ライフサイエンスコーパス: alpha-actin

1 aired CArG cis regulatory elements (SMMHC/SM alpha-actin).

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

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

4 and reduced levels of glutathiolated cardiac alpha-actin.

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

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

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

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

9 acterize this mutation in expressed human 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 te on sarcomeres to bind and recruit cardiac alpha-actin.

16 aMyHC mRNA expression and increases skeletal alpha-actin.

17 c-fos expression with no effect on SMMHC/SM alpha-actin.

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

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

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

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

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

23 of the differentiation marker smooth muscle alpha-actin.

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

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

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

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

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

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

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

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

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 n, and extensive expression of smooth muscle alpha-actin (alpha-SMA).

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

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

41 ge) we quantified the relative expression of alpha-actin, alpha-tubulin, cyclophilin A, and prolifera

42 1 at capping pointed ends of skeletal muscle alpha-actin (alphask-actin) filaments coated with alpha/

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

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

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

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

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

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

49 gelsolin expression enhanced the assembly of alpha-actin and actin filaments without significantly af

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

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

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

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

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

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

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

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

58 The expression levels of alpha-actin and cyclophilin A varied little during the c

59 the relatively constant expression levels of alpha-actin and cyclophilin A with development, suggest

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

61 ta increased the expression of smooth muscle alpha-actin and decreased the expression of gelsolin.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

94 elial monolayer with little expression of SM alpha-actin, and expression of PECAM-1 was retained in t

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

96 3A4 consisted of NT-modified enolase, ATP5b, alpha-actin, and Hsp70 family proteins including Hspa5 a

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

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

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

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

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

102 1 null mutations (absence of skeletal muscle alpha-actin) are generalized skeletal muscle weakness an

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

129 oth muscle myosin heavy chain (SMMHC) and SM alpha-actin expression and CArG-dependent promoter activ

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

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

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

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

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

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

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

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

138 was inversely associated with smooth muscle alpha-actin expression.

139 in filaments without significantly affecting alpha-actin expression.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

166 Expression of smooth muscle alpha-actin in growth factor-induced myofibroblasts and

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

191 d TGF-beta-induced assembly of smooth muscle alpha-actin; on the other hand, knocking down gelsolin e

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 ning was strongly positive, colocalized with alpha-actin-positive SMCs, and was greater in intensity

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

207 ct of MRTF-A overexpression on smooth muscle alpha-actin promoter activity was inhibited by dominant

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

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

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

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

212 d inhibitory activity toward a smooth muscle alpha-actin promoter driven by a composite TEF-1-, SRF-,

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

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

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

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

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

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

219 ation-induced SRF enrichment in the SMMHC/SM alpha-actin promoter regions, it had no effect of SRF en

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

235 myosin heavy chain promoter/enhancer, and SM-alpha-actin promoter/enhancer in non-SMCs.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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