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1                                              SRF is an essential regulator of skeletal muscle differe
2                                              SRF Ser(103) phosphorylation is bidirectionally regulate
3                                              SRF Ser(103) phosphorylation is significantly decreased
4                                              SRF subsequently funded animal research to evaluate sucr
5                                              SRF terminated Project 259 without publishing the result
6                                              SRF thickness >118.25 mum at baseline predicted requirin
7                                              SRF-VP16iHep mHCC reveal convergent Ras/MAPK and Rho/act
8                             Consistently, 35 SRF/IGF2BP1-dependent genes showing conserved associatio
9 n activator of cell contractility and MRTF-A/SRF (myocardin-related transcription factor A/serum resp
10 n is lost and correlates with reduced MRTF-A/SRF activity leading to cell adhesion defects.
11  of cell adhesion, contractility, and MRTF-A/SRF activity.
12 reviously unknown link of RASSF1A and MRTF-A/SRF in tumour suppression.
13 d for regulation of cell spreading or MRTF-A/SRF transcriptional activity.
14 ion resulting in reduced myogenically active SRF, but enhanced SRF activity on target genes involved
15  associated with stronger F-actin alignment, SRF and TEAD are up-regulated.
16 achieved when treatment aimed to resolve all SRF completely.
17 e expression but did not significantly alter SRF target gene or proliferative gene expression.
18 activated smooth muscle gene promoters in an SRF-dependent manner.
19 n proposed that coating the inner wall of an SRF cavity with superconducting thin films increases Hvp
20 ning, funding, and internal evaluation of an SRF-funded research project titled "Project 259: Dietary
21 vity-regulated transcription factors AP1 and SRF.
22 cerebellum, NR3C1 in the cerebral cortex and SRF in the basal forebrain.
23  lower volumes of NSR, RPE, sPED, fvPED, and SRF.
24 d similar efficacy in visual improvement and SRF resolution.
25 differentiate, and quantify intraretinal and SRF using area under the receiver operating characterist
26                       All individual IRC and SRF lesions were manually delineated on each of the 128
27 rrelations were computed between the IRC and SRF parameters and the baseline BCVA, final BCVA, and BC
28 s of fit of correlations between the IRC and SRF parameters and the baseline BCVA, final BCVA, and BC
29 underwent complete quantification of IRC and SRF.
30 -treated eyes, the majority had both IRF and SRF (54.7%).
31 acuity, new haemorrhage, presence of IRF and SRF on an optical coherence tomography (OCT) scan.
32 e" treatment (complete resolution of IRF and SRF) or ranibizumab "relaxed" treatment (resolution of I
33 ting the ability of Pfn to influence MKL and SRF expression.
34 sive transcription factors such as MRTFA and SRF contribute to both upregulation of morphological gen
35 rovided evidence that TCF21 blocks MYOCD and SRF association by direct TCF21-MYOCD interaction.
36 l as key SMC transcription factors MYOCD and SRF, at the RNA and protein level.
37  was complete resolution of his symptoms and SRF.
38  and intraretinal fluid (IRF; intensive arm: SRF intolerant) or resolution of all IRF only (relaxed a
39  or resolution of all IRF only (relaxed arm: SRF tolerant except for SRF >200 mum at the foveal cente
40 rrative case study method was used to assess SRF Project 259 from 1967 to 1971 based on sugar industr
41 t; however, no meaningful impact of baseline SRF status on treatment outcomes with IAI was demonstrat
42 ts of IAI over laser, regardless of baseline SRF status.
43 rs for BCVA change at month 12 were baseline SRF (P = 0.05), PVD (P = 0.03), IRC (P = 0.05), treatmen
44 f 100 was greater for patients with baseline SRF versus those without (nominal P < 0.001, for interac
45 f IAI was observed in patients with baseline SRF versus those without; however, no meaningful impact
46  letters, respectively, (those with baseline SRF) and +10.3, +10.6, and +2.5 letters, respectively, (
47 +10.9, and -2.3 letters (those with baseline SRF) and +10.6, +10.0, and +2.7 letters (those without).
48 and 8.9%, respectively, (those with baseline SRF) and 30.9%, 29.1%, and 8.2%, respectively, (those wi
49 nd 12.9%, respectively, (those with baseline SRF) and 33.3%, 30.5%, and 12.5%, respectively, (those w
50    No robust associations were found between SRF and baseline BCVA (R2 = 0.06; P = .14) or BCVA chang
51  resolution of all retinal fluid (i.e., both SRF and intra-retinal fluid [IRF]) in patients with nAMD
52                         The presence of both SRF and PVD at baseline was associated with similar BCVA
53                        In patients with both SRF and PVD at baseline, similar BCVA outcomes were obse
54     Stimulation also enhanced the long bound SRF fraction at specific timepoints (20 and 60 min) in b
55 atest and most rapid resolution, followed by SRF and PED the least.
56  cardiac myocyte hypertrophy is modulated by SRF (serum response factor) phosphorylation, constitutin
57 duced by TGF-beta1 and MYOCD, and reduced by SRF deficiency in VSMCs.
58 nce to BRAF inhibitors, which is reversed by SRF/MRTF inhibitors.
59  the binding to its transcriptional cofactor SRF.
60  follow-up; all recurrent cases had complete SRF resolution after another PDT treatment.
61 ific role of the transcription factors CREB, SRF, and MEF2 in the depression and potentiation compone
62   In this study, we tested the role of CREB, SRF, and MEF2 in ocular dominance plasticity (ODP), a pa
63 to block the transcription function of CREB, SRF, and MEF2 in the visual cortex, and measured visuall
64                          We found that CREB, SRF, and MEF2 are all required for ODP, but have differe
65 novel MRTF/SRF inhibitor, markedly decreased SRF reporter gene activity and showed a greater inhibito
66 logous mouse SRF enhancer revealed decreased SRF expression in aorta and heart tissues.
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 Forty-six (90%) study participants developed SRF during the study period, with 9 (20%) experiencing s
71 kness of 39 study participants who developed SRF at the first visit increased from 280 (26) microm at
72 e, we demonstrate that the single Drosophila SRF ortholog, termed Blistered (Bs), is expressed in all
73 tiple cancer-related pathways including Elk1/SRF, AP1, NFkappaB and STAT, and reduces EGFR expression
74 educed myogenically active SRF, but enhanced SRF activity on target genes involved in proliferation.
75                     This results in enhanced SRF-dependent transcriptional activity and promotes tumo
76                              On examination, SRF appeared as elevated, yellow-orange pockets in the f
77 genes controlled by the transcription factor SRF, and overexpression of SRF rescues impaired chromoso
78 s through their partner transcription factor SRF.
79 ial role of myocardin/serum response factor (SRF) and Notch signaling in the transcriptional regulati
80  transcription factor serum response factor (SRF) and set the chromatin state of SRF-targeted genes e
81 factor A (MRTF-A) and serum response factor (SRF) and the other using the transcriptional coactivator
82 al remodelling on the serum response factor (SRF) co-factors Megakaryoblastic Leukemia-1 and -2 (MKL1
83                       Serum response factor (SRF) has an established role in controlling actin homeos
84                       Serum response factor (SRF) mediates immediate early gene (IEG) and cytoskeleta
85 tion of Rho-dependent serum-response factor (SRF) signaling.
86 lators and to promote serum response factor (SRF) signalling has raised the question of whether MRL p
87  transcription factor serum response factor (SRF) to activate mitogen-induced transcription.
88 dering the binding of serum response factor (SRF) to the proximal CArG box.
89 teraction between the serum response factor (SRF) transcription factor and one of its principal co-ac
90                       Serum response factor (SRF) was predicted as a transcriptional regulator drivin
91 s where they activate serum response factor (SRF), a regulator of actin and other cytoskeletal protei
92 cific co-activator of serum response factor (SRF), is increased in DCM porcine and patient cardiac ti
93 )-A, a coactivator of serum-response factor (SRF), known to promote fibroblast-like behaviors in many
94 gen-responsiveness to serum response factor (SRF), which controls aggressive CaP behavior and is main
95 gnificantly inhibited serum response factor (SRF)-dependent reporter gene (SRE-LUC) activity and mRNA
96 ) are coactivators of serum response factor (SRF)-mediated gene expression.
97 lastic leukemia (MKL)/serum-response factor (SRF)-mediated gene transcription is a highly conserved m
98 ription factor (MRTF)/serum response factor (SRF)-mediated gene transcription with good potency (IC(5
99 merization results in serum response factor (SRF)-mediated transcription through nuclear retention of
100 r TGF-beta1 and MYOCD/serum response factor (SRF)-regulated TSPANs in VSMC by using RNA-seq analyses
101  transcription factor serum response factor (SRF).
102 lates the activity of serum response factor (SRF).
103  binding sites of the serum-response factor (SRF).
104 transcription factor, serum response factor (SRF); however, the mechanisms dynamically regulating SMC
105 CREB (cAMP response element binding factor), SRF (serum response factor), and MEF2 (myocyte enhancer
106                                      So far, SRF transcriptional dynamics have not been investigated
107  incomplete resolution of sub-retinal fluid (SRF) </=200 mum at the foveal centre relative to a T&E p
108 as intra-retinal (IRF) or sub-retinal fluid (SRF) were evident on SD-OCT, followed by a gradual exten
109 CRT), height of subfoveal sub-retinal fluid (SRF), central choroid thickness (CCT), mean number of PD
110 ion showed the presence of subretinal fluid (SRF) and pachychoroid supporting the diagnosis of CSCR.
111 ch as the baseline area of subretinal fluid (SRF) as measured on ultrasound images in the third cohor
112 uity (BCVA), resolution of subretinal fluid (SRF) demonstrated by optical coherence tomography (OCT),
113 cs, presence of persistent subretinal fluid (SRF) or intraretinal fluid (IRF), and on-study events (a
114                    On OCT, subretinal fluid (SRF) was detected in 77% of CM patients and 60% of UM pa
115 al cystoid fluid (IRC) and subretinal fluid (SRF) was developed.
116  was present in 86.4%, and subretinal fluid (SRF) was present in 76.3%.
117 tinal fluid (IRF), 38% had subretinal fluid (SRF), 36% had subretinal pigment epithelium (RPE) fluid,
118  intraretinal fluid (IRF), subretinal fluid (SRF), and pigment epithelial detachment (PED) were deter
119 intraretinal cysts (IRCs), subretinal fluid (SRF), and pigment epithelial detachment (PED), presentin
120 tinal cystoid fluid (IRC), subretinal fluid (SRF), and pigment epithelial detachment (PED).
121 id material and persistent subretinal fluid (SRF), but also a RPE-independent visual cycle for cone p
122 tinal cystoid fluid (IRC), subretinal fluid (SRF), pigment epithelial detachment, and vitreomacular i
123  intraretinal fluid (IRF), subretinal fluid (SRF), sub-retinal pigment epithelium (RPE) fluid, and su
124  intraretinal fluid (IRF), subretinal fluid (SRF), subretinal hyperreflective material (SHRM), retina
125 t of intraretinal fluid or subretinal fluid (SRF); (4) presence, location, and amount of hyperreflect
126 literature, respectively): subretinal fluid (SRF; 30,9), chorioretinal folds (30,68), macular exudate
127 traretinal fluid [IRF], or subretinal fluid [SRF]) versus aflibercept (q8-week).
128  was 148 mum (99) for retina, 5 mum (21) for SRF, 125 mum (107) for subretinal tissue complex, 11 mum
129  coefficient of 0.90 for IRC and of 0.96 for SRF.
130 F only (relaxed arm: SRF tolerant except for SRF >200 mum at the foveal center) before extending trea
131 Thus, competition between TCFs and MRTFs for SRF determines the balance between antagonistic prolifer
132  ubiquitin proteasome system responsible for SRF stabilization and KLF4 repression and is required fo
133 s uncover an evolutionarily ancient role for SRF in regulating muscle actin expression, and provide a
134 the most accurate CT volumetry technique for SRF and the prediction of postdonation kidney function (
135 t of the enhanced secondary radiation force (SRF).
136 l contours using a structured random forest (SRF) contour detector with fast parallel prediction and
137      In 1965, the Sugar Research Foundation (SRF) secretly funded a review in the New England Journal
138 h MYOCD to competitively displace MYOCD from SRF.
139 ters commonly evaluate split renal function (SRF) with Tc-99m-mercapto-acetyltriglycin (MAG3) scintig
140 of analytical Spontaneous Release Functions (SRF) whose parameters may be randomly sampled from appro
141                                 Furthermore, SRF delivered by CAGE exhibited significantly different
142                                 Furthermore, SRF downregulation in diploid hPSCs induces replication
143  Only 2 participants (4%) were found to have SRF at the last study visit after discontinuation of tre
144 transcription factor depletion in the heart (SRF(HKO)) or of cardiac hypertrophy triggered by transve
145       Eyes from Black individuals had higher SRF, RPE, and serous PED volumes compared with other eth
146 ctin expression, and provide a model for how SRF might function to sustain muscle fate downstream of
147                                     However, SRF alone is not sufficient for regulating smooth muscle
148                       These results identify SRF and its MRTF cofactors as major transcriptional regu
149 tor of therapy resistance, while identifying SRF/MRTF as a potential therapeutic target.
150 inding supports previous reports implicating SRF and MEF2 in long-term depression (required for Dc-OD
151 ds achieving higher acceleration gradient in SRF cavity accelerator beyond the theoretical limit of b
152 pression of a wide range of genes, including SRF itself and many important structural and regulatory
153 anchoring protein beta), such that increased SRF phosphorylation activates AP-1 (activator protein-1)
154  binding, indicating a cell type-independent SRF property.
155                   Androgen treatment induced SRF-PKN1 interaction, and PKN1 knockdown or overexpressi
156                             Using integrated SRF ChIP-seq and Hi-C data, we identified over 700 TCF-d
157 utilized Nb ellipsoid to simulate an inverse SRF cavity and investigate the effect of coating it with
158  baseline, the proportions of eyes with IRC, SRF, and PED were balanced between the aflibercept and r
159 the action of MKL that is independent of its SRF-related activity.
160  agreement between CT volumetry SRF and MAG3-SRF (bias, 95% limits of agreement: ROI vs MAG3 0.4%, -7
161  at day 3 was r = 0.85 to 0.88, between MAG3-SRF and PDKF (r = 0.84).
162 ic SRF was determined and compared with MAG3-SRF, postoperation donor kidney function, and graft func
163  the notion that modulation of the mAKAPbeta-SRF signalosome could be a new therapeutic approach for
164 to function in a similar manner to mammalian SRF in muscle maturation.
165 omatin immunoprecipitation-sequencing to map SRF-binding sites in human coronary artery SMC, showing
166                 Our findings show that mDia2-SRF-beta2 integrin signaling is critical for HSPC lodgme
167 ations associated with IIH include CNVM, ME, SRF, VSR, chorioretinal folds, choroidal infarction, and
168           Mechanistically, PI3K/Akt-mediated SRF activation promotes nuclear translocation and bindin
169 ey cardiac TFs (GATA4, NKX2-5, MEF2A, MEF2C, SRF, TBX5, TEAD1) to sensitively and reproducibly map th
170 in a possible feedback loop of the actin/MKL/SRF signaling circuit.
171  study, we examined the possible role of MKL/SRF in the context of regulation of profilin (Pfn), a ma
172 his conserved motif in the orthologous mouse SRF enhancer revealed decreased SRF expression in aorta
173                                Thus, the MRF-SRF and YAP-TEAD pathways interact indirectly through th
174 yocardin-related transcription factor (MRTF) SRF cofactor family.
175                             We compared MRTF-SRF and YAP-TEAD target gene sets and identified genes d
176 lore the impact of the actin-controlled MRTF-SRF (myocardin-related transcription factor-serum respon
177           In CAFs, expression of direct MRTF-SRF genomic targets is also dependent on YAP-TEAD activi
178          We used vav-iCre to inactivate MRTF-SRF signaling early during hematopoietic development.
179 et gene expression is also dependent on MRTF-SRF signaling.
180                                Both the MRTF-SRF and the YAP-TEAD transcriptional regulatory networks
181                        We show that the MRTF-SRF pathway is activated in cancer-associated fibroblast
182  that YAP-TEAD activity is sensitive to MRTF-SRF-induced contractility, while MRTF-SRF signaling resp
183 o MRTF-SRF-induced contractility, while MRTF-SRF signaling responds to YAP-TEAD-dependent TGFbeta sig
184 y different WH2 domains correlates with MRTF-SRF activation.
185 scription factor/Serum response factor (MRTF/SRF) pathway plays a key role in fibroblast activation a
186 scription factor/serum response factor (MRTF/SRF) pathway represents a promising therapeutic target t
187                     CCG-222740, a novel MRTF/SRF inhibitor, markedly decreased SRF reporter gene acti
188 ts of new pharmacological inhibitors of MRTF/SRF signalling in a preclinical model of fibrosis.
189          We conclude that inhibitors of MRTF/SRF-regulated gene transcription such as CCG-222740, pot
190 d showed a greater inhibitory effect on MRTF/SRF target genes than the previously described MRTF-A in
191 ed" treatment (resolution of IRF or >200 mum SRF only at foveal centre).
192 ls of HRT2 concomitantly disrupted myocardin/SRF and Notch transcription complex formation at respect
193 agged1 ligand- and Notch1-enhanced myocardin/SRF complex formation at the promoter CArG element.
194 ta indicate that TCF21 antagonizes the MYOCD-SRF pathway through multiple mechanisms, further establi
195 identified the first VSMC-enriched and MYOCD/SRF and TGF-beta1/SMAD-dependent TSPAN family member, wh
196 2 is regulated by 2 parallel pathways, MYOCD/SRF and TGF-beta1/SMAD, via distinct binding elements wi
197 cription by binding to SRF to form the MYOCD/SRF/CArG box triad (known as the ternary complex).
198  on OCT had better mean VA than eyes with no SRF (72.8 vs. 66.6 letters; P = 0.006).
199 o DeltaNT in a distinct assay (activation of SRF luciferase).
200 es observed in transcriptional activation of SRF or TEAD.
201 ndingly, TRIM32 attenuated the activation of SRF signaling and hypertrophy due to dysbindin, whereas
202               Patients with a larger area of SRF on ultrasound showed more RD progression from baseli
203 nce, and the presence and characteristics of SRF noted on optical coherence tomography.
204                             A combination of SRF, GATA6 and CRP2 required CSRP2BP for robust smooth m
205 ption factor/coactivator complex composed of SRF/Mkl1.
206  CAGE increased peak blood concentrations of SRF by 2.2-fold.
207                         The determination of SRF is conducted at a reading centre while the assessmen
208 PTEN interacts with the N-terminal domain of SRF and PTEN-SRF interaction promotes SRF binding to ess
209 ision and weak positive prognostic effect of SRF.
210 oth cell types, individual binding events of SRF molecules segregated into three chromatin residence
211 rate that IGF2BP1 promotes the expression of SRF in a conserved and N6-methyladenosine (m6A)-dependen
212 CaP patient-derived xenograft, expression of SRF target genes was maintained while AR target gene exp
213 K-regulated ternary complex factor family of SRF partner proteins.
214              A constitutively active form of SRF/Mkl1 was not sufficient to induce focal adhesion ass
215 icates cell shape is a stronger indicator of SRF and TEAD mechanosignaling pathways than coactivators
216                 The elimination half-life of SRF was also increased by 2-fold and the mean absorption
217 s in the nuclear subcellular localization of SRF and MAL.
218  37 of 46 (80%) individuals; the location of SRF accumulation varied.
219             The detection and measurement of SRF were also highly accurate with an AUC of 0.92 (range
220 ays and cofactors demonstrated modulation of SRF chromatin occupancy by actin signaling, MAP kinases,
221                            Overexpression of SRF or beta2 integrins rescues HSPC engraftment defects
222 nscription factor SRF, and overexpression of SRF rescues impaired chromosome condensation and segrega
223                              The presence of SRF did not lead to permanent ocular sequelae.
224                              The presence of SRF was common in study participants undergoing treatmen
225 ting the therapy, there was no recurrence of SRF.
226 eferentially affected androgen regulation of SRF over direct AR target genes.
227 ulated, respectively, androgen regulation of SRF target genes.
228  monthly until either complete resolution of SRF and intraretinal fluid (IRF; intensive arm: SRF into
229 isted on OCT in patients after resolution of SRF and papilledema.
230  half-time PDT showed complete resolution of SRF within 6 months after PDT, but 3 eyes that received
231  in the PDT group had complete resolution of SRF, while none of the HSML-treated patients had complet
232 , respectively, had a complete resolution of SRF.
233 -treated patients had complete resolution of SRF.
234 GE provided excellent apparent solubility of SRF tosylate (> 500 mg/mL).
235  factor (SRF) and set the chromatin state of SRF-targeted genes early growth response 1 (egr1) and c-
236 ta2 integrins are transcriptional targets of SRF.
237 y to ECM stiffness, and compare with that of SRF/MAL, which is another important regulator of differe
238                  A protocol to adjudicate on SRF has been established by the central reading centre a
239                            PKN1's effects on SRF relied on its kinase domain.
240 A via their respective DNA-binding partners (SRF and TEAD) and is therefore indirect, arising as a co
241 t Q8wks), and 52% (ranibizumab) of patients; SRF resolved in 75% (both aflibercept Q4wks/Q8wks) and 6
242 found in patient characteristics, persistent SRF or IRF, or on-study events to account for the observ
243 s that received half-dose PDT had persistent SRF before loss to follow-up at months 5, 7, and 8 (P =
244                cCSC patients with persistent SRF at the final visit of the PLACE trial were included.
245                      We highlight PGC1alpha, SRF and the MEF2 family as transcription factors that ma
246  technique for the evaluation of predonation SRF and allows a reliable prediction of donor's PDKF.
247                The difference of predonation SRF between preserved and donated kidney was the lowest
248 ain of SRF and PTEN-SRF interaction promotes SRF binding to essential promoter elements in SM-specifi
249 s with the N-terminal domain of SRF and PTEN-SRF interaction promotes SRF binding to essential promot
250 itch, namely mAKAPbeta signalosome-regulated SRF phosphorylation, that controls a transcriptional pro
251       Finally, we demonstrate that regulated SRF expression, in turn, is critical for the effects of
252 in IGF2BP1 and the transcriptional regulator SRF modulate gene expression in cancer.
253 tical coherence tomographic imaging revealed SRF beneath the interdigitation zone.
254 e was associated with lower volumes for RPE, SRF, NSR, and sPED; in second-treated eyes, older age wa
255  ranibizumab T&E protocol who tolerated some SRF achieved VA that is comparable, with fewer injection
256 l delivery of a hydrophobic drug, sorafenib (SRF).
257                      Time to first sustained SRF clearance seemed to be shorter in the IAI arms versu
258     We provide a study of single Halo-tagged SRF molecules in fibroblasts and primary neurons.
259                       Analysis of direct TCF-SRF target genes and chromatin modifiers confirmed this
260            Mechanistic studies revealed that SRF-CAGE solution spontaneously formed a self-assembled
261  driving immediate response, suggesting that SRF activity mirrors the build-up and release of sleep p
262                                          The SRF accurately reproduced the dynamics of SCRE and its d
263                                          The SRF pathway registers changes in G-actin levels, leading
264      The correlation coefficient between the SRF area at baseline and worst relative RD progression f
265 d a gene expression program initiated by the SRF/MRTF transcriptional pathway, which results in a mel
266   In conclusion, these findings identify the SRF/IGF2BP1-, miRNome- and m6A-dependent control of gene
267  TCF21, including at a novel enhancer in the SRF gene, and at the MYOCD gene promoter.
268 ro and in vivo induces the expression of the SRF (serum response factor), myocardin, and MRTFA (myoca
269 hese peaks correlated with activation of the SRF cofactors MRTF-A and MRTF-B (myocardin-related trans
270 ncer CArG box regulates transcription of the SRF gene, and mutation of this conserved motif in the or
271 by impairing the miRNA-directed decay of the SRF mRNA.
272     These data support a central role of the SRF/MRTF pathway in the pathobiology of lung fibrosis an
273 led to MRTF nuclear shuttling to promote the SRF transcriptional activity required for entosis.
274   In vitro genome editing indicated that the SRF enhancer CArG box regulates transcription of the SRF
275                        The majority of these SRF/IGF2BP1-enhanced genes, including PDLIM7 and FOXK1,
276 ated with ERM presence (P = 0.0045), thicker SRF (P = 0.0006), larger intraretinal cysts (P = 0.0015)
277 peting directly with the MRTFs for access to SRF.
278 MC-specific gene transcription by binding to SRF to form the MYOCD/SRF/CArG box triad (known as the t
279 (PKN1) transduces androgen-responsiveness to SRF.
280                     The results suggested to SRF that gut microbiota have a causal role in carbohydra
281           Furthermore, PM blebbing triggered SRF-mediated up-regulation of the metastasis-associated
282                                     In turn, SRF cooperated with MEF2 to sustain the expression of LM
283 , IGF2BP1 sustains the expression of various SRF-target genes.
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 nt with MEK inhibitors is not indicated when SRF is present.
288 bleb dynamics for cell-in-cell invasion when SRF is suppressed.
289 ecessary for both Dc-ODP and Pc-ODP, whereas SRF and MEF2 are only needed for Dc-ODP.
290  required for 2 patients (1 with VSR, 1 with SRF); others were treated with weight loss and acetazola
291           Among clinical patients, 2 (1 with SRF, 1 with CNVM) had distinctive retina-related VF defe
292 ent genes showing conserved association with SRF and IGF2BP1 expression indicate a poor overall survi
293                                    Eyes with SRF in the foveal center on OCT had better mean VA than
294             CSRP2BP directly interacted with SRF, CRP2 and myocardin.
295  transient, occurring in 9 participants with SRF (20%; 95% CI, 10%-33%).
296                      In the 26 patients with SRF, the fovea was affected in 85%.
297 nctioning as an indispensible regulator with SRF to maintain the differentiated SM phenotype.
298 tor for CRP2 that works synergistically with SRF and myocardin to regulate smooth muscle gene express
299  and FOXK1, show conserved upregulation with SRF and IGF2BP1 synthesis in cancer.
300 nt treatments compared with patients without SRF, without PVD, or without either who may require more

 
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