ライフサイエンスコーパス: SMC

1 SMC complexes reel in DNA, extruding and progressively g

2 SMC complexes, such as condensin or cohesin, organize ch

3 SMC was evaluated using data from a large, household-ran

4 SMC-derived intermediate cells, termed "SEM" cells (stem

5 SMC-specific ablation of TGF-beta signaling in Apoe(-/-)

6 SMCs seeded on TGFbeta2-loaded scaffolds also showed hig

7 of ATP (E heads), cohesin rings generate a "SMC (S) compartment" between hinge and E heads and a "kl

8 beta2 was evaluated by its ability to affect SMC proliferation as a function of its concentration.

9 ivate Lgals3 compose up to two thirds of all SMC in lesions.

10 NA-sequencing, histology, and RNAscope in an SMC-specific lineage-tracing Ahr knockout mouse model of

11 rs as well as extracellular matrix (ECM) and SMC disorganization.

12 pression in alk5-/- rescues the EC, ECM, and SMC defects.

13 erial wall with the exception of the IEL and SMC clusters in the outer media near the adventitia.

14 ecent observations indicate that the LMC and SMC are on their first passage around the Galaxy(5), tha

15 interactions between ParB-parS with ParA and SMC.

16 tablish a protective role for both TCF21 and SMC phenotypic modulation in this disease.

17 PDGFRalpha(+) cells and SMCs were involved in production of eADO from eNAD, and

18 migration and proliferation of human aortic SMC and increased expression of proinflammatory molecule

19 n vitro, knockdown of GPRC5B in human aortic SMCs resulted in increased IP-dependent cAMP production

20 Targeting Fn-EDA in human aortic SMCs suppressed the synthetic phenotype and downregulate

21 P450 reductase (CPR) were measured in aortic SMCs.

22 enotypic switching in human and mouse aortic SMCs and neointimal hyperplasia in the mouse.

23 crest (NC, ascending aorta/transverse arch) SMC lineages to model MFS aortic pathology.

24 ion of the TS was attenuated, but arteriolar SMC loss was unchanged in Col4a1(+/G498V), Notch3(+/-) m

25 scularization of the TS and focal arteriolar SMC loss in brain tissues from patients with sporadic de

26 are characterized by significant arteriolar SMC degeneration.

27 that AHR modulates the human coronary artery SMC phenotype and suppresses ossification in these cells

28 of TCF21 expression in human coronary artery SMC revealed that TCF21 suppresses a broad range of SMC

29 p SRF-binding sites in human coronary artery SMC, showing that binding is colocalized in the genome w

30 The normal pulmonary artery SMC population is heterogeneous, and we identify a Notch

31 ion was greater in PASMC versus renal artery SMC.

32 l model and in primary human coronary artery SMCs and atherosclerotic plaques obtained at carotid end

33 nal assays in cultured human coronary artery SMCs revealed that AHR modulates the human coronary arte

34 and in vitro assays in human coronary artery SMCs, with single-cell RNA-sequencing, histology, and RN

35 ogenic heterogeneity within pulmonary artery SMCs.

36 tively) and peaked in July each year, before SMC delivery began in August.

37 e IEL is a critical physical barrier between SMCs and ECs in the large elastic arteries.

38 At birth, SMC contraction drives inner layer buckling and centripe

39 ryanodine type 2 receptors (RyR2) in bladder SMCs.

40 majority of LELs in freshly isolated bladder SMCs were essentially immobile.

41 ug for acute promyelocytic leukemia, blocked SMC transition to SEM cells, reduced atherosclerotic bur

42 elial cells (BOECs), smooth muscle cells (BO-SMCs), and leukocytes were obtained from four donors.

43 quires control of chromosome organization by SMC-kleisin complexes.

44 zed by ICC, (4) NT5E is expressed chiefly by SMCs and moderately by PDGFRalpha(+) cells, (5) SIP cell

45 d not appear to be functionally expressed by SMCs or ICC.

46 as PKCdelta-mediated chemokines produced by SMCs.

47 Here we demonstrate that the non-canonical SMC family protein, SmcHD1, which is important for gene

48 escribe an efficient sequential Monte Carlo (SMC) algorithm, SeqClone, that jointly estimates the gen

49 rosclerotic lesions with smooth muscle cell (SMC) and endothelial lineage tracing to survey all plaqu

50 Rapamycin decreased smooth muscle cell (SMC) and macrophage proliferation; rapamycin also reduce

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

52 elamination arising from smooth muscle cell (SMC) dysfunction or apoptosis, degradation of or damage

53 y be related to distinct smooth muscle cell (SMC) embryologic lineages.

54 development by promoting smooth muscle cell (SMC) investment.

55 ed by progressive aortic smooth muscle cell (SMC) loss and extracellular matrix degradation, is a hig

56 thelial dysfunction, and smooth muscle cell (SMC) proliferation in the grafted vein.

57 dentified a key role for smooth muscle cell (SMC) reprogramming into a mesenchymal stem cell (MSC)-li

58 Smooth muscle cell (SMC)-specific RyR2 knockout (KO) or Rieske iron-sulfur p

59 ctions (AADs) induced by smooth muscle cell (SMC)-specific, postnatal deletion of Tgfbr1 (Tgfbr1(iko)

60 Smooth muscle cells (SMC) play a critical role in atherosclerosis.

61 lerosis and on vascular smooth muscle cells (SMC) remain to be fully elucidated.

62 scriptomes from primary smooth muscle cells (SMC), interstitial cells of Cajal (ICC), and PDGFRalpha(

63 lie contraction-primed smooth muscle cells (SMC).

64 In addition, smooth muscle cells (SMCs) along the renal arterioles transform into renin ce

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

66 contractions of colonic smooth muscle cells (SMCs) are normally suppressed by inputs from inhibitory

67 Smooth muscle cells (SMCs) are the most affected cells in HGPS individuals, a

68 EDA) is associated with smooth muscle cells (SMCs) following vascular injury.

69 croscopy for imaging of smooth muscle cells (SMCs) in atherosclerotic plaques.

70 henotypic modulation of smooth muscle cells (SMCs) in atherosclerotic tissues and promotes a fibrobla

71 ular matrix and loss of smooth muscle cells (SMCs) in the medial layer of the aortic wall.

72 hilin isotype in native smooth muscle cells (SMCs) isolated from cerebral arteries and that acute kno

73 Smooth muscle cells (SMCs) play significant roles in atherosclerosis via phen

74 n endothelial cells and smooth muscle cells (SMCs) plays a critical role not only in vascular homeost

75 Vascular smooth muscle cells (SMCs) synthesize extracellular matrix (ECM) that contrib

76 ed death was greater in smooth muscle cells (SMCs) than endothelial cells (ECs) and lower in SEAs fro

77 e of serum or HDL) onto smooth muscle cells (SMCs) that had been metabolically labeled with [(15)N]ch

78 rs that act directly on smooth muscle cells (SMCs) to induce arterial dilation and increase local blo

79 iated membrane lysis of smooth muscle cells (SMCs) triggers arterial tissue damage and inflammation.

80 ifferentiated" vascular smooth muscle cells (SMCs) which proliferate in a clonal fashion.

81 ion process in vascular smooth muscle cells (SMCs), and the requisite reducing systems that regulate

82 erentiation in vascular smooth muscle cells (SMCs), but the specific function of SMC-expressed orphan

83 plaques associated with smooth muscle cells (SMCs), inflammation, extracellular matrix remodeling, an

84 IP syncytium, including smooth muscle cells (SMCs), interstitial cells of Cajal (ICC), and cells expr

85 IP syncytium, including smooth muscle cells (SMCs), interstitial cells of Cajal (ICC), and cells expr

86 c fibroblasts (CFs) and smooth muscle cells (SMCs), whereas THY1(-) cells were predominantly restrict

87 in bladder and urethral smooth muscle cells (SMCs).

88 Cajal (ICC) but not by smooth muscle cells (SMCs).

89 differentiated vascular smooth muscle cells (SMCs).

90 P1 deletion in vascular smooth muscle cells (SMCs).

91 ed contractile vascular smooth muscle cells (SMCs).

92 Seasonal malaria chemoprevention (SMC) is a novel strategy to reduce malaria infections in

93 Seasonal malaria chemoprevention (SMC) is now widely deployed in the Sahel, including seve

94 Seasonal malaria chemoprevention (SMC) with amodiaquine and sulfadoxine-pyrimethamine prov

95 of the Structural Maintenance of Chromosome (SMC) class of proteins.

96 s have structural maintenance of chromosome (SMC) condensin complexes that were recently shown to org

97 of the Structural Maintenance of Chromosome (SMC) protein complex, cohesin, which tethers remote regi

98 of the structural maintenance of chromosome (SMC) superfamily of ATPases.

99 Structural maintenance of chromosomes (SMC) complexes are central organizers of chromatin archi

100 Structural maintenance of chromosomes (SMC) complexes are essential for genome organization fro

101 Structural maintenance of chromosomes (SMC) complexes organize chromosomes ubiquitously, thereb

102 ir of structural maintenance of chromosomes (SMC) family proteins are fundamental for the three-dimen

103 es of structural maintenance of chromosomes (SMC) proteins and kleisin subunits are essential to chro

104 n and structural maintenance of chromosomes (SMC) superfamily proteins.

105 Structural maintenance of chromosomes (SMC)-kleisin complexes organize chromosomal DNAs in all

106 or potent and targeted suppression of clonal SMC expansion in the plaque in vivo.

107 Cloud (LMC) and the Small Magellanic Cloud (SMC), the two most massive satellite galaxies of the Mil

108 ign included the Swedish Mammography Cohort (SMC) and the Cohort of Swedish Men (COSM) (1997-2017), w

109 chromosome occupancy of the Escherichia coli SMC complex, MukBEF, the chromosome is organized as a se

110 lar targets for disease therapy, we combined SMC fate mapping and single-cell RNA sequencing of both

111 The incidence rate ratio comparing SMC within the past 28 days with SMC more than 35 days a

112 hods, such as secure multiparty computation (SMC) protocols, have been developed with the aim of offe

113 rol mice revealed suppression of contractile SMC markers, extracellular matrix remodeling enzymes, an

114 nsdifferentiation of a subset of contractile SMCs into an MSC-like intermediate state that generated

115 In contrast, SMC-specific gene transfer of Prkcd accelerated reendoth

116 sification by Suzuki-Miyaura cross-coupling (SMC), resulting in new-to-nature biaryl motifs.

117 ough Csp(2)-Csp(2) Suzuki-Miyaura couplings (SMCs) are widely used in small-molecule synthesis, relat

118 In addition, DNA from damaged SMCs was engulfed by macrophages in which it activated S

119 at enhanced IP signaling in GPRC5B-deficient SMCs not only facilitates relaxation but also prevents d

120 The degradative SMC phenotype also worsens atherosclerotic disease and c

121 These vascular SMCs, termed degradative SMCs, compromise the medial properties and function of t

122 sses the transcription of CArG box-dependent SMC-specific genes including SM22alpha, SMalpha-actin an

123 The TFV-dp SMC:PBMC ratio was also significantly lower with TAF.

124 It is deficient in EC-SMC Bmpr2 double heterozygous mice in association with r

125 from mice fed with a standard diet, enhanced SMC proliferation.

126 ed by MetS-lEVs participates in the enhanced SMC proliferation, migration, proinflammatory profile, a

127 Eukaryotic SMC complexes, cohesin, condensin, and Smc5/6, use ATP h

128 The eukaryotic SMC complexes cohesin and condensin are thought to fold

129 studies suggest that the clonally expanding SMC may represent a translational target for treating at

130 le to cover the high transmission period for SMC could improve the preventive efficacy substantially.

131 of myocardin (MYOCD), a master regulator for SMC-specific gene transcription by binding to SRF to for

132 Mesenteric arteries from SMC-specific Gprc5b-KOs showed ex vivo significantly enh

133 hich is covered by mural cells distinct from SMCs and pericytes.

134 rtery disease-associated gene in fundamental SMC processes and indicating the importance of smooth mu

135 s into the regulatory mechanisms that govern SMC phenotypic modulation in the pathogenesis of vascula

136 e develop a microfluidic chip formed by HGPS-SMCs generated from induced pluripotent stem cells (iPSC

137 Our HGPS-SMCs chip represents a platform for developing treatment

138 o provide a high level of protection and how SMC might be improved.

139 Yet how SMCs contribute to the pathophysiology of atherosclerosi

140 Here, we characterize human SMC complexes condensin I and II and unveil the architec

141 PCSK6 silencing in human SMCs in vitro leads to downregulation of contractile mar

142 d by decreased MMP14 activation and impaired SMC outgrowth from aortic rings ex vivo.

143 The role of SMC-derived Fn-EDA in SMC phenotypic switching or its implication in neointima

144 Femoral artery wire injury was performed in SMC-conditional Prkcd knockout mice, and carotid angiopl

145 hus is an attractive candidate for a role in SMC-endothelial cells communication.

146 hat these signals were essentially absent in SMCs from TRPML1-knockout (Mcoln1(-/-) ) mice.

147 Lysosomal Ac in SMCs controls sEV release by regulating lysosomal TRPML1

148 D (eNAD) in colonic tunica muscularis and in SMCs, ICC and PDGFRalpha(+) cells with HPLC-FLD, we repo

149 the criteria of a master regulator of AS in SMCs.

150 lly, nuclear and mitochondrial DNA damage in SMCs and the subsequent leak of DNA to the cytosol activ

151 esponse, dedifferentiation and cell death in SMCs, and matrix metalloproteinase expression in macroph

152 NO decay in SMCs was measured following bolus addition of NO to air-

153 we observed the presence of cytosolic DNA in SMCs and macrophages and significant activation of the S

154 Specific deletion of Fn-EDA in SMCs, but not in endothelial cells, reduced intimal hype

155 Inactivation of Eln in SMCs using Sm22aCre resulted in depletion of elastic lam

156 We observed substantial (13)C enrichment in SMCs that were adjacent to [(13)C]cholesterol-loaded mac

157 NT5E was expressed in SMCs > PDGFRalpha(+) cells.

158 ents indicated that ~78% of NO metabolism in SMCs is Cygb-dependent.

159 em supporting Cygb-mediated NO metabolism in SMCs with changes in cellular B5/B5R levels modulating t

160 iscuous, proinflammatory TGFBR2 signaling in SMCs, thereby promoting AAD formation.

161 ucial for the initiation of Ca(2+) sparks in SMCs and the regulation of vascular contractility and bl

162 an TFV-dp concentration achieved with TAF in SMCs was 6% that of TFV-dp in PBMCs.

163 inhibition (carbenoxolone; 100 um) increased SMC death, inhibiting NO synthase (l-NAME, 100 um) or sc

164 PCSK6 is a novel protease that induces SMC migration in response to PDGFB, mechanistically via

165 h11-CreER(T2) lineage-tracing with inducible SMC and pericyte (SMC-P) knockout of Oct4 that Oct4 regu

166 o and in iSM-Gprc5b-KO (tamoxifen-inducible, SMC-specific knockout) mice under conditions of arterial

167 ting to ensure faithful genetic inheritance, SMCs can disrupt genome stability by trapping DNA topolo

168 the first evidence showing that YY1 inhibits SMC differentiation by directly targeting MYOCD.

169 origin-specific proteome in a validated iPSC SMC model to identify novel protein markers associated w

170 Single protein-level data from both iPSC SMCs and primary MFS aortic root aneurysm tissue confirm

171 Functionally, iPSC SMCs exhibited defective adhesion to a variety of extrac

172 HGPS-iPSC SMCs cultured under arterial flow conditions detach from

173 ometry was applied to profile LM and NC iPSC SMCs from four MFS patients and two healthy controls.

174 rformed cell biology experiments on isolated SMC-derived cells, conducted integrative human genomics,

175 endosomes and lysosomes in freshly isolated SMCs from cerebral arteries were essentially immobile.

176 ruding DNA loops, cohesin entraps within its SMC-kleisin ring (S-K) individual DNAs during G1 and sis

177 a broad range of SMC markers, as well as key SMC transcription factors MYOCD and SRF, at the RNA and

178 d transcription regulators including the key SMC transcription factor Myocardin, thereby matching man

179 We show that activated lesional SMCs attract neutrophils, triggering the ejection of neu

180 ruption of individual elastic lamellae, lost SMC contractility, and GAG production within an intra-la

181 mice treated with a MMP inhibitor show lower SMC loss in the aortic arch than controls.

182 ge-tracing models to confirm that the mature SMC can give rise to a hyperproliferative cell which app

183 This combination of medial SMC loss with marked increases in non-SMC aortic cell ma

184 Medial SMCs proliferate broadly to thicken the media, after whi

185 For old (24 months) mice, SMC death was reduced to 10% with diminished accumulatio

186 that the Ahr pathway is active in modulated SMCs in the atherosclerotic lesion cap.

187 cant increase in the proportion of modulated SMCs expressing chondrocyte markers such as Col2a1 and A

188 However, the phenotype of modulated SMCs in vivo during atherosclerosis and the influence of

189 The parent trial evaluated monthly SMC plus either azithromycin (AZ) or placebo, administer

190 A fifth monthly SMC course is needed to adequately cover the whole trans

191 factors related to adherence to the monthly SMC schedule.

192 ty and dedifferentiation in human and murine SMCs in vitro and in iSM-Gprc5b-KO (tamoxifen-inducible,

193 between endothelial (ECs) and smooth muscle (SMCs) cells.

194 ed caveolae in aECs, but not in neighbouring SMCs, impaired neurovascular coupling.

195 medial SMC loss with marked increases in non-SMC aortic cell mass induced exuberant growth and dilati

196 SMCHD1 is a noncanonical SMC family protein and implicated in epigenetic silencin

197 s adds novel insights into the complexity of SMC biology and reveals regulatory pathways for therapeu

198 ce of Chromosomes) complexes are composed of SMC dimers, kleisin and kleisin-interacting (HAWK or KIT

199 P production and consecutive facilitation of SMC relaxation.

200 e cells (SMCs), but the specific function of SMC-expressed orphan G protein-coupled receptor class C

201 rosis by regulating phenotypic modulation of SMC.

202 nd human lesions and extensive plasticity of SMC- and endothelial cell-derived cells including 7 dist

203 ealed that TCF21 suppresses a broad range of SMC markers, as well as key SMC transcription factors MY

204 ly AVF remodeling and sustained reduction of SMC proliferation.

205 tudy establishes PCSK6 as a key regulator of SMC function in vascular remodeling.

206 ) signaling was identified as a regulator of SMC to SEM cell transition, and RA signaling was dysregu

207 The role of SMC-derived Fn-EDA in SMC phenotypic switching or its im

208 ole and promoting its rupture at the site of SMC loss.

209 emphasise the need for continuing support of SMC programmes.

210 latory pathways for therapeutic targeting of SMC transitions in atherosclerotic cardiovascular diseas

211 To reveal the trajectories of SMC transdifferentiation during atherosclerosis and to i

212 the expression of Fn-EDA in the vicinity of SMC-rich neointima and peri-strut areas.

213 After 3 years of SMC deployment, the day 28 PCR-unadjusted adequate clini

214 cular injury response including apoptosis of SMCs and production of chemokines, thus is an attractive

215 plaque load and increased differentiation of SMCs in the fibrous cap.

216 ges-including in cytosolic lipid droplets of SMCs.

217 s the upstream arteriole exhibited a loss of SMCs.

218 ken the media, after which a small number of SMCs are selected to establish the neointima.

219 behaviours of LM are an emergent property of SMCs and ICC-SS.

220 identify a Notch3-marked minority subset of SMCs as the major neointimal cell of origin.

221 al vascular dimorphism, including effects on SMC differentiation.

222 also examined the direct effects of STING on SMC death and macrophage activation in vitro.

223 Global or SMC-specific LMO7 deletion enhanced neointimal formation

224 subsequently gives rise to at least 3 other SMC phenotypes within advanced lesions, including Klf4-d

225 onnecting the head domains; resembling other SMC proteins such as cohesin or condensin.

226 In particular, SMC contributed to a Myh11(-), Lgals3(+) population with

227 age-tracing with inducible SMC and pericyte (SMC-P) knockout of Oct4 that Oct4 regulates perivascular

228 condition of hyperlipidemia by potentiating SMC proliferation and migration.

229 onstrating that mTOR-dependent proliferative SMCs render the aortic wall vulnerable to dilatation and

230 LAG3+ compared to those that did not receive SMC.

231 However, children receiving SMC showed greater increases in CD4+FOXP3+ T regulatory

232 ory cells compared to children not receiving SMC.

233 venging peroxynitrite (FeTPPS, 5 um) reduced SMC death along with [Ca(2+) ](i) .

234 molecular mechanism by which TCF21 regulates SMC phenotype is not known.

235 rget genes play an important role regulating SMC phenotypic changes.

236 integrity and diminishes the disease-related SMC-to-chondromyocyte transition in atherosclerotic tiss

237 anism by which endothelial Twist1 stimulates SMC accumulation to distal PAs in PH remains unclear.

238 bsence of a calcification-inducing stimulus, SMCs assume a synthetic phenotype in response to subendo

239 -binding properties of the Bacillus subtilis SMC complex.

240 , and used pharmacological studies targeting SMC-derived cells both in vivo and in vitro.

241 Despite strong evidence that SMC is providing a high level of protection, the burden

242 ogether, these results provide evidence that SMC-derived cells within advanced mouse and human athero

243 We provide evidence that SMC-specific Klf4- versus Oct4-knockout showed virtually

244 We predict that SMC complexes in vivo constitute effectively two-sided m

245 These results reveal that SMC-derived Fn-EDA potentiates phenotypic switching in h

246 We found that SMCs transitioned to an intermediate cell state during a

247 We observed that SMCs that activate Lgals3 compose up to two thirds of al

248 The SMC (Structural Maintenance of Chromosomes) complexes ar

249 The SMC family member condensin is best known for establishi

250 The SMC-ParAB-parS system is widely employed for chromosome

251 nts, between ATP-bound engaged heads and the SMC hinge and associated kleisin, respectively.

252 e changes lies a unique group of ATPases-the SMC proteins-that act as major effectors of chromosome b

253 chimeric Mre11/Rad50 complex containing the SMC hinge of bacterial condensin MukB instead of the RAD

254 simulations suggest a critical role for the SMC coiled-coil regions, where the coils intertwine with

255 country) under observation each year in the SMC plus placebo group.

256 , respectively, in these 2 age groups in the SMC villages, with prevalence differences of 12.5% (95%

257 cases in the control villages and 270 in the SMC villages.

258 eral times higher in children who missed the SMC course preceding the survey contact, and the smalles

259 od can be used to intelligently modulate the SMC response in gelatin/PCL scaffolds making the TGFbeta

260 at ATP binding induces the transition of the SMC coiled coils from a folded-rod conformation into a m

261 The activity of the SMC complexes cohesin and condensin are linked to both t

262 its constitute the basal architecture of the SMC complexes.

263 ded coils are coupled with the motion of the SMC head domains, suggesting that the complexes may func

264 of the Rad50 hook is similar to that of the SMC hinge, which serves as rather stable dimerization in

265 While structural data exist for parts of the SMC-kleisin complexes, complete structures of the entire

266 The molecular dynamics simulations of the SMC-kleisin protein complexes suggest that these complex

267 losing, and translation along the DNA of the SMC-kleisin protein complexes would allow these motors t

268 e, single-cell RNA-sequencing studies of the SMC-specific Ahr knockout mice showed a significant incr

269 The activities of the SMC/condensin protein MukB and nucleoid-compacting prote

270 duced intimal hyperplasia and suppressed the SMC synthetic phenotype concomitant with decreased Akt1/

271 of the two HEAT-repeat subunits bound to the SMC ATPase head domains.

272 In addition, binding of ATP molecules to the SMC subunits and their hydrolysis drive dynamics of thes

273 yte-like cells, as well as return toward the SMC phenotype.

274 We also annotate loops associated with the SMC component of the dosage compensation complex (DCC) i

275 observed substantial (13)C enrichment in the SMCs adjacent to macrophages.

276 taCD before plating the macrophages onto the SMCs.

277 ation of B5 or B5R concentrations from their SMC levels showed that V(NO) exhibits apparent Michaelis

278 Despite high coverage and high adherence to SMC, the incidence of hospitalisations or deaths due to

279 Resulting depolarization conducts to SMCs, depolarizing membrane potential, activating L-type

280 Y1(-) cells were predominantly restricted to SMCs.

281 y signals from the central nervous system to SMCs via a caveolae-dependent pathway.

282 larger lesion size, increased lineage-traced SMC participation in the lesion, decreased lineage-trace

283 tion in the lesion, decreased lineage-traced SMCs in the lesion cap, and increased alkaline phosphata

284 ctility and function, in lower urinary tract SMCs.

285 omic-scale structures for several tripartite SMC-kleisin complexes, including prokaryotic condensin,

286 d BK channel activity in bladder and urethra SMCs.

287 lation to monitor the GPCR trafficking using SMCs.

288 Targeted deletion of LRP1 in vascular SMC (smLRP1(-/-)) in mice disinhibited TGFbeta1-CTGF (co

289 hat SMILR is a critical mediator of vascular SMC proliferation via direct regulation of mitotic progr

290 our data show that GPRC5B regulates vascular SMC tone and differentiation by negatively regulating IP

291 induction of ACE2 and protection of vascular SMCs, whereas stable APLN analogs provide an effective t

292 These vascular SMCs, termed degradative SMCs, compromise the medial pro

293 ently, it is important to understand whether SMC continues to provide a high level of protection and

294 g mouse to understand the mechanism by which SMC phenotypic transitions affect lesion pathogenesis.

295 c switching, a pathological process in which SMC dedifferentiation, migration, and transdifferentiati

296 o comparing SMC within the past 28 days with SMC more than 35 days ago-adjusted for age, country, and

297 endothelialization was observed in rats with SMC-specific knockdown of Prkcd.

298 ene signature that was markedly reduced with SMC-Klf4 knockout.

299 ine (eADO) by CD38, ENPP1 and NT5E, (2) with SMCs and PDGFRalpha(+) cells, eNAD is metabolized to eAD

300 In mice, Fn-EDA colocalizes with SMCs in the neointima of injured carotid arteries and pr