ライフサイエンスコーパス: myogenic

1 results highlight Ldb1 requirement for Pax3 myogenic activity and demonstrate how transcription fact

2 ohibitin2 sequesters mDia1, dampens its anti-myogenic activity and fine-tunes RhoA-mDia1 signalling t

3 ti-functional signalling effector whose anti-myogenic activity is modulated by a differentiation-depe

4 The proteomes, especially the myogenic and chromatin-related proteins including histon

5 tivity and glucose uptake, and decrease anti-myogenic and inflammatory gene expression in muscle, suc

6 tivator of transcription proteins (STATs) in myogenic and osteogenic differentiation after FN treatme

7 study was to investigate the action of FN on myogenic and osteogenic differentiation and its impact o

8 scles express dystrophin in up to 70% of the myogenic area and increased force generation following i

9 In silico, we identified myogenic as well as other cell types and constructed a "

10 mechanisms and the in-vivo-function of this myogenic autoregulation are poorly understood.

11 AMPKalpha1 deficiency had severely impaired myogenic capacity in regenerating muscle fibers.

12 1 integrin has been implicated in increasing myogenic capacity of satellite cells, therefore restorin

13 Myogenic cell expression of ICAM-1 contributed to the re

14 rganization of nuclei within myofibers after myogenic cell fusion.

15 nopathy, we investigated in vitro macrophage-myogenic cell interactions and found that Dysf-deficient

16 ese results reveal specific abnormalities in myogenic cell number and behavior associated with SPEG d

17 s and their controls however, implying a non-myogenic cell source in muscle biopsies.

18 for a paradigm in which ICAM-1 expressed by myogenic cells after muscle injury augments their adhesi

19 ast some ARMSs and the PAX3-FOXO1-expressing myogenic cells and demonstrate that fusion RNA profiling

20 is transcribed from an intergenic region of myogenic cells and its expression is upregulated during

21 tion of human non-muscle cells directly into myogenic cells by forced expression of MyoD represents o

22 tory-induced activation of Ccr2 signaling in myogenic cells contributes to aged muscle regenerative d

23 cle regeneration, and satellite cell-derived myogenic cells from EphA7(-/-) mice are delayed in their

24 e analyses of these cells along with primary myogenic cells from several developmental stages.

25 At the forelimb level, endothelial and myogenic cells migrate from adjacent somites into the li

26 ation, proliferation, and differentiation of myogenic cells obtained from striated muscle-specific Sp

27 shRNA knockdown of CD82 in myogenic cells reduces myoblast proliferation, suggestin

28 G deficiency on the survival and function of myogenic cells remains to be deciphered.

29 We show that myogenic cells secrete Fam3a, and exposure of Stat3-abla

30 ICAM-1-ICAM-1 interactions was restricted to myogenic cells, as forced expression of ICAM-1 by fibrob

31 rrecting oligomer was chosen to treat forced-myogenic cells, derived from fibroblasts from nine patie

32 rotein, and enzyme activity in all patients' myogenic cells, regardless of the nature of the mutation

33 G-deficient skeletal muscles contained fewer myogenic cells, which on further study demonstrated redu

34 e correction via homologous recombination in myogenic cells.

35 nts the adhesive and fusogenic properties of myogenic cells.

36 s one route to obtain highly desirable human myogenic cells.

37 permethylation and impaired accessibility at myogenic chromatin regions but does not result in genome

38 ial stages of progenitor cell proliferation, myogenic commitment and differentiation, myocyte fusion,

39 Although MRFs are essential for myogenic commitment and differentiation, timely repressi

40 er-anchored interactions as a consequence of myogenic commitment and differentiation.

41 sphorylation, and repression of the terminal myogenic commitment factor Myogenin.

42 le of the key paraxial mesoderm and skeletal myogenic commitment factors-mesogenin 1 (Msgn1), T-box 6

43 eir defects in mitochondrial respiration and myogenic commitment.

44 of AT1 Ra increases TRPM4 currents to induce myogenic constriction of cerebral arteries.

45 candesartan, indicating that AT1 R-mediated myogenic constriction relies on Ca(2+) -independent down

46 d knockdown of AT1 Rb selectively diminished myogenic constriction.

47 e also observed in a model of MYOD1-mediated myogenic conversion of human fibroblasts, and in primary

48 Myogenic cultures were isolated from the skeletal muscle

49 nto the myogenic program also depends on the myogenic determination factor (MyoD) family of genes, bu

50 use models, we showed that COUP-TFII hinders myogenic development by repressing myoblast fusion.

51 Of note, MTF1 formed a complex with myogenic differentiation (MYOD)1, the master transcripti

52 (genuine state), and CD34(Low), committed to myogenic differentiation (primed state).

53 that quiescent MuSCs express high levels of Myogenic Differentiation 1 (MyoD) transcript in vivo, wh

54 s such as Myogenin, myosin heavy chains, and myogenic differentiation 1 (MyoD).

55 rom Deltex2 knockout mice exhibit precocious myogenic differentiation and accelerated regeneration in

56 al lethal, we explored its potential role in myogenic differentiation and development by generating a

57 ndicate a key role of Phospho1 in regulating myogenic differentiation and mitochondrial function.

58 early in myogenesis, and its loss attenuated myogenic differentiation and potently reduced the levels

59 G translocates to the nucleus in response to myogenic differentiation and sublethal dose of cisplatin

60 mely paired box 7 (satellite cell) and early myogenic differentiation and terminal differentiation (m

61 ified that LSD1 is the only KDM required for myogenic differentiation and that KDM3B, KDM6A, and KDM8

62 el can help better understand the process of myogenic differentiation and the effects of mechanical c

63 22 was physiologically induced during normal myogenic differentiation and was transcriptionally regul

64 lecular mechanisms underlying osteogenic and myogenic differentiation by FN in C2C12 progenitor cells

65 FN treatment activates myogenic differentiation by increasing p38MAPK and decre

66 These data demonstrate that Ascl2 inhibits myogenic differentiation by targeting MRFs and facilitat

67 aling pathway, and exogenous FGF rescues the myogenic differentiation defects upon loss of MyHC-emb f

68 Accordingly, MyoD or Myog expression rescues myogenic differentiation despite Ascl2 overexpression.

69 aired gene expression and protein content of myogenic differentiation factors were preceded by decrea

70 e identified three compounds which inhibited myogenic differentiation in C2C12 myoblasts; (+)-JQ1, PF

71 show that cell migration, proliferation, and myogenic differentiation in pre-culture SBB-treated grou

72 signaling rescues CNC cell proliferation and myogenic differentiation in these mutant mice.

73 he mdx mice (paired with GFP mice) underwent myogenic differentiation in vitro and expressed markers

74 levated canonical Wnt signaling resulting in myogenic differentiation in vitro and in mouse xenograft

75 regulated in hypertrophic muscles and during myogenic differentiation in vitro and in vivo.

76 We found that Deltex2 inhibits myogenic differentiation in vitro, and that skeletal mus

77 Although various protocols achieve myogenic differentiation in vitro, resulting myotubes ty

78 The process of stem cell myogenic differentiation is interpreted as the interplay

79 Pak1 and Pak2 display delayed expression of myogenic differentiation markers and myotube formation.

80 ntrolled MyoD expression benefits functional myogenic differentiation of transdifferentiated myoblast

81 Myogenic differentiation proceeds through a highly coord

82 multiple human pluripotent stem cell (hPSC) myogenic differentiation protocols and mapped hPSC-deriv

83 HD and control myogenesis, revealing altered myogenic differentiation results in hypotrophic myotubes

84 2C12 cells, we postulate that 3-MPA promoted myogenic differentiation through the inhibition of PEPCK

85 Deletion of STIM2beta delayed myogenic differentiation through the MEF2C and NFAT4 pat

86 at exit the cell cycle during the process of myogenic differentiation to form myofibers.

87 C2C12 myogenic differentiation was significantly induced follo

88 Moreover, cell mechanical features and myogenic differentiation were significantly reduced in s

89 urthermore, the model of bexarotene-enhanced myogenic differentiation will provide an important avenu

90 entified Twist2 as a reversible inhibitor of myogenic differentiation with the remarkable ability to

91 ricular remodeling; NUP210 (expressed during myogenic differentiation) and ANK1 (cytoskeletal protein

92 ses and nuclear factor kappa B and decreased myogenic differentiation, as reflected by reduced expres

93 FSHD patient myoblasts have defective myogenic differentiation, forming smaller myotubes with

94 sults predict the kinetics of the process of myogenic differentiation, including the number of cells

95 rference revealed that BRD4 was required for myogenic differentiation, whereas BRD3 down-regulation r

96 PGC1alpha-ERRalpha axis leading to perturbed myogenic differentiation, which can effectively be rescu

97 riptional landscape of Twist2 binding during myogenic differentiation.

98 ncement of cell survival, proliferation, and myogenic differentiation.

99 critical in muscle development and regulates myogenic differentiation.

100 y the role of Wnt-beta-catenin signalling in myogenic differentiation.

101 xpressed at the sarcolemma of myotubes after myogenic differentiation.

102 as BRD3 down-regulation resulted in enhanced myogenic differentiation.

103 anscription factor myogenin, which regulates myogenic differentiation.

104 reas siRNA-mediated knockdown of Ret induced myogenic differentiation.

105 ion protein 1 (MYOD1)-mediated activation of myogenic differentiation.

106 offer a useful resource for others studying myogenic differentiation.

107 their myoblast counterparts, so is higher in myogenic differentiation.

108 ion and Dock3 KO myoblasts are defective for myogenic differentiation.

109 otubes resulted in reduced ATP synthesis and myogenic differentiation.

110 rs and epigenetic enzymes cooperate to guide myogenic differentiation.

111 Magnetism thus deploys an authentic myogenic directive that relies on an interplay between m

112 In vitro VDR knockdown induces myogenic dysregulation occurring through impaired differ

113 ting domains of Prohibitin2 reverse the anti-myogenic effects of mDia1DeltaN3, while non-interacting

114 BETi-mediated anti-myogenic effects were also observed in a model of MYOD1-

115 orphisms exist in genes that are involved in myogenic, endothelial, metabolic and neurogenic vascular

116 , sine oculis-related homeobox 1 (Six1), and myogenic factor 5 (Myf5)-in paraxial mesoderm and skelet

117 e characteristic SS18-SSX fusion oncogene in myogenic factor 5-expressing (Myf5-expressing) cells dev

118 rk for studying interactions between general myogenic factors and iTFs in evolutionary diversificatio

119 ses of Dock3 KO muscles reveal a decrease in myogenic factors and pathways involved in muscle differe

120 with 1G control, and the mRNA expression of myogenic factors such as Myod and Myh1 was elevated by 2

121 by the expression of certain combinations of myogenic factors.

122 requires tight spatiotemporal control of key myogenic factors.

123 h Ca(2+) inside the SR, thus contributing to myogenic fatigue.

124 s broadly required for the activation of the myogenic gene expression program.

125 ion were grossly impaired in null cells, and myogenic gene expression was not coordinated with cytosk

126 ction, these cells showed a dramatic rise in myogenic gene expression.

127 ogenesis through its action on MAPK-mediated myogenic gene expression.

128 rate with and phosphorylate Pol II along the myogenic gene loci.

129 differentiation and timely deployment of the myogenic gene program.

130 nistically, Linc-RAM regulates expression of myogenic genes by directly binding MyoD, which in turn p

131 osphatase directly impacts the expression of myogenic genes by promoting ATP-dependent chromatin remo

132 ion that coordinates an extensive network of myogenic genes in cooperation with MyoD; and an alpha-ca

133 s, NET39, Tmem38A, and WFS1, direct specific myogenic genes to the nuclear periphery to facilitate th

134 pigenetic changes redirect MyoD binding from myogenic genes toward oncogenic, metabolic, and growth g

135 f knock-in reporter human iPS cell lines for myogenic genes which can be used for disease modeling, d

136 ound to chromatin at the promoter regions of myogenic genes, and Cu addition stimulated this binding.

137 s, is found to activate transcription of key myogenic genes.

138 obox transcription factor that specifies the myogenic identity of muscle stem cells and acts as a nod

139 to a softer blend of PDMS muprinted with FN, myogenic index, myotube width, and myotube length on mum

140 ic beige adipocyte differentiation through a myogenic intermediate.

141 f differentiation of each myoblast along the myogenic lineage complicates teasing apart at what stage

142 nstrate that Stat3 promotes muscle stem cell myogenic lineage progression by stimulating mitochondria

143 ll muscle progenitor state - a distinct cell myogenic lineage responsible for postnatal growth and re

144 s study characterized a unique population of myogenic lineage stem cells that can be isolated from ad

145 functions in the activation of the skeletal myogenic lineage through modulation of Hedgehog, Notch,

146 the master transcriptional regulator of the myogenic lineage, at myogenic promoters.

147 ypically identified by their position in the myogenic lineage, simultaneously with the quantification

148 eper between the presomitic mesoderm and the myogenic lineage.

149 iation of activated satellite cells into the myogenic lineage.

150 t insights into the development of the human myogenic lineage.

151 e number of satellite cells committed to the myogenic lineage.

152 e and cell differentiation to osteogenic and myogenic lineages.

153 d that beta-catenin enhances MyoD binding to myogenic loci.

154 g at oncogenic loci and chromatin closing at myogenic loci.

155 yed myogenesis and lowered the expression of myogenic markers in cultured myoblasts from both species

156 tory markers and increased the expression of myogenic markers in the skeletal muscle.

157 FN significantly increased myogenic markers such as Myogenin, myosin heavy chains,

158 es TrxR1 levels and delays the expression of myogenic markers, suggesting the involvement of miR-23 i

159 genes and inhibition of the function of the myogenic master regulator PAX7.

160 (ERMS) is a childhood cancer that expresses myogenic master regulatory factor MYOD but fails to diff

161 Much is known about myogenic mechanisms in circular muscle (CM) in the gastr

162 direct transcriptional control of two major myogenic mechanisms, proliferative pathway and the Wnt s

163 We recorded myogenic MEPs after transcranial motor cortex stimulatio

164 by enhancing the interaction of an RBP and a myogenic mRNA.

165 e from the STS-131 mission exhibited reduced myogenic (Myf5 and -6) and adipogenic (Pparg, Cebpa, and

166 sal physiological mechanism that may involve myogenic, neural control as well as metabolic regulation

167 Remarkably, deletion of Tgfbr2 in myogenic or chondrogenic progenitor cells does not manif

168 a hypothesis for ancestral vertebrate trunk myogenic patterning and how it was co-opted during tail

169 selected alveolar rhabdomyosarcoma (ARMS), a myogenic pediatric cancer whose exact cell of origin is

170 ty of the transduced cells, as well as their myogenic phenotype, were determined by flow cytometry an

171 ) SCs are shifted toward more differentiated myogenic population.

172 lled labeling and monitoring of lipogenic or myogenic populations of lung fibroblasts during fibrosis

173 scle is partially responsible for diminished myogenic potential in aging and activation of hypoxia si

174 , we define miRNA cocktails that promote the myogenic potential of human MiPs.

175 Furthermore, we also observed a higher myogenic potential of MDSPCs derived from prolyl hydroxy

176 rmal and these cells had evidence of reduced myogenic potential.

177 ons of ocular and cervical vestibular evoked myogenic potentials and dynamic visual acuity.

178 ects on proliferation and differentiation of myogenic precursor cells, and these actions concertedly

179 roliferate in response to injury and provide myogenic precursors for growth and repair.

180 Most SC originate from PAX7(+) myogenic precursors set aside during development.

181 se model ectopically expressing COUP-TFII in myogenic precursors to maintain COUP-TFII activity durin

182 ental trajectory of the iPSC-derived PAX7(+) myogenic precursors.

183 ssion of TrxR1 during differentiation delays myogenic process, by negatively affecting the expression

184 eletion of Myh3 causes the depletion of both myogenic progenitor and myoblast pools.

185 rium between proliferation and quiescence of myogenic progenitor and stem cells is tightly regulated

186 nic myogenesis leads to the depletion of the myogenic progenitor cell pool and an increase in the myo

187 -erbalpha as a novel inhibitory regulator of myogenic progenitor cell properties that suppresses post

188 Furthermore, these PA scaffolds support myogenic progenitor cell survival and proliferation and

189 nse to hypertrophic stimuli and give rise to myogenic progenitor cells (MPCs) within the extracellula

190 ely via interactions between CNC-derived and myogenic progenitor cells.

191 hts into both Wnt signalling and adult human myogenic progenitor differentiation.

192 tor 2 (Ccr2) expression in non-hematopoietic myogenic progenitors (MPs) during regeneration.

193 he non-cell-autonomous effect of MyHC-emb on myogenic progenitors and myoblasts is mediated by the fi

194 n in the fusion and differentiation of human myogenic progenitors and that dominant negative inhibiti

195 of reisolated Pax3/Pax7-induced PSC-derived myogenic progenitors changes toward a postnatal molecula

196 t stem cells (PSCs) allows the generation of myogenic progenitors endowed with enhanced regenerative

197 l for a better understanding of hPSC-derived myogenic progenitors for translational applications in s

198 ospective identification and purification of myogenic progenitors from human iPS cells.

199 ng cells in vivo, specification of migratory myogenic progenitors is severely impaired.

200 Myogenic progenitors lacking Minion differentiate normal

201 man primary CD56(Pos) satellite cell-derived myogenic progenitors obtained from healthy individuals t

202 we show that in vitro-generated PSC-derived myogenic progenitors possess a molecular signature simil

203 findings demonstrate that Pax3/Pax7-induced myogenic progenitors remodel their molecular signature a

204 Somites give rise to myogenic progenitors that form all of the muscles of the

205 rentiation protocols and mapped hPSC-derived myogenic progenitors to an embryonic-to-fetal transition

206 s provide important regulatory cues to guide myogenic progenitors to differentiate into muscles in th

207 Re-orienting ghost fibers impacted myogenic progenitors' migratory paths and division plane

208 Pax3-positive migratory myogenic progenitors, marked by expression of Lbx1, are

209 of genes, but Pax3 is not expressed in these myogenic progenitors, where different gene regulatory ne

210 otential of these gene corrected PSC-derived myogenic progenitors.

211 tion of large numbers of highly regenerative myogenic progenitors.

212 Entry into the myogenic program also depends on the myogenic determinat

213 rexpression additionally targets a competing myogenic program and directs a more faithful conversion

214 erminants that control the entrance into the myogenic program and the appearance of PAX7+ cells durin

215 also restore MYOD's ability to activate the myogenic program in human senescent fibroblasts.

216 vior of these cells and their entry into the myogenic program is controlled by gene regulatory networ

217 pression that promotes the activation of the myogenic program, and is therefore termed Linc-RAM (Linc

218 bal gene transcription and repression of the myogenic program.

219 everse senescence-mediated inhibition of the myogenic program.

220 cycle progression for the activation of the myogenic program.

221 DR precluded MYOD-mediated activation of the myogenic program.

222 egulation allows the progression through the myogenic programme.

223 Here, we show that Zfp423 regulates myogenic progression during muscle regeneration.

224 RET is dynamically expressed during myogenic progression in mouse and human myoblasts.

225 nificantly enhanced proliferative growth and myogenic progression.

226 ion of Fbxl2 as both a critical regulator of myogenic proliferative processes and a susceptible gene

227 es gene expression through direct binding to myogenic promoter sequences and facilitating the binding

228 tional regulator of the myogenic lineage, at myogenic promoters.

229 Importantly, MiP myogenic propensity is influenced by somatic lineage ret

230 urthermore, methods to enhance the intrinsic myogenic properties of MiPs are likely needed, given the

231 Thus, these anti-myogenic proteins act as important inhibitors of synapse

232 Using progenitor markers, 3 distinct myogenic PW1(+) cell populations were isolated from the

233 ted statistically significant differences in myogenic reactivity between WT and KO vessels.

234 ing was found to contribute to the increased myogenic reactivity of SMTNL1 KO vessels across the 60-1

235 lpha7 integrin enhancer capable of promoting myogenic regeneration by stimulating satellite cell acti

236 (KD) on mature skeletal muscle in vivo, and myogenic regulation in vitro in C2C12 cells.

237 he physiological function of Rev-erbalpha in myogenic regulation remains largely unknown.

238 e sustained VDR-KD in C2C12 cells to analyse myogenic regulation.

239 us, we have identified MyHC-emb as a crucial myogenic regulator during development, performing dual c

240 The myogenic regulatory factor MRF4 is highly expressed in a

241 The myogenic regulatory factor MyoD has been implicated as a

242 In the present study we show that the master myogenic regulatory factor, MYOD1, is a positive modulat

243 Myogenic regulatory factors (MRFs), including Myf5, MyoD

244 myogenesis are orchestrated and regulated by myogenic regulatory factors and various downstream cellu

245 that H3K9me3 is erased from the gene loci of myogenic regulatory factors namely MYOD1, MYOG, and MYF5

246 The coordinated expression of myogenic regulatory factors, including MyoD and myogenin

247 RMS) is a pediatric malignacy of muscle with myogenic regulatory transcription factors MYOD and MYF5

248 plays an active role in both the arteriolar myogenic response and during changes in vascular tone in

249 Ang II-induced myogenic response and hypertension were greater in Apln

250 3 knockout rats exhibited impairments in the myogenic response of afferent arterioles and in renal bl

251 Using pharmacological approaches, myogenic responses of both WT and KO vessels were equall

252 in TgNotch3(R169C) and TgBAC-TIMP3 mice, and myogenic responses of brain arteries were likewise atten

253 Altered myogenic responsiveness compromises tissue perfusion, ag

254 etion of p66Shc from these rats restored the myogenic responsiveness of renal preglomerular arteriole

255 y reprograms gene expression in BAT toward a myogenic signature, including increased expression of my

256 excitation might initiate and spread in this myogenic smooth muscle.

257 er human iPS cell line for MYF5, as an early myogenic specification gene, to allow prospective identi

258 and Isl1 are required cell-autonomously for myogenic specification of ESM progenitors.

259 pment and regeneration by reprogramming each myogenic stage.

260 nd transcription factors present at distinct myogenic stages.

261 acteristics and tissues of origin, including myogenic stem and progenitor cells, stromal cells, and p

262 Satellite cells (SCs) are myogenic stem cells required for regeneration of adult s

263 Muscle satellite cells are myogenic stem cells whose quiescence, activation, self-r

264 cell cycle withdrawal in fetal and postnatal myogenic stem cells, and assign to Ptpn11 signaling a ke

265 and Six4 could participate in the genesis of myogenic stem cells.

266 tion was observed in postnatal but not fetal myogenic stem cells.

267 Our data demonstrate a lipogenic-to-myogenic switch in fibroblastic phenotype during fibrosi

268 e that a combinatorial anti-fibrotic and pro-myogenic therapy could be the foundation of future thera

269 Conversely, we observed a myogenic-to-lipogenic switch during fibrosis resolution.

270 he AT1 R blocker losartan (1 mum) diminished myogenic tone and blocked stretch-induced cation current

271 n-dependent inhibition of pressure-dependent myogenic tone consistent with previous reports of mechan

272 regulation of excitability, [Ca(2+)](i), and myogenic tone in arterial myocytes.

273 irect addition of prostaglandin D(2) rescued myogenic tone in high-fat diet-fed control mice.

274 ilatory responses to an NO donor and loss of myogenic tone in KW animals were also rescued with Nox1

275 f obesity-induced hypertension by preserving myogenic tone in resistance arteries.

276 increase in L-type Ca2+ channel activity and myogenic tone in two animal models of diabetes.

277 SMTNL1 deletion was associated with enhanced myogenic tone in vessels isolated from male, but not fem

278 y role in myogenic vasoconstriction and that myogenic tone is required to maintain local and systemic

279 f prostaglandin D(2) synthesis inhibited the myogenic tone protection in resistance arteries of endot

280 1.2 clusters, larger [Ca(2+)](i), and larger myogenic tone than male myocytes.

281 channels in arterial myocytes and increased myogenic tone upon acute hyperglycemia.

282 However, we found that development of myogenic tone was greater in arteries from AT1 Ra knocko

283 Myogenic tone was increased in obese human arteries with

284 Myogenic tone was unchanged, but over a range of transmu

285 d from patients with diabetes have augmented myogenic tone, despite reasonable blood glucose control.

286 ling output of DYRK1A on Pol II to stimulate myogenic transcription after active P-TEFb function is s

287 ation and potently reduced the levels of the myogenic transcription factor MEF2C.

288 man skin fibroblasts by forced expression of myogenic transcription factor MyoD, we performed quantit

289 8A effectively reduced the expression of the myogenic transcription factor myogenin and suppressed my

290 In contrast to myogenic transcription factor signaling, the molecular m

291 and fusion associated with dysregulation of myogenic transcription factors and disruption of the nes

292 C) are homologous proteins known to regulate myogenic transcription factors.

293 origin of the tremor, which we classify as "myogenic tremor." ANN NEUROL 2019.

294 d Rho-mediated signaling plays a key role in myogenic vasoconstriction and that myogenic tone is requ

295 Myogenic vasoconstriction is an autoregulatory function

296 In addition, animals with defective myogenic vasoconstriction showed aggravated hypotension

297 tein-coupled receptors have been involved in myogenic vasoconstriction, but the downstream signalling

298 In the absence of myogenic vasoconstriction, perfusion of peripheral organ

299 ABSTRACT: Myogenic vasoconstriction, which reflects the intrinsic

300 ucleotide exchange factor ARHGEF12 have lost myogenic vasoconstriction.