ライフサイエンスコーパス: alpha-actin

1 een the fragment of actin-binding domain and alpha-actin.

2 l muscle, with a concomitant 40% decrease in alpha-actin.

3 ther characterize the consequences of mutant alpha-actin.

4 expression of the EMT marker, smooth muscle alpha-actin.

5 and reduced levels of glutathiolated cardiac alpha-actin.

6 ructures of profilin-beta-actin and profilin-alpha-actin.

7 through the regulation of the expression of alpha-actin.

8 lective markers including smooth muscle (SM) alpha-actin.

9 ition of growth suppression attributed to SM alpha-actin.

10 erioles were immunolabeled for smooth muscle alpha-actin.

11 expression patterns identical to those of SM alpha-actin.

12 luding telokin, SM22alpha, and smooth muscle alpha-actin.

13 ithout affecting expression of smooth muscle alpha-actin.

14 in a single gene encoding smooth muscle (SM) alpha-actin.

15 aMyHC mRNA expression and increases skeletal alpha-actin.

16 ction due to the expression of smooth muscle alpha-actin.

17 acterize this mutation in expressed human SM alpha-actin.

18 te on sarcomeres to bind and recruit cardiac alpha-actin.

19 specific proteins, including MyoD and muscle alpha-actin.

20 n regulating the expression of smooth muscle alpha-actin.

21 s in the ACTA1 gene encoding skeletal muscle alpha-actin.

22 g the cyto-contractile protein smooth muscle alpha-actin.

23 ay, enhanced the expression of smooth muscle alpha-actin.

24 of the differentiation marker smooth muscle alpha-actin.

25 oxia (but hypoxic-induction of smooth muscle alpha-actin 2 was specific for a RCC cell line).

26 repressed expression of pro-fibrotic factors Alpha-Actin-2 (ACTA2) and Alpha-1 Type I Collagen (COL1A

27 int titrations of the extended smooth muscle alpha-actin 5'-flanking region demonstrated that assembl

28 In conclusion, expression levels of alpha-actin, a thin filament protein involved in contrac

29 smooth muscle cell (SMC)-specific isoform of alpha-actin (ACTA2) is a major component of the contract

30 Smooth muscle alpha-actin (Acta2) is one of six highly conserved mamma

31 ) and cardiac (alpha-CAA) to skeletal muscle alpha-actin (alpha-SKA) that, in mice, occurs during ear

32 , as shown by the induction of smooth muscle alpha-actin (alpha-SMA) and extracellular matrix protein

33 is required for the induction smooth muscle alpha-actin (alpha-SMA) by scuPA.

34 n of the MKL1/SRF target gene, smooth muscle alpha-actin (alpha-SMA) via siRNA knockdown resulted in

35 Indeed, expression of smooth muscle alpha-actin (alpha-SMA), an indicator of fibroblast acti

36 smooth muscle cell (SMC)-specific isoform of alpha-actin (alpha-SMA), cause thoracic aortic aneurysms

37 ple smooth muscle marker genes, including SM alpha-actin (alpha-SMA), SM22alpha, and calponin.

38 expression analyses detected transcripts for alpha-actin, alpha-acetylcholine (ACh) receptor (alpha-A

39 Wild-type and mutant ZASP interact with alpha-actin, alpha-actinin, and myotilin.

40 1 at capping pointed ends of skeletal muscle alpha-actin (alphask-actin) filaments coated with alpha/

41 ellate cell; aHSCs) expressing smooth muscle alpha-actin (alphaSMA) and platelet-derived growth facto

42 m of PI3K under control of the smooth muscle alpha-actin (alphaSMA) promoter was generated (Ad-SMAdnP

43 d by the de novo expression of smooth muscle alpha-actin (alphaSMA) stress fibers, plays a central ro

44 terminal sequence, Ac-EEED, of smooth muscle alpha-actin, altered both actin cytoskeleton organizatio

45 rdiac alpha-actin instead of skeletal muscle alpha-actin alters actin conformational changes upon act

46 xhibit increased expression of smooth muscle-alpha-actin and -myosin heavy chain.

47 decreased the binding of full-length NEXN to alpha-actin and abolished the interaction between the fr

48 cified genes, such as those encoding cardiac alpha-actin and alpha-myosin heavy chain, in an SRF-depe

49 and nocodazole (3 x 10(-6)m), inhibitors of alpha-actin and alpha-tubulin polymerization, respective

50 tion as a coactivator of SRF on both cardiac alpha-actin and ANF promoters.

51 mooth muscle cell (SMC)-specific isoforms of alpha-actin and beta-myosin heavy chain, two major compo

52 with the smooth muscle-specific isoforms of alpha-actin and beta-myosin, which are known to cause fa

53 Expression of alpha-actin and col3a1 genes was strongly attenuated by

54 and -challenged mice demonstrated increased alpha-actin and CT-1 mRNA expression, and airway myocyte

55 and medial and intimal cells coexpressing SM-alpha-actin and CXCR4, the SDF-1alpha receptor, was dete

56 ned by increased expression of smooth muscle alpha-actin and decreased expression of E-cadherin.

57 te cells induced expression of smooth muscle alpha-actin and endothelin-1-mediated autocrine stellate

58 e TGF-beta1 gene had increased levels of SMC alpha-actin and enhanced ability to contract a collagen

59 t also emphasize the relationship between SM alpha-actin and fibrogenesis in hepatic myofibroblasts i

60 trated elevated expressions in smooth muscle alpha-actin and myosin heavy chain in Pkd2(+/-) arteries

61 However, myosin-1, alpha-actin and myosin-4 proteins were the biomarkers th

62 retain expression of smooth muscle-specific alpha-actin and physiological responses to agonists.

63 t coexpress mural cell markers smooth muscle alpha-actin and platelet-derived growth factor receptor

64 ranscriptional repressor and it represses SM alpha-actin and PPGB expression.

65 The binding of FOXK1 to the SM alpha-actin and PPGB promoters requires the presence of

66 or the regulation of the SRF target genes SM alpha-actin and PPGB.

67 of low signal intensity correlated well with alpha-actin and Prussian blue stain- and DiI-positive ar

68 d profound suppression of smooth muscle (SM) alpha-actin and SM myosin heavy chain expression while s

69 levels of di-methyl H3K9, stimulated the SM alpha-actin and SM22 promoters, and synergistically enha

70 t of myocardin to stimulate expression of SM alpha-actin and SM22, as assessed by corresponding promo

71 -induced protein synthesis and expression of alpha-actin and SM22, indicating that eIF2B is required

72 fferentiation marker gene expression, eg, SM alpha-actin and SMMHC, via Rho kinase and myocardin and

73 on of SRF target genes such as smooth muscle alpha-actin and smooth muscle myosin heavy chain.

74 ated histone-3 binding in both smooth muscle alpha-actin and SRF promoters, epigenetically decreasing

75 ers, epigenetically decreasing smooth muscle alpha-actin and SRF transcriptional activation.

76 st that TGF-beta coordinates the increase of alpha-actin and the decrease of gelsolin to promote MSC

77 he capacity to mediate loss of smooth muscle alpha-actin and to disintegrate blood vessels.

78 beta inhibition increased mRNA expression of alpha-actin and transactivation of nuclear factors of ac

79 oreover, other contractile proteins, such as alpha-actin and tropomyosin, were not altered in SM2(-/-

80 Here, the relationship between SM alpha-actin and type 1 collagen expression (COL1A1), a m

81 hesion as well as increases in smooth muscle alpha-actin and type I collagen mRNA expression.

82 ed with enhanced expression of smooth muscle alpha-actin and vimentin that colocalized with albumin i

83 Hypoxia induced up-regulation of alpha-actin and was prevented by the calcineurin/NFAT in

84 eded with up to 85% efficiency with skeletal alpha-actin and WT yeast actin, yielding a single produc

85 ssion of smooth muscle cell alpha actin (SMC alpha-actin) and ability to contract collagen lattices.

86 in, Thy-1, PDGF receptor alpha, and vascular alpha-actin) and induced SB225002-sensitive cell invasio

87 e gene induction (calponin and smooth muscle-alpha-actin) and protein synthesis ([(3)H]leucine incorp

88 lcium channel receptor alpha-1, and Skeletal alpha-actin), and two KLF3 isoforms are upregulated duri

89 ichment of the CArG regions in the SMMHC, SM alpha-actin, and c-fos promoters in intact chromatin.

90 macrophages, M1 and M2 macrophage subtypes, alpha-actin, and DAPI was performed.

91 to nitrotyrosine (NT)-modified enolase, Ro, alpha-actin, and heat-shock proteins (HSPs) preceding pe

92 3A4 consisted of NT-modified enolase, ATP5b, alpha-actin, and Hsp70 family proteins including Hspa5 a

93 means of colocalization of DiI fluorescence, alpha-actin, and Prussian blue stain-positive cells.

94 CD31 or Ulex europaeus lectin, smooth muscle alpha-actin, and S-100, respectively, and the Y chromoso

95 ncreased cell size and up-regulated SM22, SM alpha-actin, and SM myosin heavy chain mRNA and protein

96 Because collagen and smooth muscle cell alpha-actin are coordinately expressed in the setting of

97 Ang II-induced increases in expression of SM alpha-actin are mediated through Prx1-dependent increase

98 1 null mutations (absence of skeletal muscle alpha-actin) are generalized skeletal muscle weakness an

99 ompounds for effects on skeletal and cardiac alpha-actins as well as on skeletal and cardiac myofibri

100 in expression of smooth muscle cell-specific alpha actin (ASMA), calponin, caldesmon, SM22, myosin he

101 tion, the expression levels of smooth muscle alpha actin, believed to be modulated by EIIIA-containin

102 depolarization-induced increase in SMMHC/SM alpha-actin but had no effect on c-fos expression.

103 Isolated SMCs expressed alpha-actin but not CD31, a marker of endothelial cells.

104 d reduces TGF-beta1-induced expression of SM alpha-actin by 95+/-2% (n=6, P<0.05).

105 scle-specific genes, including smooth muscle alpha-actin, by abolishing the promyogenic function of m

106 can, CD140a, and CD140b), and smooth muscle (alpha-actin, caldesmon, and calponin) markers.

107 VSMC differentiation marker genes such as SM alpha-actin, calponin, and SM-MHC are upregulated by pre

108 o effect on SRF binding to the smooth muscle alpha-actin CArG B element.

109 unting, and immunostaining was performed for alpha-actin, caspase, and macrophages.

110 ACTA2, encoding the smooth muscle isoform of alpha-actin, cause thoracic aortic aneurysms, acute aort

111 the mechanism by which loss of smooth muscle alpha-actin causes aortic disease.

112 Six of these clones (cardiac alpha-actin, cyclin G1, stathmin, NADH dehydrogenase sub

113 only suggest a molecular link between the SM alpha-actin cytoskeleton and classic fibrogenic signalin

114 which express smooth muscle alpha-actin (SM alpha-actin) de novo and produce extracellular matrix.

115 thelial denudation, and its association with alpha-actin-depleted smooth muscle cells, suggest that a

116 AE1/AE3, alpha actin, desmin, and myosin antibodies confirmed the

117 er and other muscle gene promoters (Skeletal alpha-actin, Desmin, and alpha-Myosin heavy chain) in sk

118 Deletion of SM alpha-actin did not result in any alterations in retinal

119 itical concentration for assembly than WT SM alpha-actin, driven by a high disassembly rate.

120 on, (c) NFATc3 mediates the up-regulation of alpha-actin during chronic hypoxia, and (d) NFATc3 is in

121 nse mutations in vascular smooth muscle (SM) alpha-actin encoded by ACTA2 We focus here on ACTA2-R258

122 rce requires cyclic interactions between SMC alpha-actin (encoded by ACTA2) and the beta-myosin heavy

123 ns in vascular smooth muscle alpha-actin (SM alpha-actin), encoded by ACTA2, are the most common caus

124 ns in vascular smooth muscle alpha-actin (SM alpha-actin), encoded by the gene ACTA2, are the most pr

125 ach independently repress core smooth muscle alpha-actin enhancer activity albeit in a cell type-depe

126 report a function for CAP2 in regulating the alpha-actin exchange during myofibril differentiation.

127 e, of the effect of the R258C mutation in SM alpha-actin, expressed with the baculovirus system.

128 mulation resulted in decreased smooth muscle alpha-actin expression and increased matrix metalloprote

129 ption, and an increase in smooth muscle cell alpha-actin expression compared to untreated mice.

130 on of the calcineurin-NFAT pathway decreased alpha-actin expression in cultured SMCs, suggesting that

131 atment significantly increased smooth muscle alpha-actin expression in the abdominal aorta and did no

132 ble GSK-3beta, blocked protein synthesis and alpha-actin expression induced by LiCl, SB216763, and CT

133 n dermal fibroblasts were established and SM alpha-actin expression induced with adenovirus encoding

134 owth factor-beta secretion and smooth muscle alpha-actin expression of cardiac fibroblasts because my

135 d an activated myofibroblast-like phenotype (alpha-actin expression), abundant embryonic myosin, and

136 a previously unrecognized role in regulating alpha-actin expression.

137 gical assessment and decreased smooth muscle alpha-actin expression.

138 d purification and comprehensive analysis of alpha-actin extracted from muscle tissues.

139 nfarct scar maturation, causes smooth muscle alpha-actin fiber formation, up-regulation of collagen I

140 ble to rescue the formation of smooth muscle alpha-actin filament bundles in SVAS iPSC-SMCs.

141 ly fewer organized networks of smooth muscle alpha-actin filament bundles, a hallmark of mature contr

142 ings reveal that disruption of smooth muscle alpha-actin filaments in smooth muscle cells increases r

143 Furthermore, disruption of smooth muscle alpha-actin filaments in wild-type smooth muscle cells b

144 t prepared using a 56-bp region of the mouse alpha-actin first intron containing SRF, NFAT, and AP-1

145 The skeletal muscle alpha-actin gene (ACTA1) is one of five genes for thin f

146 ylated genes, a mutant form of KRAS, and the alpha-actin gene (as a reference value) using quantitati

147 Smooth muscle alpha-actin gene activity appears in promyocardial cells

148 le, previously shown to induce smooth muscle alpha-actin gene expression in cardiac progenitor cells,

149 llaborative manner to suppress smooth muscle alpha-actin gene expression in cell types relevant to wo

150 SRF-S162 phosphorylation and an increase in alpha-actin gene expression.

151 Expression of the smooth muscle alpha-actin gene in growth-activated vascular smooth mus

152 nscriptional repression of the smooth muscle alpha-actin gene in vascular cell types.

153 s to be a signature feature of smooth muscle alpha-actin gene regulation in these cell types.

154 cal interactions necessary for smooth muscle alpha-actin gene repression.

155 Pur alpha and Pur beta repress smooth muscle alpha-actin gene transcription by means of DNA strand-se

156 letely inhibited SRF-DNA binding and blocked alpha-actin gene transcription even in the presence of p

157 rans-acting factors to control smooth muscle alpha-actin gene transcription in a cell type- and cell

158 n was increased by Ang II, also increased SM alpha-actin gene transcription in part via CArG elements

159 uired for Ang II-induced transcription of SM alpha-actin gene, and a dominant-negative form of myocar

160 the SMC differentiation marker gene, the SM alpha-actin gene.

161 ssociated with increased transcription of SM alpha-actin gene.

162 Whether SM alpha-actin has specific functional effects on cellular

163 upts cytoskeletal functions attributed to SM alpha-actin in fibroblasts and are consistent with defic

164 ed induction of both wild-type and mutant SM alpha-actin in heterozygous ACTA2-R258C cells.

165 Expression of mutant SM alpha-actin in heterozygous ACTA2-R258C fibroblasts abro

166 ued by transgenic over-expression of cardiac alpha-actin in skeletal muscles using the ACTC gene.

167 These results demonstrate that SM alpha-actin in SM cells and pericytes is not necessary f

168 Expression of alpha-actin in smooth muscle cells (SMCs) is regulated,

169 to cell-specific expression of smooth muscle alpha-actin in vivo, since substitution of c-fos consens

170 he expression of smooth muscle cell specific alpha-actin increases throughout the liver, suggesting a

171 asts abrogated the significant effects of SM alpha-actin induction on formation of stress fibers and

172 TC(Co)/KO myofibres, the presence of cardiac alpha-actin instead of skeletal muscle alpha-actin alter

173 normal retinal vascular pattern; however, SM alpha-actin is necessary for SM cells and pericytes to i

174 In the liver, smooth muscle alpha-actin (SM alpha-actin) is up-regulated in hepatic stellate cells (

175 erized actin network by overexpression of an alpha-actin isoform in Srf mutant SCs rescued their fusi

176 ral smooth muscle cell function where the SM alpha-actin isoform is present in low amounts.

177 ifferentiation is the sequential exchange of alpha-actin isoforms from smooth muscle (alpha-SMA) and

178 We then applied our method to quantify the alpha-actin isoforms in human healthy hearts and failing

179 ion, quantification, and characterization of alpha-actin isoforms, enabling assessment of their clini

180 eta2, collagen I, fibronectin, smooth muscle alpha-actin, laminin alpha1, and hyaluronan and proteogl

181 he results demonstrating that knockout of SM alpha-actin leads to reduced liver fibrosis and COL1 exp

182 ATc3 knock-out mice did not showed increased alpha-actin levels and arterial wall thickness after hyp

183 is a significant reduction in smooth muscle alpha-actin levels, whereas h-caldesmon levels are incre

184 tently upregulates the contractile marker SM alpha-actin mRNA (7.5+/-0.8-fold versus control).

185 tools to characterize a novel ACTC1 (cardiac alpha-actin) mutation identified in association with ASD

186 Age-matched SM alpha-actin null and wild-type mice were analyzed.

187 gnificant increase in RVP was observed in SM alpha-actin null mice at both postnatal day (P)50 and P7

188 eduction in both rod and cone function in SM alpha-actin null mice at P22, P45, and P75 (P<0.01 at al

189 SM alpha-actin null mice were used to determine whether vas

190 ll and pericyte ensheathing of vessels in SM alpha-actin null mice.

191 for oil red O and the SMC-specific marker SM alpha-actin of foam cell-rich lesions revealed that 50+/

192 sin light chain 20, SM22alpha, smooth muscle alpha-actin, or calponin.

193 id not activate the SM22alpha, smooth muscle alpha-actin, or smooth muscle myosin heavy chain promote

194 ter genes driven by SM22alpha, smooth muscle alpha-actin, or smooth muscle myosin heavy chain promote

195 ry was used to localize osteopontin protein, alpha-actin, osteocalcin, vascular endothelial growth fa

196 pha and beta myosin heavy chains and cardiac alpha actin, play crucial roles in atrial septal develop

197 tress and led to a 45% loss of smooth muscle alpha-actin positive cells in the eye drainage structure

198 A smooth muscle-specific alpha-actin-positive cell population developed within th

199 erized by neoplastic growth of smooth muscle-alpha-actin-positive cells that destroy lung parenchyma

200 en deposition, accumulation of smooth muscle alpha-actin-positive cells, and lipid peroxidation produ

201 cells were defined as CD68/CD3-positive and alpha-actin-positive cells.

202 e and partly co-localized with smooth muscle alpha-actin-positive cells.

203 came invested by smooth muscle cell-specific alpha-actin-positive mural cells, indicative of maturati

204 score, selective clearance of smooth muscle alpha-actin-positive myofibroblasts, reduced hepatic pro

205 tion was associated with a greater number of alpha-actin-positive VICs in neonatal aortic versus pulm

206 sion of PIAS1 significantly activated the SM alpha-actin promoter and mRNA expression, as well as SM

207 required for the transactivation of skeletal alpha-actin promoter and the expression of specific musc

208 RF binding to a probe encoding the distal SM-alpha-actin promoter CArG (CC(AT)(6)GG) element.

209 previously that MCAT elements within the SM alpha-actin promoter confer differential activity in cul

210 ficance, PIAS1 bound to SRF and activated SM alpha-actin promoter expression in wild-type but not SRF

211 fully repress the full-length smooth muscle alpha-actin promoter in cultured fibroblasts but to a le

212 criptional activation of the 2.0-kb skeletal alpha-actin promoter in differentiating C2C12 myoblasts.

213 MCAT element-containing region within the SM alpha-actin promoter in myofibroblasts, whereas transcri

214 nown coactivators of the mouse smooth muscle alpha-actin promoter in rodent fibroblasts and vascular

215 ctors (MRTF-A and MRTF-B) to a smooth muscle alpha-actin promoter is observed in response to BMP trea

216 iated with SRF and was recruited by SRF to a alpha-actin promoter SRF binding site.

217 oter, it could bind to and inhibit a cardiac alpha-actin promoter through its zinc finger domains.

218 Furthermore, the activity of skeletal alpha-actin promoter was suppressed on MSC blockade.

219 enous mRNA expression, and SRF binding to SM alpha-actin promoter within intact chromatin in cultured

220 Furthermore, AR activated the skeletal alpha-actin promoter, which lacks GRE sites, in co-trans

221 t localization of myogenic cells marked with alpha-actin promoter-driven enhanced green fluorescent p

222 so indicate that the MCAT element-mutated SM alpha-actin promoter-enhancer is a useful tool to direct

223 we generated transgenic mice harboring an SM alpha-actin promoter-enhancer-LacZ reporter gene contain

224 nsgene expression patterns with wild-type SM alpha-actin promoter-enhancer-LacZ transgenic mice.

225 intracellular loop, under the control of an alpha-actin promoter.

226 teraction of Pur beta with the smooth muscle alpha-actin promoter.

227 d not support cGMP/PKG stimulation of the SM-alpha-actin promoter.

228 se factor (SRF) and GATA6 to activate the SM-alpha-actin promoter.

229 ha1-adrenergic up-regulation of the skeletal alpha-actin promoter.

230 essed under the control of the smooth muscle alpha-actin promoter.

231 muscle myosin heavy chain and smooth muscle alpha-actin promoters and had no significant effect on t

232 of the telokin, SM22alpha, and smooth muscle alpha-actin promoters.

233 blotting, and showed diminished levels of SM alpha-actin protein and promoter activity.

234 S1P also increased smooth muscle alpha-actin protein levels in SMC but had no effect on S

235 or vessels and upregulation of smooth muscle alpha-actin protein levels.

236 Recent biochemical results with SM alpha-actin-R258C predicted that this variant will compr

237 ining with the macrophage marker CD68 and SM alpha-actin revealed that 40+/-6% (n=15) of CD68-positiv

238 Immunofluorescent staining of alpha-actin revealed that cardiomyocytes had greater sar

239 normalized levels of glutathiolated cardiac alpha-actin, reversed cardiac and myocyte hypertrophy an

240 natriuretic peptides (ANP/BNP), and skeletal alpha-actin (sACT) was increased, whereas expression for

241 tin and polylysine-induced polymerization of alpha-actin) show that the APD decays at a rate slower t

242 main or Jagged1 ligand induced smooth muscle alpha-actin (SM actin), smooth muscle myosin heavy chain

243 myofibroblasts, which express smooth muscle alpha-actin (SM alpha-actin) de novo and produce extrace

244 In the liver, smooth muscle alpha-actin (SM alpha-actin) is up-regulated in hepatic

245 Mutations in vascular smooth muscle alpha-actin (SM alpha-actin), encoded by ACTA2, are the

246 Point mutations in vascular smooth muscle alpha-actin (SM alpha-actin), encoded by the gene ACTA2,

247 are surrounded by mouse VSMCs expressing SM-alpha actin, SM myosin, SM22alpha, and calponin, all mar

248 ress a selective repertoire of genes (eg, SM alpha-actin, SM myosin heavy chain [SMMHC], myocardin) t

249 uced a strong increase in LPP, as well as SM alpha-actin, SM myosin heavy chain, and smoothelin mRNA

250 hat control expression of smooth muscle (SM) alpha-actin, SM-myosin heavy chain, and SM22alpha.

251 expression of SM-specific genes including SM alpha-actin, SM22, and others.

252 f multiple SMC markers such as smooth muscle alpha-actin, SM22alpha, and calponin in TGF-beta-treated

253 the other hand, early SMC markers such as SM alpha-actin, SM22alpha, and SM calponin were detectable

254 duced expression of SM markers, including SM alpha-actin, SM22alpha, and SM myosin heavy chain, where

255 r defects or altered expression levels of SM alpha-actin, SM22alpha, or calponin.

256 We observed the absence of myogenic alpha-actins, SM22alpha, and myocardin expression and th

257 duction for 14 days, expressed smooth muscle alpha-actin (SMA) and calponin, early and mid-SMC phenot

258 ile studying the regulation of smooth muscle alpha-actin (SMA) expression at the level of protein sta

259 The mouse vascular smooth muscle alpha-actin (SMA) gene enhancer is activated in fibrobla

260 on and down-regulation of VSMC smooth muscle alpha-actin (SMA) gene expression.

261 Smooth muscle alpha-actin (SMA) is one of the earliest markers of myob

262 in-resistance gene under the control of a SM alpha-actin (SMA) promoter.

263 One Notch target is smooth muscle alpha-actin (SMA), a differentiated smooth muscle cell m

264 ion and the differentiation of smooth muscle alpha-actin (SMA)-positive myofibroblasts.

265 ts constitutively express smooth-muscle cell alpha-actin (SMAA), deposit an excessive amount of extra

266 TGFbeta induces expression of smooth muscle alpha actin (SMalphaA) and incorporation into in stress

267 05), related to an increase in smooth muscle alpha-actin (SMalphaA) (myofibroblast phenotype) (P < 0.

268 d by the de novo expression of smooth muscle alpha-actin (SMalphaA) and normally function to assist i

269 activates transcription of the smooth muscle alpha-actin (SMalphaA) gene via dynamic interplay of nuc

270 ing expression of the vascular smooth muscle alpha-actin (SMalphaA) gene, an important determinant of

271 liferation, expression of smooth muscle cell alpha actin (SMC alpha-actin) and ability to contract co

272 only slight increases (P=not significant) in alpha actin-stained smooth muscle cells were noted in th

273 ly increased Sca1+ cells in the circulation, alpha-actin-stained vessels, and perfusion of the ischem

274 n-23) were significantly attenuated, whereas alpha-actin staining was increased in KLF4 knockout mice

275 d the formation of contractile smooth muscle alpha-actin stress fibers and the deposition of collagen

276 markers (calponin, desmin, and smooth muscle alpha actin), suggesting dedifferentiation and trans-dif

277 The delay in the alpha-actin switch coincided with the onset of motor fun

278 This alpha-actin switch was delayed in systemic CAP2 mutant m

279 This "alpha-actin switch" requires the coordinated activity of

280 The molecular machinery that controls the alpha-actin switch, however, remains enigmatic.

281 entiation markers calponin and smooth muscle alpha-actin than SMC from women.

282 ough both SMCs and myofibroblasts express SM alpha-actin, they use distinct transcriptional control m

283 f neural cadherin/beta-catenin/smooth muscle alpha actin; thus, mediating cell-cell adhesion and perm

284 restriction: caveolin, stathmin, G-1 cyclin, alpha-actin, titin, cardiac ankyrin repeat protein (CARP

285 SOCS-3 overexpression induced skeletal alpha-actin transcription in a myoblast cell line that c

286 experiments showed that RTEF-1 regulated SM alpha-actin transcription in myofibroblasts, but not in

287 n attenuated depolarization-induced SMMHC/SM alpha-actin transcription.

288 rkedly decreased basal and Ang II-induced SM alpha-actin transcription.

289 ic for myocardin decreased Ang II-induced SM alpha-actin transcription.

290 ontributed to Ang II-induced increases in SM alpha-actin transcription.

291 l (> or =90%), and smooth muscle (> or =75%) alpha-actin transcripts were also observed in the cardia

292 ated myotubes and the appearance of skeletal alpha-actin transcripts, even in the absence of ligand.

293 increases in type I collagen, smooth muscle alpha-actin, transforming growth factor-beta, and extra

294 increased physical interactions of OGA with alpha-actin, tropomyosin, and myosin light chain 1, alon

295 Expression of smooth muscle alpha-actin was not affected by rapamycin treatment, ind

296 of both LPP and palladin, like smooth muscle alpha-actin, was increased by angiotensin II, regulated

297 e, Alexa Fluor 488 to cysteine 374 of native alpha-actin, we were able to follow the binding and fold

298 hat nitrated peptides derived from titin and alpha-actin were released into the plasma of patients wi

299 pression of fibrotic markers fibronectin and alpha-actin, whereas EP1 antagonism decreased fibronecti

300 d the mesenchymal marker, smooth muscle (SM) alpha-actin; whereas the endothelial marker, PECAM-1, wa