ライフサイエンスコーパス: myocardin

1 by repressing its transcriptional regulator, Myocardin.

2 edly decreased upon RNA silencing of SRF and myocardin.

3 g the quaking response element in exon 2a of myocardin.

4 binding of histone deacetylase 5 (HDAC5) to myocardin.

5 ing with the potent tissue-specific cofactor myocardin.

6 ontractile phenotype and is regulated by SRF/myocardin.

7 regulate the transcriptional activity of the myocardin.

8 s occurs through the induction of miR-143 by myocardin.

9 y ERK1/2 through a direct phosphorylation of myocardin.

10 located within the transactivation domain of myocardin.

11 KLF5 and its downstream signaling molecule, myocardin.

12 n to promote the transcriptional activity of myocardin.

13 was achieved most efficiently with GMT plus myocardin.

14 h muscle-specific transcription coactivator, myocardin.

15 and hMSCs up-regulated the transcription of myocardin.

16 iation via competing with SRF for binding to myocardin.

17 ineage through transcriptional repression of Myocardin.

18 RP2BP directly interacted with SRF, CRP2 and myocardin.

19 lative levels of Notch1 signaling, HRT2, and myocardin.

20 h direct binding to the N-terminal region of myocardin.

21 oxf1, PDGFa, PDGFb, PDGF receptor alpha, and myocardin.

22 n, by abolishing the promyogenic function of myocardin, a key mediator of smooth muscle differentiati

23 Consistently, we found that the level of myocardin, a key transcription factor promoting contract

24 Here we show that NF-kappaB(p65) represses myocardin activation of cardiac and smooth muscle genes

25 le-specific genes, the mechanisms regulating myocardin activity are still poorly understood.

26 we identified that arterial damage triggers myocardin alternative splicing and is tightly coupled wi

27 ors, including Klf4 (Kruppel-like factor 4), myocardin and Elk-1 (ELK1, member of ETS oncogene family

28 nal interaction, p65 directly interacts with myocardin and inhibits the formation of the myocardin/SR

29 2/Cbfa1 expression and the downregulation of myocardin and Msx2.

30 criptional targets of serum response factor, myocardin and Nkx2-5 (NK2 transcription factor related,

31 FHL1 by JMJD2A was mediated through SRF and myocardin and required its demethylase activity.

32 h the contractile gene transcription factors myocardin and serum response factor (SRF), independent o

33 F-beta1 on miR143/145 was dependent upon the myocardin and serum response factor transcriptional swit

34 bone morphogenetic protein 4 and upstream of myocardin and smooth muscle cell contractile protein syn

35 yocardin by p300 enhances the association of myocardin and SRF as well as the formation of the myocar

36 nse factor (SRF), resulting in disruption of myocardin and SRF interactions and thereby attenuating e

37 Loss of Ezh2 derepresses expression of myocardin and Tbx18, which are important regulators of s

38 pression of the SRF (serum response factor), myocardin, and MRTFA (myocardin-related transcription fa

39 g GATA binding protein 4, Hand2, T-box5, and myocardin, and two microRNAs, miR-1 and miR-133, activat

40 e SAP domain-containing co-activator protein myocardin, and we show that paired sites buffer the enha

41 demonstrated simultaneous repression of both myocardin- and Notch1-induced MLCK promoter activity.

42 vely, these findings identify a function for myocardin as an SRF-independent transcriptional represso

43 We used a yeast two-hybrid screen, with myocardin as bait in a search for factors that regulate

44 We used a yeast two-hybrid screen with myocardin as bait to search for factors that may regulat

45 ne DNA glycosylase (TDG) was identified as a myocardin-associated protein.

46 ential for the expression of SMC markers and myocardin at both the mRNA and protein levels during mou

47 th muscle-specific transcriptional activator myocardin at mRNA and protein levels.

48 urthermore, we found that phosphorylation of myocardin at these sites impairs its interaction with ac

49 s through modulating the activity of the SRF-myocardin axis to either promote or inhibit differentiat

50 Myocardin belongs to the SAF-A/B, Acinus, PIAS (SAP) dom

51 fic gene expression through interfering with myocardin binding to SRF.

52 otein ligase E3 component n-recognin 5) as a myocardin-binding protein.

53 We now report the discovery of a myocardin/BMP10 (where BMP10 indicates bone morphogeneti

54 these data identify a heretofore undescribed myocardin/BMP10 signaling pathway that regulates cardiom

55 ssion of PP1alpha inhibited the induction of myocardin by MEF2C.

56 Acetylation of myocardin by p300 enhances the association of myocardin

57 nes; little is known, however, about whether myocardin can orchestrate ECM expression to act in conce

58 upting its binding to SRF and abolishing SRF-myocardin complex binding to the promoters of smooth mus

59 The serum response factor (SRF)/myocardin complex binds to CArG sequences to activate mi

60 the association of the serum response factor-myocardin complex with VSMC contractile gene promoters a

61 In this study, we demonstrated myocardin coordinate smooth muscle differentiation by in

62 Conversely, myocardin decreases p65-mediated target gene activation

63 Conversely, acetylation of myocardin decreases the binding of histone deacetylase 5

64 s extinguished, or profoundly attenuated, in myocardin-deficient hearts.

65 optotic factors are induced and activated in myocardin-deficient hearts.

66 To identify myocardin-dependent functions in smooth muscle cells (SM

67 of WNT2 signaling, leading to repression of myocardin-dependent genes.

68 ernary complexes of MEF2 and NKX2-5 bound to myocardin enhancer DNA in two crystal forms.

69 ion of a PP1alpha inhibitor, CPI-17, reduced myocardin expression and inhibited VSMC differentiation,

70 contractile phenotype by both up-regulating myocardin expression and promoting the association of th

71 ion at Ser-307 were increased, together with myocardin expression as well as SRE and NF-kappaB activi

72 NA-145 resulted in reduced KLF4 and elevated myocardin expression in aortas from ApoE(-/-) mice, cons

73 diated calcium sensitivity to MEF2-dependent myocardin expression in VSMCs through a mechanism involv

74 l role in VSMC differentiation and regulates myocardin expression, leading us to investigate whether

75 erentiation by activating ATF6 and promoting myocardin expression.

76 as well as beta-myosin heavy chain (MHC) and myocardin expressions.

77 recruiting cofactors, such as members of the myocardin family and ternary complex factors (TCFs), res

78 rum response factor (SRF), its actin-binding myocardin family coactivator, MAL, and the SRF-target 5q

79 actor megakaryoblastic leukaemia 1 (MKL1), a myocardin family member that is pivotal in cardiac devel

80 n, including serum response factor (SRF) and myocardin family members, and readily differentiate to S

81 t specific transcriptional regulators of the myocardin family might also regulate collagen gene expre

82 n of smooth muscle-specific promoters by the myocardin family of proteins.

83 Here, we show that members of the Myocardin family of transcriptional coactivators, MASTR

84 enerated a homology model of MEF2 bound to a myocardin family protein, MASTR, that acts as a potent c

85 The myocardin family proteins (myocardin, MRTF-A, and MRTF-B

86 icated important developmental functions for myocardin family proteins primarily in regulation of car

87 gh associations with MEF2 and members of the Myocardin family.

88 xpression of smooth muscle genes through the myocardin-family of co-activators.

89 istically, we found that TEAD1 competes with myocardin for binding to serum response factor (SRF), re

90 t acetylation plays a key role in modulating myocardin function in controlling cardiac and smooth mus

91 osis, revealing evolutionary conservation of myocardin function in SMCs and cardiomyocytes.

92 nally, we demonstrated that HMG2L1 abrogates myocardin function through disrupting its binding to SRF

93 effort to search for proteins that regulate myocardin function, we identified a novel HMG box-contai

94 s not required for its inhibitory effects on myocardin function.

95 Myocardin functions as a transcriptional coactivator of

96 ardiomyocyte-restricted null mutation in the myocardin gene (Myocd) develop dilated cardiomyopathy an

97 Pax3-Cre(+) mice were generated in which the myocardin gene was selectively ablated in neural crest-d

98 Inactivation of myocardin has been implicated in malignant tumor growth.

99 of Brg1, whereas miR-133 was not induced by myocardin in a Brg1-dependent manner.

100 rganization and that cell-autonomous loss of myocardin in cardiac myocytes triggers programmed cell d

101 of the serum response factor (SRF) cofactor myocardin in controlling muscle gene expression as well

102 The loss of myocardin in SMCs triggers ER stress and autophagy, whic

103 To determine the function of myocardin in the developing cardiovascular system, Myocd

104 the nuclei of SMCs and forms a complex with myocardin in vivo and in vitro.

105 This study provides the first evidence that myocardin, in addition to activating smooth muscle-speci

106 s demonstrated that in the presence of Brg1, myocardin increased SRF binding to both the miRs-143/145

107 a partially SRF-dependent, although largely myocardin-independent manner.

108 Myocardin induced expression of miRs-143/145 and miR-133

109 We found that TDG abrogates myocardin induced expression of smooth muscle-specific g

110 more, we found HMG2L1 specifically abrogates myocardin-induced activation of smooth muscle-specific g

111 miR-145 was necessary for myocardin-induced reprogramming of adult fibroblasts int

112 terfering RNA in fibroblast cells attenuated myocardin-induced smooth muscle-specific gene expression

113 ement, and this element is indispensible for myocardin-induced transactivation of TGFB1I1 promoter.

114 We have previously found that myocardin induces the acetylation of nucleosomal histone

115 Importantly, myocardin inhibits cellular proliferation by interfering

116 ly interacted with SRF without affecting SRF-myocardin interaction.

117 Myocardin is a cardiac and SM-restricted coactivator of

118 In this study, we show that myocardin is a direct target for p300-mediated acetylati

119 Myocardin is a muscle lineage-restricted transcriptional

120 Myocardin is a muscle-restricted transcriptional coactiv

121 Myocardin is a remarkably potent transcriptional coactiv

122 Myocardin is a serum response factor (SRF) co-activator

123 Myocardin is an extraordinarily powerful cofactor of ser

124 Myocardin is perhaps the most potent transcription facto

125 Here we show that myocardin is required for maintenance of cardiomyocyte s

126 onclude that the transcriptional coactivator myocardin is required for maintenance of heart function

127 Acetylation of myocardin is required for myocardin to activate smooth m

128 Ectopic expression of myocardin is sufficient to induce endogenous TGFB1I1 exp

129 rdin, which is mediated by the C terminus of myocardin, is required for the acetylation event.

130 y, we found that ERK1/2 phosphorylates mouse myocardin (isoform B) at four sites (Ser(812), Ser(859),

131 ative expression and activities of the major myocardin isoforms across disparate species.

132 p300, yet no studies have determined whether myocardin itself is similarly modified.

133 ocus for male sexual development upstream of myocardin-like 2 (MKL2) (P = 8.9 x 10(-9)), a menarche l

134 Myocardin-like protein 2 (MKL2) is a transcriptional co-

135 In hyperinsulinemic states, myocardin may act as a nuclear effector of insulin, prom

136 This myocardin-mediated induction was attenuated by dominant

137 ocardin protein expression without affecting myocardin mRNA expression.

138 that Spry1 increases, while Spry4 decreases myocardin mRNA levels.

139 The myocardin family proteins (myocardin, MRTF-A, and MRTF-B) are serum response factor

140 specification and differentiation including myocardin/Mrtf-B and the signaling factor Fgf10.

141 We found that Myocardin mutants show normal branching, despite the abs

142 activates the smooth muscle master regulator Myocardin (Myocd) and induces smooth muscle differentiat

143 y regulators of the SMC phenotype, including myocardin (MYOCD) and KLF4, have been identified, a unif

144 We examined whether the overexpression of myocardin (MYOCD) and telomerase reverse transcriptase (

145 Both TGF-beta and myocardin (MYOCD) are important for smooth muscle cell (

146 Given that TGF-beta1 and myocardin (MYOCD) are potent activators for VSMC differe

147 as serum response factor and members of the myocardin (Myocd) family.

148 Myocardin (Myocd) is a potent transcriptional coactivato

149 Myocardin (MYOCD) is a transcriptional co-activator that

150 Myocardin (MYOCD) is an essential component of a molecul

151 Myocardin (MYOCD) is the founding member of a class of t

152 serum response factor and its coactivators, myocardin (Myocd) or Myocd-related transcription factors

153 directly by the serum response factor (SRF)/myocardin (MYOCD) transcriptional switch.

154 Myocardin (MYOCD), a cardiac-specific co-activator of se

155 the transcription and the transactivation of myocardin (MYOCD), a master regulator for SMC-specific g

156 the mRNA expression and promoter activity of myocardin (Myocd), a master regulator of SM differentiat

157 One particularly strong SRF cofactor, myocardin (MYOCD), acts as a component of a molecular sw

158 Further, neither SRF nor its coactivator, Myocardin (MYOCD), was able to induce several distinct I

159 A luciferase assay showed myocardin (MYOCD)-mediated transactivation of the KCNMB1

160 We propose a new myocardin nomenclature reflecting the dominant splice va

161 Myocardin-null (Myocd) embryos and embryos harboring a c

162 ses the trans-activation of the promoters of myocardin of these genes.

163 Rs-143/145 and miR-133, whereas knockdown of myocardin only attenuated miRs-143/145 expression.

164 s, miRs-143/145 were dramatically induced by myocardin only in the presence of Brg1, whereas miR-133

165 constitutively active Notch1 in presence of myocardin or by Jagged1 ligand stimulation.

166 Here siRNAs to myocardin or NF-kappaB, as well as CHIP overexpression p

167 in multiple cell lines whereas knocking-down myocardin or SRF significantly attenuated TGFB1I1 expres

168 enotype in vitro in part through an Akt/FoxO/myocardin pathway.

169 m response factor (SRF) and its coactivator, myocardin, play a central role in the control of smooth

170 m by which interaction between NF-kappaB and myocardin plays a central role in modulating cellular pr

171 monstrate that during postnatal development, myocardin plays a unique, and important, role required f

172 the spliceosome, where it interacts with the myocardin pre-mRNA and regulates the splicing of alterna

173 ream target of PI3K/Akt signaling, represses myocardin promoter activity, and that Spry1 increases, w

174 ding to the increased binding of ATF6 on the myocardin promoter and increased its expression.

175 gene via binding of a serum response factor-myocardin protein complex to a nonconsensus CArG element

176 urthermore, we found that UBR5 can attenuate myocardin protein degradation resulting in increased myo

177 n protein degradation resulting in increased myocardin protein expression without affecting myocardin

178 tes lysine residues at the N terminus of the myocardin protein.

179 erentiation through its ability to stabilize myocardin protein.

180 We show that SRF and myocardin regulate a cardiovascular-specific microRNA (m

181 ted a cell autonomous block in expression of myocardin-regulated genes encoding SMC-restricted contra

182 rst evidence that TGFB1I1 is not only an SRF/myocardin-regulated smooth muscle marker but also critic

183 However, the underlying mechanism of myocardin regulation of cellular growth remains unclear.

184 ellular localization of activated Notch1 and myocardin related transcription factor (MRTF)-A.

185 ult depletion of either SRF or its cofactors Myocardin Related Transcription Factor (MRTF-A/-B), reve

186 Megakaryoblastic leukemia 1 (MKL1) is a myocardin-related coactivator of the serum response fact

187 subunits, CCTepsilon, as a component of the myocardin-related cotranscription factor-A (MRTF-A)/seru

188 factors (TCFs), ELK1, Sap1, and Net, and the myocardin-related factors, MKL1 and MKL2.

189 A0825 reduced TGFbeta1-induced activation of myocardin-related transcription factor (MRTF) and p38 mi

190 g events targeting the serum response factor-myocardin-related transcription factor (MRTF) complex.

191 gration, mainly by recruiting members of the myocardin-related transcription factor (MRTF) family of

192 The Rho/myocardin-related transcription factor (MRTF) pathway is

193 oskeletal gene targets for the Rho-regulated myocardin-related transcription factor (MRTF) SRF cofact

194 Myocardin-related transcription factor (MRTF) was a cent

195 CLDN-2 loss also activated myocardin-related transcription factor (MRTF), a fibroge

196 wing CD44 RNAi suggested a possible role for myocardin-related transcription factor (MRTF), a known r

197 Myocardin-related transcription factor (MRTF), a Rho/act

198 n of stress fibers results in the release of myocardin-related transcription factor (MRTF), a transcr

199 hese cells, causing nuclear translocation of myocardin-related transcription factor (MRTF)-A and MRTF

200 Myocardin-related transcription factor (MRTF)-A and MRTF

201 transduced through aberrant localization of myocardin-related transcription factor (MRTF)-A repressi

202 e able to maintain cytosolic localization of myocardin-related transcription factor (MRTF)-A, a coact

203 ding protein that specifically modulates the myocardin-related transcription factor (MRTF)-serum resp

204 hanosensors Yes-associated protein (YAP) and myocardin-related transcription factor (MRTF).

205 2-ylthiopropionic acid lead inhibitor of Rho/myocardin-related transcription factor (MRTF)/serum resp

206 al coactivator with PDZ domain (YAP/TAZ) and myocardin-related transcription factor (MRTF-A, also kno

207 We previously identified a nuclear myocardin-related transcription factor (nMRTF) resistanc

208 The roles of myocardin-related transcription factor A (MRTF-A) and MR

209 ne utilizing the transcriptional coactivator myocardin-related transcription factor A (MRTF-A) and se

210 and S1P(3) mediate this effect by activating myocardin-related transcription factor A (MRTF-A) and ye

211 at BMP4 triggers nuclear localization of the Myocardin-related transcription factor A (MRTF-A) in hum

212 Here we show that myocardin-related transcription factor A (MRTF-A) plays

213 transport and the concomitant regulation of myocardin-related transcription factor A (MRTF-A), a co-

214 stic leukemia 1 (MKL1), also known as MAL or myocardin-related transcription factor A (MRTF-A), is a

215 d transcription through nuclear retention of myocardin-related transcription factor A (MRTF-A).

216 Myocardin-related transcription factor A (MRTF-A/MAL/MKL

217 Myocardin-related transcription factor A downstream targ

218 erum response factor), myocardin, and MRTFA (myocardin-related transcription factor A) and dramatical

219 ofactors such as the coactivator MAL/MRTF-A (myocardin-related transcription factor A).

220 expression induced with adenovirus encoding myocardin-related transcription factor A, a potent coact

221 -light-chain-enhancer of activated B cells), myocardin-related transcription factor A, and Yes-associ

222 -actin-regulated transcriptional coactivator myocardin-related transcription factor A, MRTFA.

223 ivator of cell contractility and MRTF-A/SRF (myocardin-related transcription factor A/serum response

224 Furthermore, nuclear accumulation of myocardin-related transcription factor also modulated NF

225 downstream transcription factors, including myocardin-related transcription factor and Yes-associate

226 n triggers, and down-regulation of myosin or myocardin-related transcription factor prevents, this pr

227 In a screen for miRNAs regulated by myocardin-related transcription factor-A (MRTF-A), a coa

228 factor (SRF) binds to coactivators, such as myocardin-related transcription factor-A (MRTF-A), and m

229 se factor (SRF) along with its co-activator, myocardin-related transcription factor-A (MRTF-A).

230 ulation through the acutely mechanosensitive myocardin-related transcription factor-A (MRTF-A/MLK-1)

231 atios, and deregulation of mechanoresponsive myocardin-related transcription factor-A (MRTFA).

232 portance, both pathways are regulated by Rho/myocardin-related transcription factor-A and contribute

233 factors linked to fibroblast growth, MRTF-A (myocardin-related transcription factor-A) moved to the n

234 The cotranscription factor myocardin-related transcription factor-A, which affects

235 iated with decreased nuclear localization of myocardin-related transcription factor-A.

236 the impact of the actin-controlled MRTF-SRF (myocardin-related transcription factor-serum response fa

237 constraints altered the nuclear fraction of myocardin-related transcription factor.

238 d MRTF-A activity and place ATE1 upstream of myocardin-related transcription factor.

239 This review focuses on the ubiquitous myocardin-related transcription factor/serum response fa

240 The myocardin-related transcription factor/serum response fa

241 There is increasing evidence that the Myocardin-related transcription factor/Serum response fa

242 al, which establishes the importance of the myocardin-related transcription factor/serum response fa

243 The myocardin-related transcription factors (MRTF-A and MRTF

244 wth factor A induces nuclear accumulation of myocardin-related transcription factors (MRTFs) and regu

245 Myocardin-related transcription factors (MRTFs) are acti

246 The myocardin-related transcription factors (MRTFs) are coac

247 Myocardin-related transcription factors (MRTFs) are seru

248 The role of myocardin-related transcription factors (MRTFs) co-activ

249 Myocardin-related transcription factors (MRTFs) play a c

250 Myocardin-related transcription factors (MRTFs) regulate

251 Myocardin-related transcription factors (MRTFs) transloc

252 Myocardin-related transcription factors (MRTFs), through

253 mplex factors (TCFs) and the actin-regulated myocardin-related transcription factors (MRTFs), to its

254 The myocardin-related transcription factors (MRTFs), which a

255 Myocardin-related transcription factors (MRTFs), which f

256 tly binds to serum response factor (SRF) and myocardin-related transcription factors (MRTFs).

257 Myocardin-related transcription factors A and B (MRTFs,

258 tion of the SRF cofactors MRTF-A and MRTF-B (myocardin-related transcription factors).

259 ll GTPase RhoA and consecutive activation of myocardin-related transcription factors.

260 ase C, Rho-kinase, actin polymerization, and myocardin-related transcription factors.

261 (SRF) activity via SRF interaction with the myocardin-related transcriptional activator (MRTF)-A and

262 In addition, we demonstrated that myocardin represses versican through induction of miR-14

263 The effects of UBR5 on myocardin requires only the HECT and UBR1 domains of UBR

264 ccelerated calcification through a Runx2 and myocardin-serum response factor-dependent pathway.

265 y, we investigated the combinatorial role of myocardin/serum response factor (SRF) and Notch signalin

266 ctivation of TNF-alpha-induced NF-kappaB and myocardin/serum response factor (SRF) to convey hypertro

267 ls in vitro and in transgenic mice increased myocardin/serum response factor signaling and increased

268 Foxf2 attenuated myocardin/serum response factor signaling in smooth musc

269 Expression of myocardin/serum response factor-regulated myofibrillar g

270 ndependently regulated by TGF-beta1/SMAD and myocardin/serum response factor.

271 Our data demonstrated that myocardin significantly represses versican expression in

272 kt1 deficiency was associated with decreased myocardin, SRF, and alphaSMA expressions in vivo.

273 rdin and SRF as well as the formation of the myocardin-SRF-CArG box ternary complex.

274 tened levels of HRT2 concomitantly disrupted myocardin/SRF and Notch transcription complex formation

275 led both Jagged1 ligand- and Notch1-enhanced myocardin/SRF complex formation at the promoter CArG ele

276 ion or the promyogenic transcription factors myocardin/SRF in a CHIP-dependent manner.

277 myocardin and inhibits the formation of the myocardin/SRF/CArG ternary complex in vitro and in vivo.

278 s demonstrated that TDG binds to a region of myocardin that includes the SRF binding domain.

279 s including the key SMC transcription factor Myocardin, thereby matching many of the criteria of a ma

280 Acetylation of myocardin is required for myocardin to activate smooth muscle genes.

281 to aspartate has no effect on the ability of myocardin to activate SRF.

282 Although previous studies have shown myocardin to be a critical transcription factor for stim

283 nthetic capacity through enhanced binding of myocardin to CArG box DNA sequences present within the p

284 UBR5 significantly augmented the ability of myocardin to induce expression of endogenous SMC marker

285 ontaining SWI/SNF complexes are required for myocardin to induce expression of miRs-143/145 in smooth

286 CRP2 that works synergistically with SRF and myocardin to regulate smooth muscle gene expression.

287 bility of the 4xD (but not of 4xA) mutant of myocardin to stimulate expression of SM alpha-actin and

288 Myocardin transactivated the Bmp10 gene via binding of a

289 ion of ATF6 and leads to further increase of myocardin transcription.

290 s bait in a search for factors that regulate myocardin transcriptional activity.

291 Up-regulation of myocardin was accompanied by down-regulation of WNT-depe

292 The interaction between TDG and myocardin was confirmed in vitro by glutathione S-transf

293 n serum response factor and its co-activator myocardin was reduced by overexpression of Yap1 in a dos

294 1(-/-) mice, and the differentiation inducer myocardin was undetectable.

295 , the interaction domains between HMG2L1 and myocardin were mapped to the N termini of each of the pr

296 ) significantly impairs activation of SRF by myocardin, whereas the phosphodeficient mutation of all

297 ingly, a direct interaction between p300 and myocardin, which is mediated by the C terminus of myocar

298 , we test this model in vivo by inactivating Myocardin, which prevented airway smooth muscle differen

299 alcium signaling increased the expression of myocardin, which was sensitive to ROCK and p38 MAPK inhi

300 hibition resulted in increased expression of myocardin, while ectopic expression of PP1alpha inhibite