ライフサイエンスコーパス: MEF2

1 ption factor (TF) myocyte enhancer factor-2 (MEF2).

2 ion of upstream regulators of KLF2 (ERK5 and MEF2).

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

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

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

6 a significantly different fashion than Notch-Mef2.

7 trolled by the transcription factors SRF and MEF2.

8 This loss is attenuated by expression of MEF2.

9 the exclusively nuclear transcription factor Mef2.

10 ession is the conserved transcription factor Mef2.

11 or of the master muscle transcription factor MEF2.

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

13 o show that these compounds directly bind to MEF2.

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

15 lates MuRF1 through the transcription factor MEF2.

16 ates dendritic spine number and type through Mef2.

17 on of the core cardiac transcription factor, MEF2.

18 er under control of the transcription factor MEF2.

19 the activity-regulated transcription factor MEF2.

20 at overlap significantly with the targets of MEF2.

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

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

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

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

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

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

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

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

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

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

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

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

35 induced a significantly greater increase in MEF2 activity.

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

37 tabilizing a repressor complex that controls MEF2 activity.

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

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

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

41 MEF2 and FMRP cooperatively regulate the expression of P

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

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

44 des of interactions between MEF2 and NKX2-5: MEF2 and NKX bind to adjacent DNA sites to recognize DNA

45 acent DNA sites to recognize DNA in cis; and MEF2 and NKX bind to different DNA strands to interact w

46 e crystal structures of ternary complexes of MEF2 and NKX2-5 bound to myocardin enhancer DNA in two c

47 MEF2 and NKX2-5 transcription factors interact with each

48 l two possible modes of interactions between MEF2 and NKX2-5: MEF2 and NKX bind to adjacent DNA sites

49 cular mechanisms of the interactions between MEF2 and NKX2.5 and their roles in cardiogenesis.

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

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

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

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

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

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

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

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

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

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

60 ce for genetic interaction between Ube3a and Mef2 as simultaneous dosage manipulation in different ti

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

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

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

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

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

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

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 pposing functions of Setd1a on promoters and Mef2-bound enhancers.

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

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

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 ng a functional departure from the canonical MEF2 corepressor function of class IIa HDACs.

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

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

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

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

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

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

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

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

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

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

96 MEF2-dependent synapse elimination is rescued in Fmr1 KO

97 SIK2 activates MEF2-dependent transcription and relieves repression of

98 on of HDAC4, thereby relieving inhibition of Mef2-dependent transcription of K(+) and water transport

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

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

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

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

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

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

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

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

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

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

109 ete zone bordering the infarct switch from a MEF2-driven homeostatic lineage-specific to an AP-1-driv

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

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

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

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

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

115 , partially sequestering Myf5 and inhibiting MEF2 expression.

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

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

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

119 n regulatory roles exerted by members of the MEF2 family and MEF2B's involvement in B-cell lymphoma.

120 We highlight PGC1alpha, SRF and the MEF2 family as transcription factors that may potentiall

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 kely representative for other members of the MEF2 family.

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

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

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

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

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

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

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

138 , we found no adverse effects of attenuating 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 Of the four mammalian Mef2 genes, Mef2d is highly expressed in the suprachiasm

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

165 a upregulation of myocyte enhancer factor 2 (MEF2) induces KLF2 expression.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

181 Mef2 is the key transcription factor for muscle developm

182 MEF2 is thus a critical transcriptional switch in the ad

183 scription factor, myocyte enhancer factor-2 (MEF2), is required for normal circadian behavior in Dros

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

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

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

187 Analysis of MEF2 isoform-specific function in neonatal cardiomyocyte

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

212 thousands of cardiomyocyte lineage-specific MEF2-occupied regulatory elements that lost accessibilit

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

214 s with a striking overlap between Setd1a and Mef2 on enhancers.

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

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

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

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

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

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

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

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

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

224 articularly notable for the angiogenic VEGFA-MEF2 pathway, otherwise active in adult hearts and durin

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

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

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

228 argets of miR-135a, including members of the Mef2 protein family, are identified that begin to explai

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

230 In contrast, Mettl21c knockout increased Mef2 protein levels in slow muscles.

231 euronal targets of miR-135a, including Mef2a Mef2 proteins are key regulators of excitatory synapse d

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

233 scle differentiation by depleting individual MEF2 proteins in myoblasts.

234 ese studies are the first to show a role for MEF2 proteins in the brain outside of the hippocampus, a

235 ngs add to the growing body of evidence that MEF2 proteins play important roles in the brain.SIGNIFIC

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

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

238 MEF2 recognizes DNA and interacts with transcription cof

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

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

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

242 Moreover, Mef2 regulates microRNAs that have emerged as important

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

244 The angiogenic VEGFA-MEF2 regulatory pathway is predominantly active in endoc

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

261 MEF2 target gene activation is directly linked to VEGFA-

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

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

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

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

266 Mef2 therefore transmits clock information to machinery

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

268 d interactions between UBE3A/Ube3a and MEF2C/Mef2, thus contributing to the characterization of the u

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 ed nuclear export in cardiomyocytes, freeing MEF2 to stimulate progrowth genes; it was generally assu

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

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

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 Myocyte enhancer factor 2 (MEF2) transcription factors are key regulators of the de

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

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

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

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

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

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

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

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

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 ression of each single orthologous gene (Da, Mef2, Ube3a, Zfh1, XNP) and in pairwise combinations.

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

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