ライフサイエンスコーパス: SRF

1 SRF is also dispensable for the KLF3-mediated repression

2 SRF is an essential regulator of skeletal muscle differe

3 SRF is an essential transcription factor in hematopoiesi

4 SRF regulates neutrophil migration, integrin activation,

5 SRF split renal function was measured by using the area

6 SRF subsequently funded animal research to evaluate sucr

7 SRF terminated Project 259 without publishing the result

8 SRF thickness >118.25 mum at baseline predicted requirin

9 SRF-deficient macrophages fail to spread, transmigrate,

10 SRF-VP16iHep mHCC reveal convergent Ras/MAPK and Rho/act

11 SRF/MRTF-A-dependent gene transcription is activated whe

12 lators of smooth muscle expression (miR-145, SRF, Nfatc4, and Crip1).

13 The main aim of this study was to compare 2D SRFs between neurons in the noise-selective region (NSR)

14 for retina (ICC = 0.84; 95% CI, 0.83-0.86), SRF (ICC = 0.88; 95% CI, 0.86-0.89), and subretinal tiss

15 2 reduced the nuclear accumulation of MRTF-A.SRF complexes and consequently inhibited alpha-SMA promo

16 It describes how the MRTF-A/SRF pathway is intricately linked to all the key regulat

17 ription factor/serum response factor (MRTF-A/SRF) transcription pathway as a potential novel therapeu

18 polymerization de-repress MRTFs and activate SRF-dependent genes.

19 conditionally express constitutively active SRF-VP16 in hepatocytes, thereby controlling subsets of

20 ued by expression of a constitutively active SRF.

21 ion resulting in reduced myogenically active SRF, but enhanced SRF activity on target genes involved

22 ng the formation of transcriptionally active SRF/MRTF-A complexes.

23 ically interacted with SRF without affecting SRF-myocardin interaction.

24 All SRF-VP16iHep mice develop hyperproliferative liver nodul

25 enrichment of RNase L and TTP targets among SRF-regulated genes suggesting that the RNase L/TTP axis

26 activated smooth muscle gene promoters in an SRF-dependent manner.

27 n proposed that coating the inner wall of an SRF cavity with superconducting thin films increases Hvp

28 ning, funding, and internal evaluation of an SRF-funded research project titled "Project 259: Dietary

29 essive DNA binding complexes and suppress an SRF-dependent transcriptional program that supports surv

30 transmigrate, and phagocytose bacteria, and SRF-deficient neutrophils show defective chemotaxis in v

31 cerebellum, NR3C1 in the cerebral cortex and SRF in the basal forebrain.

32 d similar efficacy in visual improvement and SRF resolution.

33 differentiate, and quantify intraretinal and SRF using area under the receiver operating characterist

34 All individual IRC and SRF lesions were manually delineated on each of the 128

35 rrelations were computed between the IRC and SRF parameters and the baseline BCVA, final BCVA, and BC

36 s of fit of correlations between the IRC and SRF parameters and the baseline BCVA, final BCVA, and BC

37 rvention, exudative features such as IRC and SRF resolved rapidly in 74% of eyes, whereas PED respond

38 underwent complete quantification of IRC and SRF.

39 ual outcome only in combination with IRC and SRF.

40 acuity, new haemorrhage, presence of IRF and SRF on an optical coherence tomography (OCT) scan.

41 e" treatment (complete resolution of IRF and SRF) or ranibizumab "relaxed" treatment (resolution of I

42 entiates TNF-alpha in inducing NF-kappaB and SRF/SRE activities.

43 us, despite the shared phenotype of KLF3 and SRF-deficient mice, cooperation of these factors appears

44 ting the ability of Pfn to influence MKL and SRF expression.

45 in which RNase L and TTP target SRF mRNA and SRF-induced transcripts.

46 F), resulting in disruption of myocardin and SRF interactions and thereby attenuating expression of s

47 set of genes associated with high Notch and SRF activity.

48 tile melanoma cells had increased Notch- and SRF-dependent transcription.

49 scription factors (MRTFs), which function as SRF coactivators, serve as sensors of actin polymerizati

50 rrative case study method was used to assess SRF Project 259 from 1967 to 1971 based on sugar industr

51 CREB/ATF family, heat-shock factor 1, ATF6, SRF, and E2F1 transcription factors.

52 Baseline SRF had no effect on visual recovery; however, recurrenc

53 rs for BCVA change at month 12 were baseline SRF (P = 0.05), PVD (P = 0.03), IRC (P = 0.05), treatmen

54 No robust associations were found between SRF and baseline BCVA (R2 = 0.06; P = .14) or BCVA chang

55 resolution of all retinal fluid (i.e., both SRF and intra-retinal fluid [IRF]) in patients with nAMD

56 via distinct mechanisms, the actions of both SRF and MRTF-A.

57 The presence of both SRF and PVD at baseline was associated with similar BCVA

58 In patients with both SRF and PVD at baseline, similar BCVA outcomes were obse

59 inal cysts resolved most rapidly followed by SRF, whereas PED decreased at a slower rate and intensit

60 duced by TGF-beta1 and MYOCD, and reduced by SRF deficiency in VSMCs.

61 follow-up; all recurrent cases had complete SRF resolution after another PDT treatment.

62 ific role of the transcription factors CREB, SRF, and MEF2 in the depression and potentiation compone

63 In this study, we tested the role of CREB, SRF, and MEF2 in ocular dominance plasticity (ODP), a pa

64 to block the transcription function of CREB, SRF, and MEF2 in the visual cortex, and measured visuall

65 We found that CREB, SRF, and MEF2 are all required for ODP, but have differe

66 novel MRTF/SRF inhibitor, markedly decreased SRF reporter gene activity and showed a greater inhibito

67 gether, these results suggest that decreased SRF expression induces replicative stress and chromosoma

68 act as general antagonists of MRTF-dependent SRF target gene expression, competing directly with the

69 C data, we identified over 700 TCF-dependent SRF direct target genes involved in signaling, transcrip

70 1 patients; 16 of these eyes (84%) developed SRF on OCT.

71 Forty-six (90%) study participants developed SRF during the study period, with 9 (20%) experiencing s

72 kness of 39 study participants who developed SRF at the first visit increased from 280 (26) microm at

73 upon postnatal and adult depletion of either SRF or its cofactors Myocardin Related Transcription Fac

74 tiple cancer-related pathways including Elk1/SRF, AP1, NFkappaB and STAT, and reduces EGFR expression

75 observation), when exudative signs emerged (SRF in 3/6 eyes and retinal cystoid spaces in 5/6 eyes).

76 -induced SM gene transcription by empowering SRF binding to CArG box in SM gene promoters.

77 educed myogenically active SRF, but enhanced SRF activity on target genes involved in proliferation.

78 xpression of Olfm2 dose dependently enhanced SRF binding.

79 of the CCTepsilon subunit by siRNA enhances SRF signaling in cultured mammalian cells by an actin as

80 On examination, SRF appeared as elevated, yellow-orange pockets in the f

81 genes controlled by the transcription factor SRF, and overexpression of SRF rescues impaired chromoso

82 s through their partner transcription factor SRF.

83 transcription factor serum-response factor (SRF) along with its co-activator, myocardin-related tran

84 ial role of myocardin/serum response factor (SRF) and Notch signaling in the transcriptional regulati

85 transcription factor serum response factor (SRF) and set the chromatin state of SRF-targeted genes e

86 factor A (MRTF-A) and serum response factor (SRF) and the other using the transcriptional coactivator

87 The serum response factor (SRF) binds to coactivators, such as myocardin-related tr

88 al remodelling on the serum response factor (SRF) co-factors Megakaryoblastic Leukemia-1 and -2 (MKL1

89 Serum response factor (SRF) controls multiple genes governing adhesion and migr

90 tic leukemia-1 (MKL1)/serum response factor (SRF) during myofibroblast differentiation resulted in de

91 (MRTFs) co-activating serum response factor (SRF) in this process is largely unknown.

92 Serum response factor (SRF) is a ubiquitously expressed transcription factor an

93 scriptional regulator serum response factor (SRF) is controlled by both Ras/MAPK (mitogen-activated p

94 We demonstrate that serum response factor (SRF) is induced by both platelet-derived growth factor (

95 oding proteins of the serum response factor (SRF) pathway are located on 5q.

96 ion factor-A (MRTF-A)/serum response factor (SRF) pathway.

97 es, especially in the serum response factor (SRF) pathway.

98 tion of Rho-dependent serum-response factor (SRF) signaling.

99 lators and to promote serum response factor (SRF) signalling has raised the question of whether MRL p

100 transcription factor serum response factor (SRF) to activate mitogen-induced transcription.

101 -kappaB and myocardin/serum response factor (SRF) to convey hypertrophy signaling in cardiac myoblast

102 teraction between the serum response factor (SRF) transcription factor and one of its principal co-ac

103 levated expression of serum-response factor (SRF), a master regulator of mitogen-induced transcriptio

104 s where they activate serum response factor (SRF), a regulator of actin and other cytoskeletal protei

105 cardin for binding to serum response factor (SRF), resulting in disruption of myocardin and SRF inter

106 transcription factor Serum Response Factor (SRF), suffer from loss of BBB integrity and intracerebra

107 scriptional regulator serum response factor (SRF), whereas another is calcineurin Abeta.

108 ator that activates a serum response factor (SRF)-dependent gene program required for cardiogenesis a

109 gnificantly inhibited serum response factor (SRF)-dependent reporter gene (SRE-LUC) activity and mRNA

110 tes the expression of serum-response factor (SRF)-dependent target genes in response to the Rho-actin

111 ) are coactivators of serum response factor (SRF)-mediated gene expression.

112 lastic leukemia (MKL)/serum-response factor (SRF)-mediated gene transcription is a highly conserved m

113 merization results in serum response factor (SRF)-mediated transcription through nuclear retention of

114 r TGF-beta1 and MYOCD/serum response factor (SRF)-regulated TSPANs in VSMC by using RNA-seq analyses

115 binding sites of the serum-response factor (SRF).

116 tional coactivator of serum response factor (SRF).

117 romoter activity in a serum response factor (SRF)/CArG box-dependent manner.

118 transcription factor, serum response factor (SRF); however, the mechanisms dynamically regulating SMC

119 CREB (cAMP response element binding factor), SRF (serum response factor), and MEF2 (myocyte enhancer

120 was controlled by the transcription factors SRF and MEF2.

121 sue by quantifying spatial receptive fields (SRFs) in two functionally distinct cortical regions in t

122 incomplete resolution of sub-retinal fluid (SRF) </=200 mum at the foveal centre relative to a T&E p

123 as intra-retinal (IRF) or sub-retinal fluid (SRF) were evident on SD-OCT, followed by a gradual exten

124 sed hole showed persistent subretinal fluid (SRF) after gas absorption.

125 uity (BCVA), resolution of subretinal fluid (SRF) demonstrated by optical coherence tomography (OCT),

126 F corresponded to areas of subretinal fluid (SRF) on spectral-domain OCT and was found to persist in

127 On OCT, subretinal fluid (SRF) was detected in 77% of CM patients and 60% of UM pa

128 al cystoid fluid (IRC) and subretinal fluid (SRF) was developed.

129 intraretinal cysts (IRCs), subretinal fluid (SRF), and pigment epithelial detachment (PED), presentin

130 tinal cystoid fluid (IRC), subretinal fluid (SRF), and pigment epithelial detachment (PED).

131 intraretinal cysts (IRCs), subretinal fluid (SRF), and pigment epithelial detachments (PEDs), decreas

132 intraretinal fluid (IRF), subretinal fluid (SRF), and sub-retinal pigment epithelium (RPE) fluid and

133 id material and persistent subretinal fluid (SRF), but also a RPE-independent visual cycle for cone p

134 tinal cystoid fluid (IRC), subretinal fluid (SRF), pigment epithelial detachment, and vitreomacular i

135 intraretinal fluid (IRF), subretinal fluid (SRF), sub-retinal pigment epithelium (RPE) fluid, and su

136 ccult CNV, and presence of subretinal fluid (SRF).

137 coefficient of 0.90 for IRC and of 0.96 for SRF.

138 ivation of SRF by GSK-3 that is critical for SRF-dependent axon growth in mammalian central neurons.

139 asis, underscoring an essential function for SRF and its pathway in health and disease.

140 Thus, competition between TCFs and MRTFs for SRF determines the balance between antagonistic prolifer

141 This serine phosphorylation is necessary for SRF activity and for its interaction with MKL-family cof

142 ollectively, our results identify a role for SRF in proliferation and migration during craniofacial d

143 the most accurate CT volumetry technique for SRF and the prediction of postdonation kidney function (

144 In 1965, the Sugar Research Foundation (SRF) secretly funded a review in the New England Journal

145 ters commonly evaluate split renal function (SRF) with Tc-99m-mercapto-acetyltriglycin (MAG3) scintig

146 Furthermore, SRF downregulation in diploid hPSCs induces replication

147 We generated SRF-VP16iHep mice, which conditionally express constitut

148 Only 2 participants (4%) were found to have SRF at the last study visit after discontinuation of tre

149 transcription factor depletion in the heart (SRF(HKO)) or of cardiac hypertrophy triggered by transve

150 However, SRF alone is not sufficient for regulating smooth muscle

151 These results identify SRF and its MRTF cofactors as major transcriptional regu

152 inding supports previous reports implicating SRF and MEF2 in long-term depression (required for Dc-OD

153 ds achieving higher acceleration gradient in SRF cavity accelerator beyond the theoretical limit of b

154 We hypothesize that impairments in SRF/MRTF activity contribute to human SVD pathology.

155 pression of a wide range of genes, including SRF itself and many important structural and regulatory

156 h insulin alone, insulin+TNF-alpha increased SRF/SRE binding and beta-MHC expression, which was rever

157 ein 70-interacting protein (CHIP), increased SRF activity, as well as beta-myosin heavy chain (MHC) a

158 At the molecular level, direct and indirect SRF/MRTF target genes, encoding structural components of

159 Olfm2 expression inhibited TGF-beta-induced SRF binding to SM gene promoters in a chromatin setting,

160 P axis represents a viable target to inhibit SRF-driven proliferation in neoplastic diseases.

161 It did so both by independently inhibiting SRF gene expression and nuclear import of MRTF-A.

162 Using integrated SRF ChIP-seq and Hi-C data, we identified over 700 TCF-d

163 utilized Nb ellipsoid to simulate an inverse SRF cavity and investigate the effect of coating it with

164 Specific alterations, such as IRC, SRF, and PED, as baseline or follow-up features are sign

165 baseline, the proportions of eyes with IRC, SRF, and PED were balanced between the aflibercept and r

166 the action of MKL that is independent of its SRF-related activity.

167 agreement between CT volumetry SRF and MAG3-SRF (bias, 95% limits of agreement: ROI vs MAG3 0.4%, -7

168 at day 3 was r = 0.85 to 0.88, between MAG3-SRF and PDKF (r = 0.84).

169 ic SRF was determined and compared with MAG3-SRF, postoperation donor kidney function, and graft func

170 wever, in severely dilated kidneys, the mean SRF split renal function measurement was underestimated

171 atypical actin-regulatory protein, mediates SRF/MRTF-A-dependent gene transcription elicited by nerv

172 r actin as a regulatory switch that mediates SRF/MRTF-A-dependent gene transcription.

173 in a possible feedback loop of the actin/MKL/SRF signaling circuit.

174 study, we examined the possible role of MKL/SRF in the context of regulation of profilin (Pfn), a ma

175 Furthermore, disruption of the MKL1/SRF target gene, smooth muscle alpha-actin (alpha-SMA) v

176 tify the transcription factor binding motifs SRF and PRDM1 as important regulators of PIP3-sensitive

177 Thus, the MRF-SRF and YAP-TEAD pathways interact indirectly through th

178 yocardin-related transcription factor (MRTF) SRF cofactor family.

179 MRTF-SRF signaling is thus critical for expression of genes r

180 We compared MRTF-SRF and YAP-TEAD target gene sets and identified genes d

181 lore the impact of the actin-controlled MRTF-SRF (myocardin-related transcription factor-serum respon

182 In CAFs, expression of direct MRTF-SRF genomic targets is also dependent on YAP-TEAD activi

183 ts stabilizing partner KLHL40, enhances MRTF-SRF activity.

184 We used vav-iCre to inactivate MRTF-SRF signaling early during hematopoietic development.

185 et gene expression is also dependent on MRTF-SRF signaling.

186 Both the MRTF-SRF and the YAP-TEAD transcriptional regulatory networks

187 We show that the MRTF-SRF pathway is activated in cancer-associated fibroblast

188 that YAP-TEAD activity is sensitive to MRTF-SRF-induced contractility, while MRTF-SRF signaling resp

189 o MRTF-SRF-induced contractility, while MRTF-SRF signaling responds to YAP-TEAD-dependent TGFbeta sig

190 y different WH2 domains correlates with MRTF-SRF activation.

191 scription factor/Serum response factor (MRTF/SRF) pathway plays a key role in fibroblast activation a

192 scription factor/serum response factor (MRTF/SRF) pathway represents a promising therapeutic target t

193 CCG-222740, a novel MRTF/SRF inhibitor, markedly decreased SRF reporter gene acti

194 ts of new pharmacological inhibitors of MRTF/SRF signalling in a preclinical model of fibrosis.

195 We conclude that inhibitors of MRTF/SRF-regulated gene transcription such as CCG-222740, pot

196 d showed a greater inhibitory effect on MRTF/SRF target genes than the previously described MRTF-A in

197 ed" treatment (resolution of IRF or >200 mum SRF only at foveal centre).

198 ckness of the retina was Delta = 5+/-67 mum, SRF was Delta = 1.5+/-35 mum, and subretinal tissue comp

199 ls of HRT2 concomitantly disrupted myocardin/SRF and Notch transcription complex formation at respect

200 agged1 ligand- and Notch1-enhanced myocardin/SRF complex formation at the promoter CArG element.

201 promyogenic transcription factors myocardin/SRF in a CHIP-dependent manner.

202 identified the first VSMC-enriched and MYOCD/SRF and TGF-beta1/SMAD-dependent TSPAN family member, wh

203 2 is regulated by 2 parallel pathways, MYOCD/SRF and TGF-beta1/SMAD, via distinct binding elements wi

204 two regions: (1) compared with NSR neurons, SRF properties of FMSR neurons were more strongly depend

205 on OCT had better mean VA than eyes with no SRF (72.8 vs. 66.6 letters; P = 0.006).

206 , induces MRTF translocation to the nucleus, SRF-activation and CCN1/2 transcription.

207 al a novel phosphorylation and activation of SRF by GSK-3 that is critical for SRF-dependent axon gro

208 o DeltaNT in a distinct assay (activation of SRF luciferase).

209 ndingly, TRIM32 attenuated the activation of SRF signaling and hypertrophy due to dysbindin, whereas

210 gnal-responsive transcriptional activator of SRF.

211 nce, and the presence and characteristics of SRF noted on optical coherence tomography.

212 A combination of SRF, GATA6 and CRP2 required CSRP2BP for robust smooth m

213 ption factor/coactivator complex composed of SRF/Mkl1.

214 nt to overcome the axonal growth deficits of SRF-deficient and GSK-3-inhibited neurons.

215 The determination of SRF is conducted at a reading centre while the assessmen

216 SRF interaction promoted the dissociation of SRF from HERP1, a transcriptional repressor.

217 PTEN interacts with the N-terminal domain of SRF and PTEN-SRF interaction promotes SRF binding to ess

218 K-regulated ternary complex factor family of SRF partner proteins.

219 A constitutively active form of SRF/Mkl1 was not sufficient to induce focal adhesion ass

220 t of CCG-1423, a small molecule inhibitor of SRF/MRTF-A-dependent transcription that exhibits efficac

221 s in the nuclear subcellular localization of SRF and MAL.

222 37 of 46 (80%) individuals; the location of SRF accumulation varied.

223 Loss of SRF leads to defects in B-cell and T-cell development.

224 xpression levels are maintained with loss of SRF, integrin activation and trafficking are disrupted.

225 and RS renal scintigraphy for measurement of SRF split renal function was shown in patients with mode

226 The detection and measurement of SRF were also highly accurate with an AUC of 0.92 (range

227 nscription factor SRF, and overexpression of SRF rescues impaired chromosome condensation and segrega

228 The presence of SRF did not lead to permanent ocular sequelae.

229 Agreement on presence of SRF was 87% and sub-RPE fluid was 80%, with more SD OCT

230 The presence of SRF was common in study participants undergoing treatmen

231 ller total CNV leakage area, and presence of SRF.

232 t on visual recovery; however, recurrence of SRF during follow-up showed a tendency for an additional

233 g SRF activity antagonizes Myc repression of SRF target genes, attenuates Myc-induced apoptosis, and

234 half-time PDT showed complete resolution of SRF within 6 months after PDT, but 3 eyes that received

235 eyes for up to 8 years despite resolution of SRF.

236 ssociated with improved VA and resolution of SRF.

237 genomics approach to investigate the role of SRF (serum response factor) in the serum response of fib

238 eview focuses, in particular, on the role of SRF in myeloid maturation and neutrophil function.

239 Here we elucidate the role of SRF in neutrophils, the primary defense against infectio

240 The well-established dual role of SRF with alternative cofactors and responsiveness to two

241 factor (SRF) and set the chromatin state of SRF-targeted genes early growth response 1 (egr1) and c-

242 y to ECM stiffness, and compare with that of SRF/MAL, which is another important regulator of differe

243 Olfm2-SRF interaction promoted the dissociation of SRF from HE

244 A protocol to adjudicate on SRF has been established by the central reading centre a

245 Similar effects of PGE2 on SRF gene expression were observed in fibroblasts from th

246 revealing essential requirements of ongoing SRF/MRTF activity for maintenance of cerebral small vess

247 ying peripheral areas of previous or ongoing SRF and choroidal hyperpermeability that can assist in t

248 A via their respective DNA-binding partners (SRF and TEAD) and is therefore indirect, arising as a co

249 t Q8wks), and 52% (ranibizumab) of patients; SRF resolved in 75% (both aflibercept Q4wks/Q8wks) and 6

250 ow-up period, but 1 eye exhibited persistent SRF, which was resolved progressively during the 12 mont

251 s that received half-dose PDT had persistent SRF before loss to follow-up at months 5, 7, and 8 (P =

252 GSK-3 binds to and directly phosphorylates SRF on a highly conserved serine residue.

253 technique for the evaluation of predonation SRF and allows a reliable prediction of donor's PDKF.

254 The difference of predonation SRF between preserved and donated kidney was the lowest

255 ain of SRF and PTEN-SRF interaction promotes SRF binding to essential promoter elements in SM-specifi

256 s with the N-terminal domain of SRF and PTEN-SRF interaction promotes SRF binding to essential promot

257 Finally, we demonstrate that regulated SRF expression, in turn, is critical for the effects of

258 a mechanism by which RNase L down-regulates SRF-induced genes.

259 cofactor usage, leading to a PDGF-responsive SRF-driven transcriptional program in the midface.

260 Restoring SRF activity antagonizes Myc repression of SRF target ge

261 nd performed manual measurements of retinal, SRF, and subretinal tissue complex thicknesses at the fo

262 tical coherence tomographic imaging revealed SRF beneath the interdigitation zone.

263 absence of either RNase L or TTP stabilized SRF mRNA, and a subset of established TTP targets was al

264 k regulation in which RNase L and TTP target SRF mRNA and SRF-induced transcripts.

265 Analysis of direct TCF-SRF target genes and chromatin modifiers confirmed this

266 Here we report that SRF is phosphorylated and activated by GSK-3 to promote

267 We have previously shown that SRF is essential for megakaryocyte maturation and platel

268 The SRF pathway registers changes in G-actin levels, leading

269 The SRF target gene and actin-binding protein, vinculin, is

270 ly with increasing sound levels; and (3) the SRF size and centroid elevation were correlated with the

271 RNase L destabilized the SRF transcript and formed a complex with SRF mRNA in cel

272 Disruption of the SRF pathway results in myelodysplasia and immune dysfunc

273 These data support a central role of the SRF/MRTF pathway in the pathobiology of lung fibrosis an

274 led to MRTF nuclear shuttling to promote the SRF transcriptional activity required for entosis.

275 We hypothesized that the SRF/MRTF pathway inhibitor CCG-203971 would modulate myo

276 peting directly with the MRTFs for access to SRF.

277 hrough interfering with myocardin binding to SRF.

278 of Ras homolog family member A signaling to SRF, results in aberrant myeloid differentiation and hyp

279 The results suggested to SRF that gut microbiota have a causal role in carbohydra

280 Furthermore, PM blebbing triggered SRF-mediated up-regulation of the metastasis-associated

281 In turn, SRF cooperated with MEF2 to sustain the expression of LM

282 However, the molecular mechanisms underlying SRF-dependent axon growth remains unknown.

283 rane (Collagen IV), were down-regulated upon SRF depletion.

284 orrelation between predonation CT volumetric SRF of the preserved kidney and PDKF at day 3 was r = 0.

285 Preoperation CT volumetric SRF was determined and compared with MAG3-SRF, postopera

286 alysis showed agreement between CT volumetry SRF and MAG3-SRF (bias, 95% limits of agreement: ROI vs

287 lone overcomes the MZ B cell deficiency when SRF is absent.

288 nt with MEK inhibitors is not indicated when SRF is present.

289 bleb dynamics for cell-in-cell invasion when SRF is suppressed.

290 ecessary for both Dc-ODP and Pc-ODP, whereas SRF and MEF2 are only needed for Dc-ODP.

291 the SRF transcript and formed a complex with SRF mRNA in cells providing a mechanism by which RNase L

292 Eyes with SRF in the foveal center on OCT had better mean VA than

293 Olfm2 physically interacted with SRF without affecting SRF-myocardin interaction.

294 CSRP2BP directly interacted with SRF, CRP2 and myocardin.

295 oters show enriched genome-wide overlap with SRF ChIP-seq peaks, PDGF selectively activates a network

296 transient, occurring in 9 participants with SRF (20%; 95% CI, 10%-33%).

297 In the 26 patients with SRF, the fovea was affected in 85%.

298 nctioning as an indispensible regulator with SRF to maintain the differentiated SM phenotype.

299 tor for CRP2 that works synergistically with SRF and myocardin to regulate smooth muscle gene express

300 nt treatments compared with patients without SRF, without PVD, or without either who may require more