ライフサイエンスコーパス: muscle cell

1 A function within the cerebrovascular smooth muscle cell.

2 ing and function in the skeletal and cardiac muscle cell.

3 istributed evenly along the periphery of the muscle cell.

4 nderlies the contraction-relaxation cycle of muscle cells.

5 onal responses that are propagated along the muscle cells.

6 r the regulation of actin homeostasis in non-muscle cells.

7 d lipid metabolism in human primary skeletal muscle cells.

8 uman airway epithelial progenitor and smooth muscle cells.

9 sels are comprised of endothelial and smooth muscle cells.

10 ic acid (3-MPA), a PEPCK inhibitor, on C2C12 muscle cells.

11 to the PAA endothelium into vascular smooth muscle cells.

12 the presence of the underlying medial smooth muscle cells.

13 esional macrophages, endothelial, and smooth muscle cells.

14 and the role of canonical IL-6 signaling in muscle cells.

15 Ki significantly relax human ureteral smooth muscle cells.

16 are the core regulator of mineral amount in muscle cells.

17 f AChR clusters both in vivo and in cultured muscle cells.

18 or maintenance of contractile apparatuses in muscle cells.

19 by the nuclear actions of ERalpha in smooth muscle cells.

20 mponents of contractile stress fibers in non-muscle cells.

21 in vitro, reminiscent of t-tubule system in muscle cells.

22 terior wnt1+ signaling center within midline muscle cells.

23 tipotent etv2 progenitor cells into skeletal muscle cells.

24 itioned medium (CM) from lamin A/C-deficient muscle cells.

25 ing to an increase in ventricular and smooth muscle cells.

26 mesoderm containing chondrocytes and smooth muscle cells.

27 type 2 diabetes, into primary human skeletal muscle cells.

28 promotes muscle fiber formation in cultured muscle cells.

29 eletal assemblies embedded in the cytosol of muscle cells.

30 and during differentiation of primary human muscle cells.

31 orporate into myofilament and is degraded in muscle cells.

32 ne modifiers of polyglutamine aggregation in muscle cells.

33 ely by comparing it with data from perturbed muscle cells.

34 CD47 and other oncogenes in arterial smooth muscle cells.

35 gitudinal proliferation of arteriolar smooth muscle cells.

36 side on the plasma membranes of live Xenopus muscle cells.

37 ygen consumption, and glycolysis in skeletal muscle cells.

38 L-4 in human bronchi and human airway smooth muscle cells.

39 helial cells, pericytes, and vascular smooth muscle cells.

40 ytes compared to neurons and vascular smooth muscle cells.

41 28) microbleeds, both Abeta (4%) and smooth muscle cells (4%) were almost never present in the vesse

42 (1), cardiomyocytes(2-4) and vascular smooth muscle cells(5), where they are involved in the regulati

43 its transient protonation, which occurs upon muscle cell acidification.

44 ammation and remodeling via decreased smooth muscle cell activation and neutrophil transendothelial m

45 SCAP knockdown in vascular smooth muscle cells alleviates atherosclerosis plaque formation

46 fiber disruption, and an increase in smooth muscle cell alpha-actin expression compared to untreated

47 from the shape of the relaxed and contracted muscle cell and the Young's modulus of the matrix withou

48 altered intracellular calcium homeostasis in muscle cells and an indirect toxicity through the trigge

49 n gene, highly expressed in arteries' smooth muscle cells and chondrocytes.

50 P-1) in endothelial cells or vascular smooth muscle cells and decreased monocytes adhesion to endothe

51 (2) as a regulator of ion channels in smooth muscle cells and endothelial cells-the two major classes

52 led proliferation of pulmonary artery smooth muscle cells and fibroblasts.

53 In primary muscle cells and in muscles of mice without NO66, riboso

54 DNF is also secreted by differentiated human muscle cells and induces insulin secretion in human isle

55 collecting lymphatic vessels, via lymphatic muscle cells and one-way valves, to transport lymph from

56 Mural cells (smooth muscle cells and pericytes) are integral components of b

57 These data implicate replication in skeletal muscle cells and release of IL-6 as important mediators

58 s (~750 bases) in aortic endothelial, smooth muscle cells and THP-1 (human leukemia monocytic cell li

59 t regulates contractile pericytes and smooth muscle cells and thus blood flow.

60 lial cells with 2 abluminal layers of smooth muscles cells and matrix.

61 sm and its underlying mechanisms in skeletal muscle cells, and evaluated whether the observed effects

62 tude, fast signals, e.g. those in dendrites, muscle cells, and immune cells.

63 adhesion complexes (IACs) at borders between muscle cells, and is required for locomotion of the anim

64 ional autophagy in endothelial cells, smooth muscle cells, and macrophages, plays a detrimental role

65 types, including platelets, vascular smooth muscle cells, and neuronal cells.

66 ectures, including Drosophila neurons, mouse muscle cells, and rodent oligodendrocytes.

67 p53 in lamin A/C-deficient muscles and C2C12 muscle cells, and the p16Ink4a may induce senescence-ass

68 al to AChR clustering, was reduced in mutant muscle cells; and expressing rapsyn in muscles attenuate

69 1) Treatments of human aortic smooth muscle cells (AoSMCs) with SIRT1 activators (SRT1720 and

70 nctions, all ~15 individual synapses on each muscle cell are shared by a 1 degrees Mn bouton and at l

71 Results show that CFS skeletal muscle cells are unable to utilise glucose to the same e

72 ults identify P2Y(2) receptors in RTN smooth muscle cells as requisite determinants of respiratory ch

73 also identify P2Y(2) receptors in RTN smooth muscle cells as the substrate responsible for this respo

74 ized pacemaker cells, termed atypical smooth muscle cells (ASMCs), are thought to drive the peristalt

75 t impact on the contraction of airway smooth muscle cells (ASMCs).

76 evaluates the changes in rat vascular smooth muscle cell biomechanics following statin-mediated chole

77 de or genetic deletion of P2Y(2) from smooth muscle cells blunted the ventilatory response to CO(2),

78 outgrowth endothelial cells (BOECs), smooth muscle cells (BO-SMCs), and leukocytes were obtained fro

79 rix is united across the entire width of the muscle cell both at birth and in mature muscle.

80 PIX-1 localizes to IACs at muscle cell boundaries, M-lines and dense bodies.

81 of the PIX signaling pathway show defects at muscle cell boundaries.

82 ctivated Rac in muscle, and abnormal IACs at muscle cell boundaries.

83 zed cytoskeletal organization is typical for muscle cells, but muscle cells with reduced PABPN1 level

84 d within the mitochondria of vascular smooth muscle cells can drive an hour-long disruption.

85 , like endothelial cells and vascular smooth muscle cells, cardiac myocytes and inflammatory cells, l

86 ly on mouse and human coronary artery smooth muscle cells (caSMCs) and caECs, resulting in soluble ad

87 In cultured coronary arterial smooth muscle cells (CASMCs) from Asah1(fl/fl)/SM(Cre) mice, hi

88 ctivation by RNA interference selectively in muscle cells caused muscular atrophy in larval stages an

89 bnormal proliferation of the vascular smooth muscle cells causes the marked tortuosity of retinal art

90 When expressed in excitable nerve and muscle cells, ChRs can be used to control the membrane p

91 or paxillin interacts with HDAC6 in skeletal muscle cells, colocalizes with AChR aggregates, and regu

92 nt transgenic PDE3A overexpression in smooth muscle cells confirmed that mutant PDE3A causes hyperten

93 tracellular Ca(2+) levels in arterial smooth muscle cells, constricted arterioles ex vivo and in vivo

94 We find that all muscle cells contain highly connected myofibrillar netwo

95 Skeletal muscle cells contain hundreds of myonuclei within a shar

96 f glutamate to embryonic vertebrate skeletal muscle cells cultured before innervation is necessary an

97 with what we know of endothelial and smooth muscle cells cultured from blood vessels.

98 rol depletion remodels total vascular smooth muscle cell cytoskeletal orientation that may additional

99 erfamily that is implicated in human cardiac muscle cell death from oxidative stress, based on gene s

100 urther role for MAP4K4 was proposed in heart muscle cell death triggered by cardiotoxic anti-cancer d

101 herapeutic target in DOX-induced human heart muscle cell death.

102 nels at myoendothelial projections to smooth muscle cells decreases resting blood pressure in nonobes

103 ammatory actions of TWEAK on vascular smooth muscle cells, decreasing NF-kB activation, cytokines and

104 coding NOTCH3 and results in vascular smooth muscle cell degeneration, stroke, and dementia.

105 nd MAP2K6) have an important role to play in muscle cell degradation, development and motility.

106 on of TRPV4 channels mitigates aortic smooth muscle cell-dependent inflammatory cytokine production a

107 trategy whereby human endothelial and smooth muscle cells derived from blood progenitors from the sam

108 gnificant delay in induction of apoptosis in muscle cells derived from mice and humans, as well as in

109 ond, about half of all foam cells are smooth muscle cell-derived, retaining smooth muscle cell transc

110 l myosin heavy chain cluster during skeletal muscle cell differentiation.

111 At all stages of skeletal muscle cells differentiation, we show a permanent flux o

112 Transdifferentiation of human non-muscle cells directly into myogenic cells by forced expr

113 tylase (AADAC) expression in vascular smooth muscle cells (dVSMCs) differentiated from patient-derive

114 Additionally, insulin resistant lymphatic muscle cells exhibited elevated intracellular calcium an

115 We now report that vascular smooth muscle cells express all three subunits of the IL-2R, an

116 Smooth muscle cells express Kv7.4 and Kv7.5 voltage-dependent p

117 PCR and immunostaining that mouse lymphatic muscle cells expressed Ca(v)3.1 and Ca(v)3.2 and produce

118 In muscle cells, expression of NO66, but not of demethylase

119 40/DCC controls the growth of dendritic-like muscle cell extensions towards motoneurons and is requir

120 Here, we demonstrate that striated muscle cells form a continuous myofibrillar matrix linke

121 xidation and metabolic flexibility in soleus muscle cells from ABA-treated mice with DIO.

122 Compared with renal vascular smooth muscle cells from Add3 transgenic rats, those from FHH r

123 lisation of different substrates by skeletal muscle cells from CFS patients (n = 9) and healthy contr

124 ntiated human macrophages, and aortic smooth muscle cells from humans with diabetes), MCC950 signific

125 n freshly isolated pulmonary arterial smooth muscle cells from Kcnk3-mutated rats.

126 duced-pluripotent-stem-cell-derived skeletal muscle cells from patients with Becker MD and mdx mice s

127 3) are elevated in pulmonary arterial smooth muscle cells from patients with pulmonary arterial hyper

128 ssion of P2Y(2) receptors only in RTN smooth muscle cells fully rescued the CO(2)/H(+) chemoreflex.

129 d medial endothelial, macrophage, and smooth muscle cell function.

130 by the intracellular ATP level of the living muscle cells, further demonstrating that membrane diffus

131 Vascular smooth muscle cells going from a proliferative and motile circu

132 p was strongly associated with airway smooth muscle cell growth in vitro.

133 has previously been shown that CFS skeletal muscle cells have lower levels of ATP and have AMP-activ

134 rimary human coronary artery vascular smooth muscle cells (HCASMCs).

135 Human pulmonary artery smooth muscle cells (HPASMCs) demonstrated hypoxic induction of

136 In human airway smooth muscle cells, IL-13 and IL-4, but not IL-5 and IL-17A, e

137 displayed diminished replication in skeletal muscle cells in a mouse model of CHIKV disease.

138 lly by treating human coronary artery smooth muscle cells in an in vitro calcification assay.

139 Endothelial and smooth muscle cells in arterial tissue expressed CARD8 and CARD

140 patial localization patterns of neuronal and muscle cells in embryonic stages appear to foreshadow la

141 e expressed predominantly on vascular smooth muscle cells in lesions of athero-prone Apoe(-/-) mice.

142 the expression of CD47 from arterial smooth muscle cells in mice.

143 r cells (previously termed 'atypical' smooth muscle cells) in the murine and cynomolgus monkey pelvis

144 ociated with rare specialized regions of the muscle cell, including markers of the myotendinous junct

145 The co-expression of rapsyn in muscle cells induced AChR clustering and facilitated rec

146 Distinct loss of function of IDO in smooth muscle cells, inflammatory cells, or cardiomyocytes does

147 e inhibition of HDAC9 in human aortic smooth muscle cells inhibited calcification and enhanced cell c

148 Gt); UAS:GFP cells differentiate as skeletal muscle cells instead of contributing to vasculature in e

149 In fat and skeletal muscle cells, insulin-responsive amino peptidase (IRAP)

150 -1 secretion and attenuated leukocyte-smooth muscle cell interactions under high glucose or lipopolys

151 fferentiation and fragmentation of syncytial muscle cells into mononucleate myoblasts and depends on

152 ough activation of nuclear ERalpha in smooth muscle cells, inviting to revisit the mechanisms of acti

153 role of the protein Kv2.1 in arterial smooth muscle cells is to form K(+) channels in the sarcolemma.

154 d ongoing proliferation of intestinal smooth muscle cells (ISMC) with expression of platelet-derived

155 ascular endothelial cells (iVECs) and smooth muscle cells (iSMCs) by direct reprogramming of healthy

156 glomeruli and primary renal vascular smooth muscle cells isolated from these rats.

157 Cardiac muscle cells lack regenerative capacity in postnatal mam

158 Knockdown of ARNT in a primary muscle cell line impaired differentiation in vitro.

159 Finally, we confirmed in non-muscle cell lines that TBK1 phosphorylation occurs in th

160 which is associated with damage to lymphatic muscle cells (LMCs), is a biomarker of disease progressi

161 CD31(+) microvessel growth, and media smooth muscle cell loss, compared with those from Apoe(-/-) con

162 Multiple subtypes were observed for smooth muscle cells, macrophages, and T lymphocytes, suggesting

163 ulations including endothelial cells, smooth muscle cells, mast cells, B cells, myeloid cells, and T

164 xtra, short-A-bands lying close to the outer muscle cell membrane and between normally spaced A-bands

165 rol depletion may coordinate vascular smooth muscle cell migration and adhesion to different extracel

166 Smooth muscle cell migration is essential for many diverse biol

167 ockdown by shRNA reduced human airway smooth muscle cell migration, which was restored by Abi1 rescue

168 s is in the axial direction, while lymphatic muscle cell nuclei and actin fibers are oriented in both

169 ne-rich repeat 3 (SPRR3), in vascular smooth muscle cells of atheromas.

170 ellular Ca(2+) waves are generated in smooth muscle cells of colonic longitudinal muscles (LSMC).

171 ed from the kidney and renal vascular smooth muscle cells of FHH rats was associated with the disrupt

172 or protein p66Shc is overexpressed in smooth muscle cells of renal resistance vessels of hypertensive

173 eous cytosolic Ca(2+) oscillations in smooth muscle cells of renal vessels mediate their spontaneous

174 Neuronal and muscle cells of the 2 glands in particular showed differ

175 gnatures of mesangial cells, vascular smooth muscle cells of the afferent and efferent arterioles, pa

176 Smooth muscle cells of the muscularis mucosa, in close proximit

177 eleased endothelin-1 were recorded in smooth muscle cells of the renal arteries.

178 Genetic disruption of autophagy in smooth muscle cells of young mice exposed to hyperlipidemia led

179 ice harboring specific endothelial or smooth muscle cells or cardiomyocyte or myeloid cell deficiency

180 ltered metabolism in pulmonary artery smooth muscle cells (PASMCs) and endothelial cells (PAECs) cont

181 a(2+) signaling in pulmonary arterial smooth muscle cells (PASMCs) plays an important role in pulmona

182 rked accumulation of pulmonary artery smooth muscle cells (PASMCs) represents one of the major pathol

183 ormal phenotype of pulmonary arterial smooth muscle cells (PASMCs), a major contributor of PAH pathob

184 te cardiac lineages, such as vascular smooth muscle cells, pericytes, and fibroblasts.

185 on of IL-2Ralpha varies with vascular smooth muscle cell phenotype.

186 siology, regulating vascular tone and smooth-muscle cell phenotype.

187 low the investigation of pericyte and smooth muscle cell physiology and their role in regulating rCBF

188 Despite its important role in muscle cell physiology suggested by various in vitro stu

189 After gastrulation, when similar muscle cell populations in the post-anal tail are genera

190 ian models, 20(R)-ginsenoside Rh(2) enhanced muscle cell proliferation and accelerated recovery from

191 sociated with an increase in vascular smooth muscle cell proliferation and changes in vessel morpholo

192 Further, expression of genes associated with muscle cell proliferation and differentiation were affec

193 Furthermore, IgG antibodies enhanced smooth muscle cell proliferation in vitro in an Fc receptor-dep

194 inding to fibrin, (ii) stimulation of smooth-muscle cell proliferation, and (iii) stimulation of LDL

195 hma and additionally increases airway smooth muscle cell proliferation.

196 d expression of HDAC9 in human aortic smooth muscle cells promoted calcification and reduced contract

197 ression of alpha-dbn or alphakap in cultured muscle cells promotes the formation of large agrin-induc

198 f Akt1E17K to endothelial, cardiac or smooth muscle cells resulted in viable offspring and remodeled

199 energy availability (EA) on potent skeletal muscle cell signalling pathways (regulating mitochondria

200 where DNA-content functions as a limiter of muscle cell size.

201 validation in human adipocytes and skeletal muscle cells (SKMCs) confirmed the relevance of the key

202 advanced atherosclerotic lesions with smooth muscle cell (SMC) and endothelial lineage tracing to sur

203 Rapamycin decreased smooth muscle cell (SMC) and macrophage proliferation; rapamyci

204 It has been thought that smooth muscle cell (SMC) degeneration at the site of arteriolar

205 s of aortic delamination arising from smooth muscle cell (SMC) dysfunction or apoptosis, degradation

206 ion in MFS may be related to distinct smooth muscle cell (SMC) embryologic lineages.

207 rotic plaque development by promoting smooth muscle cell (SMC) investment.

208 n (AAD), caused by progressive aortic smooth muscle cell (SMC) loss and extracellular matrix degradat

209 lopment and identified a key role for smooth muscle cell (SMC) reprogramming into a mesenchymal stem

210 Smooth muscle cell (SMC)-specific RyR2 knockout (KO) or Rieske

211 sms and dissections (AADs) induced by smooth muscle cell (SMC)-specific, postnatal deletion of Tgfbr1

212 Smooth muscle cells (SMC) play a critical role in atheroscleros

213 ge of atherosclerosis and on vascular smooth muscle cells (SMC) remain to be fully elucidated.

214 collected transcriptomes from primary smooth muscle cells (SMC), interstitial cells of Cajal (ICC), a

215 ernal to which lie contraction-primed smooth muscle cells (SMC).

216 In addition, smooth muscle cells (SMCs) along the renal arterioles transform

217 Neointima arises from smooth muscle cells (SMCs) and not endothelium.

218 Smooth muscle cells (SMCs) are the most affected cells in HGPS

219 domain A (Fn-EDA) is associated with smooth muscle cells (SMCs) following vascular injury.

220 ERS (iSERS) microscopy for imaging of smooth muscle cells (SMCs) in atherosclerotic plaques.

221 required for phenotypic modulation of smooth muscle cells (SMCs) in atherosclerotic tissues and promo

222 s in extracellular matrix and loss of smooth muscle cells (SMCs) in the medial layer of the aortic wa

223 undant junctophilin isotype in native smooth muscle cells (SMCs) isolated from cerebral arteries and

224 Smooth muscle cells (SMCs) play significant roles in atheroscle

225 Vascular smooth muscle cells (SMCs) synthesize extracellular matrix (ECM

226 (in the absence of serum or HDL) onto smooth muscle cells (SMCs) that had been metabolically labeled

227 dilatory factors that act directly on smooth muscle cells (SMCs) to induce arterial dilation and incr

228 subset of "dedifferentiated" vascular smooth muscle cells (SMCs) which proliferate in a clonal fashio

229 NO dioxygenation process in vascular smooth muscle cells (SMCs), and the requisite reducing systems

230 ility and differentiation in vascular smooth muscle cells (SMCs), but the specific function of SMC-ex

231 herosclerotic plaques associated with smooth muscle cells (SMCs), inflammation, extracellular matrix

232 cells of the SIP syncytium, including smooth muscle cells (SMCs), interstitial cells of Cajal (ICC),

233 neurons and SIP syncytium, including smooth muscle cells (SMCs), interstitial cells of Cajal (ICC),

234 contractility in bladder and urethral smooth muscle cells (SMCs).

235 itial cells of Cajal (ICC) but not by smooth muscle cells (SMCs).

236 regulator in differentiated vascular smooth muscle cells (SMCs).

237 y differentiated contractile vascular smooth muscle cells (SMCs).

238 corporation of target sequences for skeletal muscle cell-specific miR-206.

239 Smooth muscle cell-specific overexpression of Smad7 completely

240 of coordinated reduction in vascular smooth muscle cell stiffness and actin cytoskeletal orientation

241 sh that transgenically express GFP on smooth muscle cells (Tg[acta2:GFP]), to visualize the beating h

242 rentially arranged layers of vascular smooth muscle cells that are separated by concentrically arrang

243 rostaglandin E(2) signaling in airway smooth muscle cells that eventually triggered cAMP/PKA-dependen

244 through contraction of the basic unit of the muscle cell, the sarcomere.

245 n filaments from overgrowing, whereas in non-muscle cells, their function has remained elusive.

246 ates phenotypic switching of vascular smooth muscle cells through plasma membrane potential-dependent

247 id necrosis of the entire nervous system and muscle cells throughout the entire organism.

248 We identify a rare population of muscle cells tightly associated with photoreceptor axons

249 t to their role in muscle myofibrils, in non-muscle cells, Tmods bind actin-tropomyosin filaments to

250 Myosin II is the motor protein that enables muscle cells to contract and nonmuscle cells to move and

251 and Kv7.5 alpha-subunits in vascular smooth muscle cells to determine which components are essential

252 in migration and adhesion of vascular smooth muscle cells to extracellular matrix proteins fibronecti

253 Exposure of muscle cells to high concentrations of BCKAs resulted in

254 ontribution of CHIKV replication in skeletal muscle cells to pathogenesis, we engineered a CHIKV stra

255 at escaped germline stem cells induce nearby muscle cells to reach out and wrap around them, forming

256 phenolic metabolites on the ability of human muscle cells to take up and metabolize glucose.

257 smooth muscle cell-derived, retaining smooth muscle cell transcripts rather than transdifferentiating

258 hesion, and migration of human airway smooth muscle cells transfected with PKAc variants containing a

259 C; optimized intraperitoneal and periocular muscle cell transplantation; and epifluorescence and con

260 lated by simulating lipotoxicity in skeletal muscle cells treated with saturated FA, palmitate.

261 e peristaltic contractions of typical smooth muscle cells (TSMCs) in the renal pelvis.

262 Our single-cell expression map of skeletal muscle cell types will further the understanding of the

263 hypercontraction of the head and pharyngeal muscle cells, ultimately resulting in rapid necrosis of

264 r vesicles secreted by human coronary smooth muscle cells upon exposure to atherogenic conditions.

265 generate both the motor neurons and skeletal muscle cells used.

266 le force was applied to live vascular smooth muscle cells using a fibronectin-functionalized atomic f

267 ted the gene expression patterns of skeletal muscle cells using RNA-seq of subtype-pooled single huma

268 ed that DGAT1 was dominant in human skeletal muscle cells utilizing fatty acids (FAs) derived from va

269 In vascular smooth muscle cells (VMSCs), stimulation of Ca(2+) -permeable c

270 rallel myofibrils comprising the bulk of the muscle cell volume.

271 ol management on primary rat vascular smooth muscle cell (VSMC) biomechanics.

272 Vascular smooth muscle cell (VSMC) function is regulated by Nox-derived

273 ression patterns that define vascular smooth muscle cell (VSMC) phenotype.

274 determine the role of YY1 in vascular smooth muscle cell (VSMC) phenotypic modulation both in vivo an

275 Fbeta1) is a major driver of vascular smooth muscle cell (VSMC) phenotypic switching, an important pa

276 Vascular smooth muscle cell (VSMC) remodeling is a pathological hallmark

277 n mitochondrial dynamics and vascular smooth muscle cell (VSMC) senescence.

278 m to investigate the role of vascular smooth muscle cell (VSMC) TFEB in the development of AAA and es

279 ation of seizures in SE, and vascular smooth muscle cell (VSMC) TRPC3 channels participate in vasocon

280 Vascular smooth muscle cells (VSMCs) are critical in the development of

281 Vascular smooth muscle cells (VSMCs) can be derived in large numbers fro

282 he role of several miRNAs in vascular smooth muscle cells (VSMCs) has been extensively characterized,

283 Vascular smooth muscle cells (VSMCs) in the normal arterial media contin

284 Vascular smooth muscle cells (VSMCs) play critical roles in the stabilit

285 ical fluctuations applied to vascular smooth muscle cells (VSMCs) regulates mitochondrial network str

286 Vascular smooth muscle cells (VSMCs) show a remarkable phenotypic plasti

287 In vascular smooth muscle cells (VSMCs), activation of Ca(2+) -permeable st

288 id phenotype of striated and vascular smooth muscle cells (VSMCs), we performed lineage tracing studi

289 mide deacetylase (AADAC), in vascular smooth muscle cells (VSMCs).

290 vessel wall, is mediated by vascular smooth muscle cells (VSMCs).

291 elial cells and alpha-SMA(+) vascular smooth muscle cells were detected within all cellular zones in

292 CFS skeletal muscle cells were shown to oxidise galactose and fatty a

293 om human lung tissue and human airway smooth muscle cells were treated for 2 and 1 day(s), respective

294 function and spontaneous beating of cardiac muscle cells, which are important functions of cardiac t

295 This is especially true in skeletal muscle cells, which contain hundreds of myonuclei distri

296 CaN phosphatase activity in vascular smooth muscle cells, which express MKK7gamma mRNA, enhances JNK

297 was localized in centrosomes of human smooth muscle cells, which regulated centrosome maturation and

298 4 is notoriously difficult to detect in FSHD muscle cells, while DUX4 target gene expression is an in

299 rganization is typical for muscle cells, but muscle cells with reduced PABPN1 levels (named as shPAB)

300 The integration of muscle cells with soft robotics in recent years has led