CREB1 and HDACIIa/MEF2 complexes.

78 MEF2D bound to a MEF2 consensus site in the region of the mtDNA that cont

79 Importantly, MEF2 constitutively binds to the Nur77 promoter in neuro

80 y relied on overexpression of a constitutive MEF2 construct that impairs memory formation or knockdow

81 The loss of phosphorylated MEF2 contributes to loss of anabolic enzyme expression i

82 The nuclear localization of the MEF2 corepressor HDAC4 is impaired by Mrf4 knockdown, su

83 tudies revealed that IRF2BP2 is required for MEF2-dependent activation of Kruppel-like factor 2.

84 n heavy-chain Arg403Gln, (MHC(403/+)) and an Mef2-dependent beta-galactosidase reporter transgene.

85 The temporal and spatial relationship of Mef2-dependent gene activation with myocyte necrosis and

86 MASTR, that acts as a potent coactivator of MEF2-dependent gene expression.

87 MEF2-dependent genes represent the top-ranking gene set

88 Activation of MEF2-dependent inflammatory pathway genes by PKCalpha-CT

89 t links RhoA-mediated calcium sensitivity to MEF2-dependent myocardin expression in VSMCs through a m

90 ssion, VEGF stimulated transcription from an MEF2-dependent promoter.

91 ith necrotic cells, MHC(403/+) myocytes with Mef2-dependent reporter activation reexpressed the fetal

92 tially increased in MHC(403/403) hearts, but Mef2-dependent reporter activation was patchy.

93 equential analyses showed myocytes increased Mef2-dependent reporter activity before death.

94 us cyclin T1 in murine C2C12 cells abolishes MEF2-dependent reporter gene expression as well as trans

95 In hypertrophic hearts, activation of the Mef2-dependent reporter was remarkably heterogeneous and

96 nuclear accumulation of HDAC inhibiting the MEF2-dependent Sost bone enhancer, and class I HDACs are

97 MEF2-dependent synapse elimination is rescued in Fmr1 KO

98 SIK2 activates MEF2-dependent transcription and relieves repression of

99 Activation of MEF2-dependent transcription induced by serum starvation

100 P-TEFb is a critical step for stimulation of MEF2-dependent transcription, therefore providing a fund

101 s, whereas overexpression of P-TEFb enhances MEF2-dependent transcription.

102 atellite cell differentiation and identify a MEF2-dependent transcriptome associated with skeletal mu

103 However, the MEF2-depleted fibers showed impaired integrity and a lac

104 l end of the MEF2 domain may allow different MEF2 dimers to recognize different DNA sequences in the

105 However, MEF2 does not show a major requirement in the maintenanc

106 ediately following the C-terminal end of the MEF2 domain may allow different MEF2 dimers to recognize

107 resent the crystal structure of the MADS-box/MEF2 domain of MEF2A bound to DNA.

108 previous structural studies showing that the MEF2 domain of MEF2A is partially unstructured, the pres

109 ructured, the present study reveals that the MEF2 domain participates with the MADS-box in both dimer

110 -terminal domain referred to as the MADS-box/MEF2 domain.

111 kely to be of major importance in regulating MEF2-driven cardiac remodeling in the presence of sympat

112 egative feedback circuit between miR-92b and Mef2 efficiently maintains the stable expression of both

113 evelopment and differentiation, such as SRF, MEF2, ETS1, SMAD, and GATA.

114 Interestingly, ablation of Mef2 expression at later stages of development showed ME

115 Knocking down Mef2 expression via RNAi or expressing a repressor form

116 Deletion of miR-92b caused abnormally high Mef2 expression, leading to muscle defects and lethality

117 , partially sequestering Myf5 and inhibiting MEF2 expression.

118 gene regulatory elements, thus establishing MEF2 factors as the transcriptional effectors of VEGFA s

119 cells at the angiogenic front, we found that MEF2 factors directly transcriptionally activate the exp

120 To investigate the potential involvement of MEF2 factors in muscle regeneration, we conditionally de

121 These results suggest that individual MEF2 family members are able to recognize specific targe

122 These results reveal that mammalian MEF2 family members have distinct transcriptional functi

123 nd determine the requirements for individual MEF2 family members in Bdnf regulation.

124 ved splicing process of transcription factor MEF2 family members that yields different MEF2 isoforms

125 ese data show that individual members of the MEF2 family of transcription factors differentially regu

126 The MEF2 family of transcription factors regulates many deve

127 The Mef2 family of transcription factors regulates muscle di

128 enhancer factor 2 (MEF2) C, a member of the MEF2 family of transcription factors that plays an impor

129 lved in calcium signaling and members of the MEF2 family of transcription factors.

130 scription factors as MYOD and members of the MEF2 family.

131 Members of the myocyte enhancer factor 2 (MEF2) family of transcription factors play essential rol

132 on factors in the myocyte enhancer factor 2 (MEF2) family play important roles in cell survival by re

133 interaction with Myocyte Enhancer Factor-2 (MEF2) for their recruitment to specific genomic loci.

134 Here we examine Mef2 function in early heart development in zebrafish.

135 gnaling as a potent regulator of endothelial MEF2 function in the developing cardiovascular system.

136 hat impairs memory formation or knockdown of MEF2 function that increases spine numbers and enhances

137 , we found no adverse effects of attenuating Mef2 function.

138 leading to GSK3beta-dependent inhibition of MEF2 function.

139 ical to transcriptional control modulated by MEF2, GATA-4, and Tbx5, thereby enhancing gene expressio

140 MEF2 gene transcripts are subject to alternate splicing

141 We show that deletion of individual Mef2 genes has no effect on muscle regeneration in respo

142 not been seen in analyses of the function of Mef2 genes in other examples of myogenesis.

143 scriptional regulatory hierarchy, CLK/CYC- > Mef2- > Fas2, indicate that it influences the circadian

144 Furthermore, we demonstrate that Mef2 has temporally separable functions in this remodell

145 The transcription factor Mef2 has well established roles in muscle development in

146 Myocyte enhancer factor 2 (Mef2) has been implicated in RV development, regulating

147 n young rat cortical neurons, MHCI regulates MEF2 in an activity-dependent manner and requires calcin

148 Studies attempting to address the role of MEF2 in brain have largely relied on overexpression of a

149 onal targets among apelin-APJ, Galpha13, and MEF2 in endothelial cells, which are significantly decre

150 dentified as a key transcriptional target of MEF2 in hippocampal neurons, and siRNA-mediated knockdow

151 upports previous reports implicating SRF and MEF2 in long-term depression (required for Dc-ODP), and

152 esults therefore establish the importance of Mef2 in multiple roles in examples of myogenesis that ha

153 rocesses during development, but the role of MEF2 in neural stem/progenitor cells (NSPCs) in the adul

154 study, we tested the role of CREB, SRF, and MEF2 in ocular dominance plasticity (ODP), a paradigm of

155 of the transcription factors CREB, SRF, and MEF2 in the depression and potentiation components of OD

156 Here, we describe a role for Mef2 in the Drosophila pacemaker neurons that regulate c

157 the transcription function of CREB, SRF, and MEF2 in the visual cortex, and measured visually evoked

158 Similarly, inhibition of endogenous MEF2 increases synapse number in wild-type but not Fmr1

159 Treg cells led to myocyte enhancer factor 2 (Mef2)-induced expression of genes important to oxidative

160 f the Pcdh10-proteasome interaction inhibits MEF2-induced PSD-95 degradation and synapse elimination.

161 FMRP target mRNA, sequester Mdm2 and prevent MEF2-induced PSD-95 ubiquitination and synapse eliminati

162 Here we report that MEF2 induces a Protein phosphatase 2A (PP2A)-mediated de

163 nscription factor myocyte enhancer factor 2 (MEF2) induces excitatory synapse elimination in mouse ne

164 r corepressor 1 axis, which in turn promotes Mef2 inhibition, closing a self-limiting feedback loop,

165 t negative MEF2, while constitutively active MEF2 is able to induce myofibre hypertrophy.

166 However, we show here that Mef2 is absolutely required for a diverse range of Droso

167 of Mef2 RNAi constructs, we demonstrate that MEF2 is critical at the early stages of adult myoblast f

168 By contrast, vertebrate MEF2 is encoded by four distinct genes, Mef2a, -b, -c, a

169 In vivo, Mef2 is essential for the development of the Drosophila

170 r heart formation in Drosophila, but whether Mef2 is essential for vertebrate cardiomyocyte (CM) diff

171 Mef2 is inhibited by histone/protein deacetylase-9 (Hdac

172 We found that Mef2 is normally produced in all adult clock neurons and

173 tic and biochemical approaches, we find that MEF2 is phosphorylated at a conserved site in healthy fl

174 howed that Brg1 interacts with MEF2 and that MEF2 is required for Brg1 recruitment to target genes in

175 D-mef2 is required for heart formation in Drosophila, but

176 Most important, dysregulation of MHCI and MEF2 is required for the MIA-induced reduction in neural

177 We show here that Mef2 is required for this daily fasciculation-defascicul

178 We show that Mef2 is required in the fat body for anabolic function a

179 Mef2 is the key transcription factor for muscle developm

180 MEF2 is thus a critical transcriptional switch in the ad

181 nscription factor myocyte enhancer factor 2 (MEF2) is expressed throughout the central nervous system

182 ctopic expression of myogenin and a specific Mef2 isoform induced myogenic differentiation without ac

183 tational analysis of regulatory regions from MEF2 isoform-dependent gene sets identified the Notch an

184 pathways as key determinants in coordinating MEF2 isoform-specific control of antagonistic gene progr

185 Analysis of MEF2 isoform-specific function in neonatal cardiomyocyte

186 ted inducible knockout of all brain-enriched Mef2 isoforms (Mef2a/c/d) specifically from neural stem

187 de opportunities to modulate the activity of MEF2 isoforms and their respective gene programs in skel

188 Genetic deletion of individual MEF2 isoforms in brain during embryogenesis demonstrated

189 detailed information on the localization of MEF2 isoforms in the mammalian brain.

190 ghout the central nervous system, where four MEF2 isoforms play important roles in neuronal survival

191 These two MEF2 isoforms were co-expressed in virtually all neurons

192 or MEF2 family members that yields different MEF2 isoforms with differential effects on cardiac hyper

193 ural gene expression: after myoblast fusion, Mef2 knockdown did not interrupt expression of major str

194 aker neurons to become desynchronized, while Mef2 knockdown strongly dampens molecular rhythms.

195 Contrary to our hypothesis, inducible Mef2 KO mice also displayed an increase in YFP(+) neuron

196 rther validated these findings in vivo using MEF2-LacZ reporter mice.

197 l survival factor myocyte enhancer factor 2 (MEF2) leading to its inactivation and loss.

198 itionally, overexpression of miR-92b reduced Mef2 levels and caused muscle defects similar to those s

199 ng microRNA sponge techniques also increased Mef2 levels and caused muscle defects similar to those s

200 MHCI and MEF2 levels are higher, and synapse density is lower, on

201 Precise control of Mef2 levels is essential for muscle development as diffe

202 d synthesis by Myriocin, or reducing Pdk1 or Mef2 levels, all effectively suppress neurodegeneration

203 To better understand the mechanisms of MEF2-mediated regional gene regulation in the heart, we

204 s in both synapse development/maturation and MEF2-mediated synapse remodeling.

205 movement of signaling proteins that initiate MEF2-mediated transcriptional reprogramming events.

206 We hypothesized a critical role of a Mef2-microRNAs axis in RV failure.

207 our results uncover a muscle-restricted p38K-Mef2-MnSOD signaling module that influences life span an

208 that in Drosophila, a p38 MAP kinase (p38K)/Mef2/MnSOD pathway is a coregulator of stress and life s

209 ng factor), SRF (serum response factor), and MEF2 (myocyte enhancer factor 2) play critical roles in

210 tch and the pleiotropic transcription factor Mef2 (myocyte enhancer factor 2), which profoundly influ

211 The functional role of MEF2/MyoD-binding sites and neighboring three CpG cluste

212 MEF2A is a member of the MEF2 (myogenic enhancer factor 2) family of transcriptio

213 n is lost, and the activity of MEF2 changes--MEF2 now associates with the TATA binding protein to bin

214 opment of the Drosophila larval musculature: Mef2-null embryos have no differentiated somatic muscle.

215 IIa HDACs by blocking their interaction with MEF2 on DNA.Weused X-ray crystallography and (19)F NMRto

216 Mutations in certain E-box, NFkappaB, MEF2, or Ets family binding sites--known to be important

217 tered molecular clocks in pacemaker neurons: Mef2 overexpression causes the oscillations in individua

218 produced in all adult clock neurons and that Mef2 overexpression in clock neurons leads to long perio

219 ects similar to those seen in Mef2 RNAi, and Mef2 overexpression led to reversal of these defects.

220 es demonstrate correlation between Notch and Mef2 paralogues and support the notion that Notch-MEF2 s

221 ther SIK1 couples cAMP signaling to the HDAC-MEF2 pathway during myogenesis and how this response cou

222 The MHCI-MEF2 pathway identified here also mediates the effects o

223 ults indicate that an iron/sphingolipid/Pdk1/Mef2 pathway may play a role in FRDA.

224 sponse to activation of a Trk-dependent ERK5/MEF2 pathway, and our data indicate that this pathway pr

225 ice also activates an iron/sphingolipid/PDK1/Mef2 pathway, indicating that the mechanism is evolution

226 ced KLF2 expression in part through the ERK5/MEF2 pathway.

227 ntiation block by interfering with MYOD1 and MEF2 pro-differentiation activities.

228 ry muscle precursor cells profoundly impairs MEF2 protein accumulation and myogenic differentiation.

229 ssential for muscle development as different Mef2 protein levels activate distinct sets of muscle gen

230 Finally, we show that Mef2 proteins cooperate with the products of their targe

231 scle differentiation by depleting individual MEF2 proteins in myoblasts.

232 extensive redundancy, we show that mammalian MEF2 proteins regulate a significant subset of nonoverla

233 Knockdown of individual MEF2 proteins, MEF2A, -C, and -D, in primary neonatal ca

234 MEF2 recognizes DNA and interacts with transcription cof

235 specific targets among the entire cohort of MEF2-regulated genes in the muscle genome.

236 However, the downstream factors that mediate MEF2-regulated survival are unknown.

237 The transcription factor Mef2 regulates activity-dependent neuronal plasticity an

238 ubiquitously expressed transcription factor MEF2 regulates an intricate transcriptional program in n

239 Moreover, Mef2 regulates microRNAs that have emerged as important

240 Myocyte enhancer factor 2 (MEF2) regulates specific gene expression in diverse deve

241 ude that in the context of adult myogenesis, MEF2 remains an essential factor, participating in contr

242 creased histone H3 acetylation and increased MEF2 reporter activity in a PKD-dependent manner, consis

243 king gene set enriched after Mrf4 RNAi and a MEF2 reporter is inhibited by co-transfected MRF4 and ac

244 mory in vivo, and its effects are reliant on Mef2, revealing a novel cell-intrinsic molecular pathway

245 ugh stage- and tissue-specific expression of Mef2 RNAi constructs, we demonstrate that MEF2 is critic

246 When Mef2 RNAi was induced in muscles following eclosion, we

247 used muscle defects similar to those seen in Mef2 RNAi, and Mef2 overexpression led to reversal of th

248 To consider Mef2 roles in severe HCM, we studied homozygous MHC(403/

249 eural stem cells and their progeny confirmed Mef2's requirement for Isx-9-induced increase in hippoca

250 reported the critical nature of calpain-CDK5-MEF2 signaling in governing dopaminergic neuronal loss i

251 entify a previously unknown MHCI-calcineurin-MEF2 signaling pathway that regulates the establishment

252 s, a putative Stat and/or Ets element, and a MEF2 site, and muscle transcription factors myogenin and

253 nal SOX binding sites and a single essential MEF2 site.

254 dent effects on transcription in vivo Paired MEF2 sites are prevalent in cardiac enhancers, suggestin

255 We show that two MEF2 sites in the enhancer function cooperatively due to

256 ons; however, only the Mef2c gene encodes an MEF2 splice variant that lacks the gamma repressor-domai

257 paralogues and support the notion that Notch-MEF2 synergy may be significant for modulating human mam

258 MEF2 target gene activation is directly linked to VEGFA-

259 nt of the histone acetyltransferase EP300 to MEF2 target gene regulatory elements, thus establishing

260 (ER)alpha gene, which we show to be a direct MEF2 target gene.

261 ChIP-Chip analysis identified numerous Mef2 target genes implicated in neuronal plasticity, inc

262 ssion as well as transcription of endogenous MEF2 target genes, whereas overexpression of P-TEFb enha

263 MEF2 binding sites in the promoter region of MEF2 target genes.

264 locked the recruitment of class IIa HDACs to MEF2-targeted genes to enhance the expression of those t

265 scribed indirect regulation by NRF1 of other MEF2 targets in muscle such as GLUT4.

266 ila, this process is controlled, in part, by MEF2, the sole member of an evolutionarily conserved tra

267 Mef2 therefore transmits clock information to machinery

268 vated by Mef2 and subsequently downregulates Mef2 through binding to its 3'UTR, forming a negative re

269 ession at later stages of development showed MEF2 to be more dispensable for structural gene expressi

270 requires calcineurin-mediated activation of MEF2 to limit synapse density.

271 In turn, SRF cooperated with MEF2 to sustain the expression of LMOD3 and other compon

272 nase-1 (Pdk1) and myocyte enhancer factor-2 (Mef2) to trigger neurodegeneration of adult photorecepto

273 time extensive cytoplasmic localization of a MEF2 transcription factor in the mammalian brain in vivo

274 for chromatin-mediated transcription of the Mef2 transcription factor.

275 nhibiting the nuclear receptor NURR1 and the MEF2 transcription factor.

276 MEF2 transcription factors (TFs) play essential roles in

277 Here, we identify MEF2 transcription factors as crucial regulators of spro

278 Mef2 transcription factors have been strongly linked wit

279 specific genes, many of which are targets of MEF2 transcription factors.

280 scription complex CLK/CYC directly regulates Mef2 transcription.

281 at members of the myocyte enhancer factor 2 (MEF2) transcription factor family bind a regulatory elem

282 n Drosophila, the Myocyte Enhancer Factor-2 (MEF2) transcription factor is important for all types of

283 hat activation of myocyte enhancer factor 2 (Mef2) transcription factors (TFs) by the pre-BCR is nece

284 The myocyte enhancer factor 2 (MEF2) transcription factors have been implicated in cell

285 euronal activity, myocyte enhancer factor 2 (MEF2) transcription factors induce robust synapse elimin

286 Myocyte enhancer factor 2 (MEF2) transcription factors play critical roles in diver

287 The Myocyte Enhancer Factor 2 (MEF2) transcription factors suppress an excitatory synap

288 that requires the myocyte enhancer factor 2 (MEF2) transcription factors.

289 ced nuclear export, suppressed flow-mediated MEF2 transcriptional activity and expression of KLF2 and

290 on, our results suggest a mechanism in which MEF2 transcriptional activity is differentially recruite

291 yocyte enhancer factor-2 (MEF2) and enhanced MEF2 transcriptional activity, which leads to expression

292 ear translocation of HDAC4 and repression of MEF2 transcriptional activity.

293 st step in molecularly dissecting vertebrate MEF2 transcriptional function in skeletal muscle differe

294 expression of the myocyte enhancer factor 2 (MEF2) transcriptional target Kruppel-like factor 2.

295 a direct transcriptional target of SOX10 and MEF2 via this evolutionarily conserved enhancer.

296 tivity of MEF2 and that forced expression of MEF2-VP16 can restore expression of the collagen X repor

297 signals activated myocyte enhancer factor-2 (Mef2), we studied mice carrying the HCM mutation, myosin

298 class II histone deacetylases that activate Mef2 were substantially increased in MHC(403/403) hearts

299 ion by inhibiting myocyte enhancer factor 2 (MEF2), which activates a distant bone enhancer.

300 fibre size is prevented by dominant negative MEF2, while constitutively active MEF2 is able to induce