ライフサイエンスコーパス: RBF

1 RBF also responded to treatment with RPC-conditioned med

2 RBF and GFR response to acetylcholine was blunted in RVD

3 RBF associates with dE2F and dDP in vivo and is a stoich

4 RBF combines several of the structural features of pRB,

5 RBF correlated significantly between the two techniques

6 RBF modifies these effects by reducing E2F1/Sd interacti

7 RBF specifically repressed E2F-dependent transcription a

8 RBF was measured 60 and 150 minutes after the end of isc

9 RBF was phosphorylated by a cyclin E-associated kinase i

10 RBF, renal vascular resistance (RVR), GFR, and urine flo

11 RBF-280, a mutant form of RBF that has four putative cdk

12 between the two techniques (RBF(MD) = 0.96 . RBF(EB) mL/min; R = 0.77, P < .01).

13 udy also examined whether AngII would affect RBF in mice lacking AT1A receptors due to gene targeting

14 arboxyl-terminal 20-kDa fragment of alpha2M (RBF), which is capable of binding to both LRP and the si

15 tment (12 h after LPS injection) ameliorated RBF and RVR but did not restore GFR.

16 s-of-function cyclin E mutations enhanced an RBF overexpression phenotype, consistent with the idea t

17 l shift assays required the generation of an RBF-maltose fusion protein (RBF-MBP), which specifically

18 allows an a priori evaluation of whether an RBF(3)K reagent will likely engender "fast", "slow", or

19 luciferase reporter vector, together with an RBF expression vector construct, into steroid treated hu

20 We infer that dE2F and RBF function specifically in cell cycle control, and tha

21 L-NAME), and compared its effects on GFR and RBF with those of S-methylisothiourea (SMT), a selective

22 DNP, resulting in decreased UcGMPV, GFR, and RBF and increased distal FNaR.

23 Mean arterial pressure (MAP) and RBF were measured continuously, 18 h/d, in uninephrectom

24 tracted videointensity measured from MCE and RBF obtained from fluorescent microspheres were calculat

25 averaged 91 +/- 0.5 and 89 +/- 0.4 mmHg, and RBF averaged 8.0 +/- 0.1 and 7.8 +/- 0.1 ml/min in the c

26 uld improve renal function, oxygenation, and RBF in patients with atherosclerotic renal artery stenos

27 onths after infusion, cortical perfusion and RBF rose in the STK (151.8-185.5 ml/min, P=0.01); contra

28 otic kidney cortical/medullary perfusion and RBF were measured using contrast-enhanced multidetector

29 rtical and medullary volumes, perfusion, and RBF using multidetector computed tomography.

30 etween physiological fluctuations in RAP and RBF.

31 mbranes resulted in greater PD reduction and RBF, but there is a lack of high-quality comparative stu

32 These changes in RVR and RBF were associated with no significant change in renal

33 is element and is supershifted when the anti-RBF polyclonal antibody is added.

34 In each case, total arterial RBF and blood flow per unit of renal volume were calcula

35 by a Doppler flow wire in the renal artery), RBF and renal vascular resistance (RVR) were evaluated.

36 t analyses, and by competition EMSAs between RBF-MBP and the N-terminal domain.

37 iations, or 95% confidence interval) between RBF measurements obtained with the PAH-clearance hematoc

38 lature by modelling the relationship between RBF and oxygen.

39 We determined that the relationship between RBF and PaO2 can be modelled as a combination of hyperbo

40 reduced hippuran clearance (P < 0.003), but RBF was unchanged (P > 0.17).

41 ivia's overall diarrheal disease burden, but RBF resulted in an estimated health burden that is only

42 e that the repression of E2F target genes by RBF is necessary for the maintenance but not the initiat

43 t this hid enhancer is directly repressed by RBF through an E2F binding site.

44 and posterior to the second mitotic wave by RBF.

45 cycle progression via the well-characterized RBF/E2F pathway, but our understanding of how growth is

46 Consistently, RBF, a negative regulator of dE2F1, negates this synergy

47 By contrast, RBF-280 does not block activated Ras-induced cellular gr

48 f dE2F or overproduction of its corepressor, RBF, retarded cell proliferation.

49 e responses but did not prevent the cortical RBF decreases.

50 tively remove each component of the dE2F/dDP/RBF pathway, and we examined the genome-wide changes in

51 dvantage of the stream-lined Drosophila dE2F/RBF pathway, which has only two E2Fs (dE2F1 and dE2F2),

52 Instead, dE2F/RBF-mediated repression is exerted on genes that encode

53 xpectedly, there is a second program of dE2F/RBF-dependent transcription, in which dE2F2/RBF1or dE2F2

54 As a result, dE2F/RBF regulation is used to link gene expression with cell

55 We propose that dE2F/RBF complexes should not be viewed simply as a cell cycl

56 strategy for studying regulation of the dE2F/RBF pathway in vivo.

57 These genes are repressed by dE2F2/RBF and a recently identified RB-containing complex, dRE

58 First, dE2F2/RBF and dREAM/MMB employ histone deacetylase (HDAC) acti

59 ed for the stability of the repressive dE2F2/RBF complexes at their promoters during S phase.

60 identify suppressors that overcome the dE2F2/RBF-dependent proliferation block.

61 h NOS inhibitors increased MAP but decreased RBF, but only L-NAME reduced GFR and increased sodium ex

62 stration in these NLA-treated dogs decreased RBF (2.5+/-0.3 ml/min per g; n = 4) to a similar extent,

63 NLA treatment decreased RBF (5.3+/-0.3 to 3.6+/-0.2 ml/min per g) and sodium exc

64 When bound to avian genomic DNA, RBF generates saturable high-affinity binding sites for

65 the multisubunit protein complex Drosophila RBF, E2F, and Myb (dREAM) that contains homologs of the

66 vator in the generally repressive Drosophila RBF, E2F2, and Myb (dREAM)/Myb-MuvB complex.

67 plexes represent the predominant form of E2F/RBF repressor complexes in Drosophila.

68 E2F2, RBF, and Mip130/LIN-9 acted in opposition to Myb by repr

69 ne expression by Myb, Mip130/LIN-9, and E2F2-RBF in vivo, and also provide an explanation for the abi

70 RAB-27 potentially acts through its effector RBF-1 to promote soluble N-ethylmaleimide-sensitive fact

71 The receptor-binding factor (RBF) for the avian oviduct progesterone (Pg) receptor (P

72 Steroid receptor binding factor (RBF) was originally isolated from avian oviduct nuclear

73 ing (BOP) reduction, radiographic bone fill (RBF), and mucosal recession.

74 -4.2 and +3.5) during riverbank filtration (RBF) at the river Thur was studied using both spatiotemp

75 interventions, such as riverbank filtration (RBF), are used in developing countries to treat irrigati

76 d in terms of the Richards-Baker Flashiness (RBF) index).

77 al artery stenosis reduces renal blood flow (RBF) and amplifies stenotic kidney hypoxia.

78 filtration rate (GFR), and renal blood flow (RBF) and decreased distal fractional sodium reabsorption

79 ular disease (RVD) reduces renal blood flow (RBF) and GFR and accelerates poststenotic kidney (STK) t

80 We measured single-kidney blood flow (RBF) and GFR and established the degree of renal damage

81 ributes to the decrease in renal blood flow (RBF) and GFR observed during LPS-induced sepsis was test

82 Basal renal blood flow (RBF) and glomerular filtration rate (GFR) were similarly

83 Retinal blood flow (RBF) and mean circulation time (MCT) were evaluated by v

84 ) may mediate decreases of renal blood flow (RBF) and/or GFR associated with LPS-induced sepsis.

85 ed dogs (n = 9) to examine renal blood flow (RBF) autoregulatory efficiency before and after saturati

86 feasibility of determining renal blood flow (RBF) by using a technique based on intravenous administr

87 e and the TGF mechanism in renal blood flow (RBF) control at the very earliest stages of diabetes.

88 ssure (MABP), no change in renal blood flow (RBF) due to an increase in renal vascular conductance (R

89 fter infusion of AngII and renal blood flow (RBF) fell by 3.3 ml min(-1) .

90 In vivo, PGI2 increased retinal blood flow (RBF) in control and diabetic animals.

91 , mediating increases in retinal blood flow (RBF) in response to several autoregulatory stimuli.

92 Retinal blood flow (RBF) increases in response to a reduction in oxygen (hyp

93 Renal blood flow (RBF) is often reduced in patients with chronic CHF and m

94 This rat renal blood flow (RBF) study quantified the impact of nitric oxide synthas

95 n an immediate increase in renal blood flow (RBF) to the remnant kidney, followed by compensatory ren

96 Retinal blood flow (RBF) was measured in rats to test the hypotheses that hy

97 Renal blood flow (RBF) was measured using an ultrasonic transit-time flowm

98 Regional blood flow (RBF) was measured with fluorescent microspheres at basel

99 a [ET-1] increased 66% and renal blood flow (RBF) was reduced by 38% compared with baseline.

100 dynamic characteristics of renal blood flow (RBF) was studied in conscious dogs by testing the respon

101 Hippuran clearance and renal blood flow (RBF) were measured twice, before and after treatment wit

102 in mean arterial pressure, renal blood flow (RBF), and renal capillary perfusion at 4 hours, which we

103 s in the autoregulation of renal blood flow (RBF), but the underlying mechanisms are unknown.

104 Renal blood flow (RBF), mean arterial pressure (MAP), and heart rate (HR)

105 trol decreases in cortical renal blood flow (RBF), measured with laser Doppler flowmetry, were 58+/-9

106 t arterial pressure (ABP), renal blood flow (RBF), renal vascular conductance (RVC), mean right atria

107 circulation time (RCT), retinal blood flow (RBF), treatment-emergent adverse events, and other safet

108 filtration rate (GFR) and renal blood flow (RBF).

109 filtration rate (GFR), and renal blood flow (RBF).

110 = +18 to 26 mmHg), reduced renal blood flow (RBF, Delta = -1.8 to 2.9 ml min(-1)), increased renal va

111 the gadolinium chelate perfusion method for RBF measurement and discusses potential applications.

112 a that the SWI/SNF proteins are required for RBF-mediated repression and suggest that a requirement f

113 s of the full-length amino acid sequence for RBF predicts a DNA-binding motif involving a beta-sheet

114 s a solution, we present Random Bits Forest (RBF), a classification and regression algorithm that int

115 ith a recombinant receptor binding fragment (RBF) from rat alpha1M and murine macrophages demonstrate

116 ned and expressed receptor binding fragment (RBF) to the recently described alpha2M signaling recepto

117 Radial Basis Function (RBF) outperformed polynomial and linear kernel functions

118 nd dDP) as bait, we identified a novel gene, RBF.

119 Total and hemispheric RBF, retinal nerve fiber layer (RNFL), and ganglion cell

120 raction tests with a DROSOPHILA: Rb homolog, RBF, indicate that CycD-Cdk4 can counteract the cell cyc

121 retion (P < 0.001) without altering MAP, HR, RBF, or CrCl.

122 ozin (0.9 mg kg(-1)) did not change MAP, HR, RBF, or creatinine clearance (CrCl) in SD rats (n = 7).

123 xtent, compared with ATP, but did not impair RBF autoregulation.

124 pression may explain the biphasic changes in RBF observed in diabetes.

125 No changes in RBF occurred in medical treatment only subjects.

126 used to estimate stimulus-induced changes in RBF.

127 ynitrite generation, reversed the decline in RBF, capillary perfusion, and glomerular filtration rate

128 nt capillary permeability or the decrease in RBF and capillary perfusion, which suggests that these e

129 rectomized rats caused a greater decrease in RBF on days 2 and 7 compared with controls, whereas by 1

130 reated dogs resulted in further decreases in RBF (2.8+/-0.2 ml/min per g), GFR (0.58+/-0.05 ml/min pe

131 -9 mmHg), leading to associated decreases in RBF (from 5.5+/-0.2 to 4.6+/-0.4 ml/min x g) and sodium

132 The decreases in RBF and GFR after LPS were attenuated in TP-KO mice vers

133 tan chronically still exhibited decreases in RBF in response to a bolus dose of Ang II, further studi

134 Furthermore, the early drop in RBF during the initial weeks after inducing diabetes in

135 , p = 0.0005), which led to a marked fall in RBF in every patient (mean values 376 +/- 36 to 146 +/-

136 ton resonance parameter () of the R group in RBF(3)K, allows an a priori evaluation of whether an RBF

137 ted fibrogenic activity, and improvements in RBF and GFR greater than those observed with placebo, EL

138 94% +/- 6% (P < 0.05; n = 5) the increase in RBF (94% +/- 7%; P < 0.05) elicited by the intravitreal

139 ter nephrectomy, there was a 49% increase in RBF (corrected per gram of kidney weight), a 25% increas

140 ad no effect on the 103% +/- 12% increase in RBF (P < 0.05; n = 5) induced by the nitric oxide donor

141 Whether the increase in RBF after unilateral nephrectomy is mediated by nitric o

142 ay play an important role in the increase in RBF and GFR in diabetes.

143 caused a marked and progressive increase in RBF in the diabetic rats, averaging 10 +/- 6% above cont

144 d before nephrectomy blocked the increase in RBF seen at 2 and 7 d and retarded the renal hypertrophy

145 es in rats, as well as the later increase in RBF, both correlated with levels of retinal PSF.

146 ethyl ester (L-NAME) blocked the increase in RBF.

147 ressure, there were significant increases in RBF (26+/-11%) and urine flow (43+/-19%) and proportiona

148 Hg), and there were significant increases in RBF (from 5.4+/-0.2 to 6.8+/-0.4 ml/min x g) and decreas

149 potension, elicited substantial increases in RBF and proportionally much greater increases in sodium

150 These very rapid increases in RBF and transfer function gain suggest that autoregulati

151 ectomy, immediate and sustained increases in RBF are mediated at least in part by NO.

152 In addition, no significant increases in RBF could be elicited by 2.5 to 25 nmol 8-bromo-cAMP (n

153 adenosine caused dose-dependent increases in RBF of 79% +/- 4% (P < 0.05; n = 5) and 323% +/- 61% (P

154 espectively 2.9 and 5.5 log10 units lower in RBF-treated water than in the river water.

155 ed mutation of Lys-1374 (human numbering) in RBF to Arg or Ile residues almost completely abolishes s

156 1, -4A2 and -4A3 attenuated the reduction in RBF and the consequent increase in RVR by L-NAME with a

157 tion that leads to an important reduction in RBF.

158 ent, dose-dependent, selective reductions in RBF in AT1A knockout mice as well as wild-type mice.

159 rength and speed of the myogenic response in RBF but not hindlimb autoregulation, an action dependent

160 e multisubunit protein complex that includes RBF, repressor E2Fs and Myb, in what was termed the dREA

161 attenuated postprocedural hypoxia, increased RBF, and improved kidney function in this pilot trial.

162 The increased RBF was diverted to the medulla.

163 Although VEGF increases RBF and reduces MCT, HGF did not affect either.

164 53D) was blocked by the cell cycle inhibitor RBF, and required normal activity of the growth effector

165 With prior IPC, RBF after 30 and 60 minutes of ischemia was 21+/-1 and 1

166 Control (0 minutes' ischemia) RBF was 22+/-3 ml/100 g per minute (mean +/- SE).

167 er 5, 30, 60, 75, or 90 minutes of ischemia, RBF was 15+/-2 (NS), 11+/-1, 8+/-2, 8+/-1, and 10+/-1 ml

168 er 5, 30, 60, 75, or 90 minutes of ischemia, RBF was 18+/-3 (NS), 13+/-1, 12+/-3, 12+/-2, and 11+/-1

169 -185.5 ml/min, P=0.01); contralateral kidney RBF increased (212.7-271.8 ml/min, P=0.01); and STK rena

170 Stenotic kidney RBF rose (202+/-29-262+/-115 mL/min; P=0.04) 3 months af

171 governing simple on-farm interventions like RBF can be intermediary solutions for communities in urb

172 dotoxemia is beneficial because it maintains RBF and GFR.

173 vasopressin produced greater changes in MAP, RBF, and RVR in septic mice than in controls.

174 LPS-injected mice displayed lower MAP, RBF, and GFR than controls (P < 0.001).

175 Mean RBF was reduced in the abnormal hemisphere compared with

176 In the 5 healthy subjects, mean RBF was 3.4 +/- 0.4 mL/min/g.

177 idney on each slice and pooled to yield mean RBF.

178 -circle scanning pattern was used to measure RBF.

179 ard genetic screen for mutants mislocalizing RBF-1 rabphilin, a RAB-27 effector.

180 , a 12% increase in ABP, no change in mRAtP, RBF or GFR, but increases of 75 and 100% in urine flow a

181 ith the idea that the biological activity of RBF is negatively regulated by endogenous cyclin E.

182 to the overall short-term autoregulation of RBF.

183 PR in the c-myc gene promoter is composed of RBF dimers bound to a specific single-stranded DNA eleme

184 reprogramming and that these consequences of RBF/RB function are present in both flies and human cell

185 The dimers of RBF are generated by C-terminal leucine zipper and the D

186 Only the N-terminal domain of RBF binds the RBF DNA element as demonstrated by southwe

187 ometric analysis of the C-terminal domain of RBF demonstrates its potential to form noncovalent prote

188 pment can enhance or suppress the effects of RBF and E2F on development of the eye.

189 teract the cell cycle suppressive effects of RBF, but that its growth promoting activity is mediated

190 enosine receptor blockade for enhancement of RBF and improvement of renal function in patients with c

191 Expression of RBF-280 in the developing eye revealed that RBF-280 does

192 RBF-280, a mutant form of RBF that has four putative cdk phosphorylation sites mut

193 te that most, if not all, of the function of RBF during development is mediated through E2F.

194 cating that this differentiation function of RBF is mediated by its regulation of dE2F1 activity.

195 uce quantitative maps (parametric images) of RBF.

196 ethods were employed to assess the impact of RBF on consumer health burdens for Giardia, Cryptosporid

197 In addition, there was marked impairment of RBF autoregulatory efficiency during ATP infusion.

198 ctivation and synergize with inactivation of RBF, suggesting that they may act in parallel to dE2F.

199 Interestingly, reducing the level of RBF restored the normal pattern of cell proliferation in

200 Parametric mapping of RBF with PET and H(2)(15)O provides a straightforward, n

201 ninvasive method for quantitative mapping of RBF, which may prove useful in research applications and

202 give the promise of clinical measurements of RBF.

203 The results indicate that the mechanisms of RBF regulation at these two types of E2F targets are dif

204 amp led to a dose-dependent normalization of RBF and renal vascular resistance within 2 h of cross-cl

205 n-sensitive site is predominantly outside of RBF.

206 The phenotype of RBF-deficient embryos suggests that rbf has a function t

207 6-6.3 h, demonstrated the great potential of RBF systems to degrade organic micropollutants and simul

208 The properties of RBF suggest that it is the intermediary factor that was

209 tion activator rather than a co-repressor of RBF during Drosophila development.

210 Characterization of the role of RBF in Cyclin D/Cdk4-mediated cellular growth showed tha

211 erated and analyzed to determine the role of RBF in this process.

212 We have examined the role of RBF, the Drosophila RB family homolog, in cell cycle pro

213 e may be differential effects of diabetes on RBF versus nonrenal BF control.

214 (0.92+/-0.04 to 0.90+/-0.06 ml/min per g) or RBF autoregulatory efficiency.

215 drolysis of potassium organotrifluoroborate (RBF(3)K) reagents to the corresponding boronic acids (RB

216 ressure (MAP), and increased cardiac output, RBF, and medullary NO content.

217 F protein to identify a minimal 54-base pair RBF-binding element in the matrix-associated region (MAR

218 TB endothelin antagonist L-754,142 preserves RBF and sodium reabsorption, leading to a significant im

219 Before treatment with probenecid, RBF was linearly related to hippuran clearance (r(2) = 0

220 cle regulatory pathways (the Rb-like protein RBF and the E2F transcription factor complex components

221 generation of an RBF-maltose fusion protein (RBF-MBP), which specifically binds this element and is s

222 omologs of the RB and E2F family of proteins RBF and dE2F1 have been identified.

223 f phenylephrine did not significantly reduce RBF or renal oxygen delivery.

224 Reduced RBF and RNFL and GCC loss also are observed in the perim

225 Reduced RBF is associated with thinner RNFL and GCC in the corre

226 The cause of reduced RBF is multifactorial and involves systemic as well as l

227 uch responsiveness may contribute to reduced RBF and GFR during endotoxemia.

228 Discontinuation of ATP infusion restored RBF autoregulatory efficiency.

229 ncrease in renal vascular conductance (RVC = RBF/MABP) and falls in urine flow and absolute sodium ex

230 , Losartan induced an increase in basal RVC, RBF, urine flow and UNaV whilst hypoxia induced falls in

231 ing in complex solvolytic profiles with some RBF(3)K reagents.

232 Stenotic RBF was reduced compared with RBF of contralateral kidne

233 For each subject, RBF was measured with a standard technique of p-aminohip

234 Compared with healthy control subjects, RBF was significantly decreased in patients with renal d

235 Classification methods such as SVM, RBF Neural Nets, MLP Neural Nets, Bayesian, Decision Tre

236 f the classification methods including; SVM, RBF Neural Nets, MLP Neural Nets, Bayesian, Decision Tre

237 ed significantly between the two techniques (RBF(MD) = 0.96 . RBF(EB) mL/min; R = 0.77, P < .01).

238 of activated Ras to induce growth, and that RBF may have a role in regulating growth in the prolifer

239 We concluded that RBF compensated for decreases in arterial oxygen content

240 In addition, we demonstrate that RBF-1 (rabphilin) is an effector of RAB-27.

241 These findings indicate that RBF plays a critical role in the regulation of cell prol

242 R2, two E2F-regulated genes, indicating that RBF is required for their transcriptional repression.

243 RBF-280 in the developing eye revealed that RBF-280 does not inhibit G1/S transition in the second m

244 , and the results presented here showed that RBF is required at multiple stages of development.

245 D/Cdk4-mediated cellular growth showed that RBF-280 blocks Cyclin D/Cdk4 induced cellular growth in

246 Recent studies have shown that RBF binds to a 54 bp element in the 5'-flanking region o

247 vine) Machine Learning Repository shows that RBF outperforms other popular methods in both accuracy a

248 90 +/- 3 mmHg), an increase in RVC such that RBF was unchanged, and falls in glomerular filtration ra

249 These observations suggest that RBF has additional functions besides dE2F1 binding that

250 er treatment with probenecid, to verify that RBF is not affected.

251 The RBF (19.3 +/- 8.4 mul/minute), RNFL (103.7 +/- 20.6 mum)

252 The RBF was correlated with RNFL (r = 0.41; P = 0.02) and GC

253 The RBF was derived from the recorded Doppler frequency shif

254 The RBF was similar in both groups, averaging 7 ml/min per g

255 the E2F2 transcriptional repressor, and the RBF and Mip130/LIN-9 tumor suppressor proteins reside in

256 Only the N-terminal domain of RBF binds the RBF DNA element as demonstrated by southwestern blot ana

257 fection of this MAR sequence, containing the RBF element and cloned into a luciferase reporter vector

258 h flank an intervening domain containing the RBF element.

259 In contrast, the RBF and RVR responses to angiotensin II, NE, or L-NAME w

260 atous eyes with single-hemifield damage, the RBF is significantly reduced in the hemisphere associate

261 clear matrix-like attachment sites flank the RBF element.

262 (a)(u)du - k integral C(u)du, where F is the RBF, k is the tissue-to-blood clearance rate, C is the P

263 ons containing only the parent vector of the RBF expression construct.

264 priate gearing of the hydrolysis rate of the RBF(3)K reagent with the rate of catalytic turnover.

265 in/nuclear matrix structure, composed of the RBF-DNA element complex which is flanked by nuclear matr

266 ears to regulate growth independently of the RBF/E2f pathway.

267 e treatment are used to demonstrate that the RBF-maltose binding protei (MBP) fusion protein binds to

268 of transcription, dependent on E2F2 and the RBFs.

269 We conclude that Cx40 contributes to RBF autoregulation by transducing TGF-mediated signals t

270 The total RBF (34.6+/-12.2 mul/minute) and venous cross-sectional

271 internalization and degradation of wild-type RBF and K1374R; however, internalization and degradation

272 signal transduction as compared to wild-type RBF.

273 The weaker RBF effects are most likely due to the absence of the AT

274 was reduced to 85 mmHg (P < 0.001), as were RBF (5.0 versus 9.3 ml/min per g kidney wt; P < 0.001) a

275 vers a previously unknown mechanism in which RBF and E2F1 modify Hippo signaling responses to modulat

276 western blot and DNA gel shift analyses with RBF protein to identify a minimal 54-base pair RBF-bindi

277 dE2F1 that disrupts dE2F1's association with RBF [the Drosophila retinoblastoma protein (Rb) homolog]

278 form of de2f1 that disrupts the binding with RBF but retains the transcription activation function do

279 Stenotic RBF was reduced compared with RBF of contralateral kidneys (225.2 mL/min vs 348 mL/min

280 Receptor-associated protein competes with RBF for binding to the lower but not the higher affinity

281 ntensity ratio significantly correlated with RBF data (r=0.79; p < 0.0001).

282 Similar results were observed with RBF.

283 The WM RBF was 2.1 mm for groups 3 and 4.

284 Embryos lacking both maternal and zygotic RBF products show constitutive expression of PCNA and RN