ライフサイエンスコーパス: myocardin

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

2 ineage through transcriptional repression of Myocardin.

3 RP2BP directly interacted with SRF, CRP2 and 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 was achieved most efficiently with GMT plus myocardin.

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

11 located within the transactivation domain of myocardin.

12 KLF5 and its downstream signaling molecule, myocardin.

13 n to promote the transcriptional activity of 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 lative levels of Notch1 signaling, HRT2, and myocardin.

18 induced suppression of SMC marker genes, and myocardin.

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

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

21 by repressing its transcriptional regulator, Myocardin.

22 edly decreased upon RNA silencing of SRF and myocardin.

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

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

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

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

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

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

29 n, binds the C-terminal activation domain of myocardin and enhances myocardin-mediated transcriptiona

30 regulated by actin dynamics, upregulated by myocardin and expressed in the neointima of injured aort

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

32 2/Cbfa1 expression and the downregulation of myocardin and Msx2.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

58 Acetylation of myocardin by p300 enhances the association of myocardin

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

60 scription factors Nkx2.5, Tbx5, and cofactor myocardin; cardiac proteins 24 h later; and a sarcomeric

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

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

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

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

65 Conversely, myocardin decreases p65-mediated target gene activation

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

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

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

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

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

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

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

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

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

75 ociated with a decrease in Nkx2.5, Tbx5, and myocardin expression in the WB F344 cells.

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

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

78 erentiation by activating ATF6 and promoting myocardin expression.

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

80 H3K9 methylation and that the effects of the myocardin factors on SMC-specific transcription may invo

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

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

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

84 assays demonstrated that Jmjd1a bound all 3 myocardin family members, and further mapping studies sh

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

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

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

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

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

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

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

92 globular (G) actin ratio, known to regulate myocardin family transcription factors, was also decreas

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

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

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

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

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

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

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

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

101 Myocardin functions as a transcriptional coactivator of

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

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

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

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

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

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

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

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

110 was found to compete with SRF for binding to myocardin in vitro and in vivo, suggesting that TDG can

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

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

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

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

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

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

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

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

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

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

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

122 Importantly, myocardin inhibits cellular proliferation by interfering

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

124 es, at least in part, through disrupting SRF/myocardin interactions.

125 Myocardin is a cardiac and SM-restricted coactivator of

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

127 Myocardin is a muscle lineage-restricted transcriptional

128 Myocardin is a muscle-restricted transcriptional coactiv

129 Myocardin is a remarkably potent transcriptional coactiv

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

131 Myocardin is an extraordinarily powerful cofactor of ser

132 Myocardin is perhaps the most potent transcription facto

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

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

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

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

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

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

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

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

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

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

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

144 This myocardin-mediated induction was attenuated by dominant

145 activation domain of myocardin and enhances myocardin-mediated transcriptional activation of VSMC-sp

146 ocardin protein expression without affecting myocardin mRNA expression.

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

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

149 Mice harboring loss-of-function mutations in myocardin, MRTF-A, and MRTF-B, respectively, display dis

150 ted transcription factors (MRTFs), including myocardin, MRTF-A/MKL1/MAL, and MRTF-B/MKL2, comprise a

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

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

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

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

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

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

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

158 Myocardin (Myocd) is a potent transcriptional coactivato

159 Myocardin (Myocd) is a serum response factor (SRF) coact

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

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

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

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

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

165 transcription by reducing the expression of Myocardin (Myocd), a potent SMC-specific nuclear coactiv

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

167 gh levels of serum response factor (SRF) and myocardin (MYOCD), two interacting transcription factors

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

189 erentiation through its ability to stabilize myocardin protein.

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

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

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

193 Taken together, these data demonstrate that myocardin regulates expression of genes required for the

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 MAL/MKL1/myocardin-related transcription factor A is cytoplasmic,

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

224 s genome and cDNA databases, we identified a myocardin-related transcription factor expressed specifi

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

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

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

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

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

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

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

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

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

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

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

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

237 The myocardin-related transcription factor/serum response fa

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

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

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

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

242 nuclear localization and recruitment of the myocardin-related transcription factors (MRTF-A and MRTF

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

244 Myocardin-related transcription factors (MRTFs) are acti

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

246 Myocardin-related transcription factors (MRTFs) are seru

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

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

249 Myocardin-related transcription factors (MRTFs) regulate

250 Myocardin-related transcription factors (MRTFs) transloc

251 Myocardin-related transcription factors (MRTFs), includi

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

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

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

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

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

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

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

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

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

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

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

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

270 Our data demonstrated that myocardin significantly represses versican expression in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

286 Myocardin transactivated the Bmp10 gene via binding of a

287 We and others have previously shown that the myocardin transcription factors play critical roles in t

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

289 by specific small interfering RNA attenuates myocardin transcriptional activation in cultured cells.

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 ator for the major VSMC transcription factor myocardin, which is required for VSMC differentiation to

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