ライフサイエンスコーパス: ANF

1 ANF alone had no effect but inhibited PE-induced increas

2 ANF binding to the recombinant protein was chloride conc

3 ANF binding was measured using the purified recombinant

4 ANF binds in a distinctly different orientation in P450

5 ANF forms spontaneously in solutions of polymer actin co

6 ANF increases the rates of formation for NR metabolites

7 ANF induced a rapid increase in ERK phosphorylation and

8 ANF induced minimal phosphorylation of JNK or p38, indic

9 ANF is one of the earliest markers of cardiac differenti

10 ANF reacts with antibodies to both the N- and C-terminal

11 ANF spike trains therefore provide a window into the ope

12 ANF treatment caused MEK phosphorylation and activation

13 ANF-induced activation of ERK was mimicked by cGMP analo

14 ANF-induced ERK phosphorylation was eliminated by PD0980

15 ANF-induced extracellular signal-regulated protein kinas

16 ANF-RGC is the prototype membrane guanylate cyclase, bot

17 ANFs displayed KV7.2 and KV7.3 at heminodes, nodes, inte

18 ANFs from successfully lesioned animals exhibited signif

19 kably, each IHC is the sole partner of 10-30 ANFs with a range of spontaneous firing rates (SRs).

20 ncreases in CSA, but it completely abolished ANF-induced inhibition of PE-induced increases.

21 ection assays indicate that Csx can activate ANF reporter gene expression to the same extent that GAT

22 roles for JNK and c-Jun in calcium-activated ANF expression.

23 n of Csx and GATA4 synergistically activates ANF reporter gene expression.

24 cumulation of GATA4, whereas beta-adrenergic ANF transcription was suppressed by dominant negative GA

25 4 plays an important role in beta-adrenergic ANF transcription.

26 e the third individual had approximately all ANF-related ancestry.

27 The transcriptional activity of an ANF promoter-reporter in rat neonatal ventricular myocyt

28 II (alpha, deltaB, and deltaC) along with an ANF promoter/luciferase reporter gene.

29 vator of SRF on both cardiac alpha-actin and ANF promoters.

30 es mediate betaAR-induced Akt activation and ANF transcription in cardiac myocytes.

31 he expression of beta-myosin heavy chain and ANF mRNA was greater in male versus female LVH hearts.

32 yte surface area, total protein content, and ANF expression, whereas dominant negative Akt blocked IS

33 IL-18 induced cardiomyocyte hypertrophy and ANF gene transcription via PI3K, PDK1, Akt, and GATA4.

34 iction-induced increases in cardiac mass and ANF expression were not inhibited.

35 bryos: (&agr;)MHC, betaMHC, MLC2A, MLC2V and ANF, whereas they were expressed in wild-type embryos.

36 rlier spectroscopic investigations of NR and ANF cooperativity, and a mechanism of ANF heteroactivati

37 otein synthesis, sarcomere organization, and ANF expression both at baseline and in response to pheny

38 nt did not respond to pressure overload, and ANF was induced in the absence of Nkx2-5.

39 ed AngII-induced intracellular oxidation and ANF promoter activity, while N19RhoA partially inhibited

40 nzylation was stimulated by progesterone and ANF, and 7-BFC did not inhibit testosterone or progester

41 individuals had a mixture of WHG-related and ANF-related ancestry, one of them with approximately 50%

42 as evidenced by increased ANF secretion and ANF promoter-driven reporter gene activity.

43 the CN and their colocalization with Sp5 and ANF terminals following injections of anterograde tracer

44 ned species-specific ECVs for anidulafungin (ANF), caspofungin (CSF), micafungin (MCF), fluconazole (

45 mulations showed that two molecules of 9-AP, ANF or 1-PB can be adequately docked to two individual s

46 NKX2.6 was inactive at ANF but weakly activated transcription of a Cx40 promote

47 tes negligible binding cooperativity between ANF and TST.

48 howed a lack of positive correlation between ANF oxidation and stimulation of progesterone 6beta-hydr

49 ation of progesterone 6beta-hydroxylation by ANF, indicating that ANF binds at two sites within CYP3A

50 C-ANF was functionalized with 1,4,7,10-tetraazacyclododeca

51 We demonstrated that (64)Cu-DOTA-C-ANF is a promising candidate tracer for in vivo PET of N

52 (64)Cu-DOTA-C-ANF uptake in the atherosclerotic region was visible on

53 ial of a C-type atrial natriuretic factor (C-ANF) to image developing plaque-like lesions in vivo.

54 bution of interspike intervals (ISIs) of cat ANFs during spontaneous activity can be modeled as resul

55 vestigate nonrenewal properties of these cat-ANF spontaneous spike trains, manifest as negative seria

56 In contrast, ANFs colabeled predominantly with VGLUT1.

57 Chloride-dependent ANF-receptor binding may function as a feedback-control

58 utation of these elements results in ectopic ANF promoter activity in the kidneys, facial muscles, an

59 orter gene in vivo recapitulating endogenous ANF expression, which was markedly reduced in tamoxifen-

60 iption repressor Hey2, similar to endogenous ANF expression.

61 no marked preference for either environment; ANF preferentially bound to the membrane, and miconazole

62 aturation-binding studies showed that excess ANF cannot overcome loss of binding caused by low chlori

63 he relationship between the cells expressing ANF and tissue pathology.

64 expression of ANF and that cells expressing ANF are found in regions of tissue pathology.

65 nd expressed less atrial natriuretic factor (ANF) and brain natriuretic peptide (BNP) and more glucos

66 arkedly decreased atrial natriuretic factor (ANF) and connexin 40 (cx40) transcription, implicating t

67 h partners at the atrial natriuretic factor (ANF) and connexin-40 (Cx40) promoters and its specific D

68 rtrophy including atrial natriuretic factor (ANF) and myosin light chain-2.

69 transcription of atrial natriuretic factor (ANF) by beta-adrenergic receptors in cardiac myocytes.

70 cer region of the atrial natriuretic factor (ANF) contains several putative Csx binding sites and con

71 oxidase activity, atrial natriuretic factor (ANF) expression, and cardiac mass were inhibited in gp91

72 r genes, increase atrial natriuretic factor (ANF) expression, and promote myofilament organization, n

73 activation of the atrial natriuretic factor (ANF) gene and enlargement (hypertrophy) of the cells.

74 n shown to induce atrial natriuretic factor (ANF) gene expression in adult cardiomyocytes.

75 The atrial natriuretic factor (ANF) gene is initially expressed throughout the myocardi

76 activators of the atrial natriuretic factor (ANF) gene, a cardiac-specific marker of hypertrophic sig

77 In the cardiac atrial natriuretic factor (ANF) gene, a promoter-proximal serum response element (S

78 e promoter of the atrial natriuretic factor (ANF) gene, an in vivo target gene of Csx/Nkx2.5.

79 icates a role for atrial natriuretic factor (ANF) in renal salt regulation, other studies have found

80 Atrial natriuretic factor (ANF) inhibits proliferation in non-myocardial cells and

81 Atrial natriuretic factor (ANF) is abundantly expressed in atrial cardiomyocytes th

82 P inhibited basal atrial natriuretic factor (ANF) mRNA expression, the stretch-induced increase in AN

83 activation of the atrial natriuretic factor (ANF) promoter (measured by the activity of a transfected

84 ucine uptake, and atrial natriuretic factor (ANF) promoter activity.

85 ort here that the atrial natriuretic factor (ANF) promoter is a target of PITX2.

86 pression from the atrial natriuretic factor (ANF) promoter, a genetic marker that is activated during

87 oters such as the atrial natriuretic factor (ANF) promoter.

88 tion, we used the atrial natriuretic factor (ANF) promoter.

89 rkedly attenuated atrial natriuretic factor (ANF) reporter gene expression induced by alpha1-adrenerg

90 the mechanism of atrial natriuretic factor (ANF) transcription by isoproterenol (ISO), an agonist fo

91 GFP-tagged preproatrial natriuretic factor (ANF) was expressed in nerve growth factor-treated PC12 c

92 pecific promoter (atrial natriuretic factor (ANF)) alone and synergistically with other transcription

93 These include atrial natriuretic factor (ANF), beta-myosin heavy chain (beta-MHC), and skeletal m

94 (mRNA) levels of atrial natriuretic factor (ANF), beta-myosin heavy chain, sarcoplasmic reticulum Ca

95 similar levels of atrial natriuretic factor (ANF), brain natriuretic peptide (BNP), the RNA helicase

96 genes, including atrial natriuretic factor (ANF), has been documented in experimental models of card

97 m cells including atrial natriuretic factor (ANF), Nkx2.5 and Tbx5.

98 ase expression of atrial natriuretic factor (ANF), whereas N17Rac1 inhibited endothelin 1-stimulated

99 the expression of atrial natriuretic factor (ANF), which is a genetic marker of in vivo cardiac hyper

100 We found that atrial natriuretic factor (ANF), which is normally expressed in the atria and trabe

101 es, including the atrial natriuretic factor (ANF).

102 mbryonic gene for atrial natriuretic factor (ANF).

103 ac-specific gene, atrial natriuretic factor (ANF).

104 trophy-associated atrial natriuretic factor (ANF, 2.1-fold) and skeletal alpha-actin (SK, 2.2-fold) g

105 pha (RXR alpha) on atrial naturietic factor (ANF) gene transcription was investigated.

106 in dimer acts as an actin nucleating factor (ANF), decreasing the half-time for spontaneous actin pol

107 pertrophic genes (atrial natriuretic factor [ANF] and c-myc) and also enhanced protein synthesis were

108 E on soybean seed anti-nutritional factors (ANF's) were examined under three different agro-climatic

109 In family ANF, however, FAA was not linked to any locus previously

110 primarily from Anatolian Neolithic farmers (ANFs).

111 deefferentation, acute auditory nerve fiber (ANF) recordings were made from lesioned animals, lesion

112 inner hair cell (IHC)/auditory nerve fiber (ANF) synapse is the first synapse of the auditory pathwa

113 Phase locking of auditory-nerve-fiber (ANF) responses to the fine structure of acoustic stimuli

114 Phase locking of auditory-nerve-fiber (ANF) responses to the temporal fine structure of acousti

115 imary afferent (type I auditory-nerve fiber; ANF) are mainly determined by a single ribbon synapse in

116 Auditory nerve fibers (ANFs) exhibit a range of spontaneous firing rates (SRs)

117 Auditory-nerve fibers (ANFs) in the cat have been subdivided according to spont

118 of CN, whereas type I auditory nerve fibers (ANFs) project to the magnocellular areas of the VCN (VCN

119 red from responses of auditory-nerve fibers (ANFs) to threshold- and moderate-level tones and tone co

120 nt along the axons of auditory nerve fibers (ANFs).

121 NF binding rather than reducing affinity for ANF.

122 e factor (SRF), was shown to be critical for ANF induction in primary cardiac myocytes transfected wi

123 ad MICs less than or equal to the ECVs), for ANF, CSF, MCF, FLC, PSC, and VRC, respectively, were 0.1

124 is-regulatory DNA elements are essential for ANF expression selectively in the developing heart.

125 iscs were 4.0 microm for TNS, 5.8 microm for ANF, 0.45 microm for miconazole, and 0.45 microm for bro

126 Activation of p38 was required for ANF expression induced by the hypertrophic agonists.

127 on a neighboring subunit is responsible for ANF formation.

128 atch extracellular recordings were made from ANF dendrites using acutely excised rat cochlear prepara

129 Because re-expression of the fetal gene ANF is mostly associated with hypertrophy, a hallmark of

130 on levels of the putative GATA4 target genes ANF, BNP, MEF2C, Nkx2-5, cyclin D2, and BMP4 were unchan

131 ats of both sexes, we show that, for a given ANF, the period histograms obtained at all stimulus leve

132 or and the signal transducer of the hormones ANF and BNP.

133 I collagen expression in adult normal human (ANF) and scleroderma (SF) fibroblasts.

134 ver, during cardiac failure and hypertrophy, ANF expression can reappear in adult ventricular cardiom

135 of Ranvier in the peripheral axons of type I ANFs in the rat cochlea with immunohistochemistry and co

136 statistics and endogenous firing in immature ANFs.

137 the NF-kappaB inhibitory effect on COL1A1 in ANF and SF were carried out; in this regard, immunopreci

138 igates whether these SR-based differences in ANF connections are unique to the cat.

139 -activators of type I collagen expression in ANF and SF.

140 expression, the stretch-induced increase in ANF mRNA expression was not inhibited by MnTMPyP.

141 ine, and virtually abolished the increase in ANF reporter gene expression induced by GTPase-deficient

142 inhibitory effect on COL1A1 transcription in ANF, whereas only the siRNAs targeting Sp3 and c-Krox pr

143 l locations of voltage-gated ion channels in ANFs are unknown.

144 e-dependent manner as evidenced by increased ANF secretion and ANF promoter-driven reporter gene acti

145 Kinase-inactive GSK3beta increased ANF transcription.

146 igate the mechanism whereby pacing increases ANF, pacing was tested for its ability to regulate mitog

147 echanisms in shaping responses of individual ANFs.SIGNIFICANCE STATEMENT Phase locking of auditory-ne

148 nal of the deltaB isoform was able to induce ANF reporter gene expression, albeit to a lesser extent

149 Most importantly, IL-18 induced ANF gene transcription and hypertrophy of neonatal rat v

150 Furthermore, IL-18 induced ANF gene transcription in a time-dependent manner as evi

151 are capable of inhibiting TNF-alpha-induced ANF-promoter up-regulation and increase in cardiomyocyte

152 1)-adrenergic receptor (alpha(1)-AR)-induced ANF expression.

153 ISO-induced ANF transcription was not affected by inhibition of mito

154 nositides) was also required for ISO-induced ANF transcription.

155 MEKK1-induced ANF expression was also negatively regulated by expressi

156 hibited both MEKK- and phenylephrine-induced ANF expression, indicating an additional requirement for

157 Rlf-induced ANF promoter activation required Ral and Cdc42 but not R

158 h necessary and sufficient for Rlf-inducible ANF expression.

159 extent than srcF527 and also did not inhibit ANF-luciferase expression in response to phenylephrine.

160 Overexpression of GSK3beta inhibited ANF transcription, which was reversed by ISO.

161 ile a dominant negative MEKK mutant inhibits ANF expression induced by PE.

162 Likewise, ANF expression-a molecular marker of trabecular myocardi

163 Period histograms from phase-locked ANF responses to low-frequency tones exhibit spike-rate

164 expression level of the hypertrophy marker, ANF, compared to C57BL/6 mice.

165 ese JMJ-binding sites do not seem to mediate ANF repression by JMJ.

166 aling, defines a mechanism of IL-18-mediated ANF gene transcription, and further supports a role for

167 f an ATF6 antisense RNA blocked p38-mediated ANF induction through the ANF SRE.

168 e II also potentiated phenylephrine-mediated ANF gene expression, and this effect was blocked by KN-9

169 esults suggest that the alpha1-AdrR mediates ANF gene expression through a Ras-MEKK-JNK pathway and t

170 ing that calcineurin only partially mediates ANF transcription.

171 gen-activated protein kinase family members, ANF promoter activity, and the trans-activation domain o

172 Transfection of mutant ANF promoter-reporter gene constructs demonstrated that

173 )coumarin (7-BFC), and alpha-naphthoflavone (ANF) as substrates.

174 2.7 A resolution with alpha-naphthoflavone (ANF) bound in the active site cavity.

175 enebutanol (1-PB), and alpha-naphthoflavone (ANF) show cooperative spectral binding and yielded 2:1 s

176 nesulfonic acid (TNS), alpha-naphthoflavone (ANF), miconazole, and bromocriptine) binding to CYP3A4 i

177 ic allosteric effector alpha-naphthoflavone (ANF).

178 testosterone (TST) and alpha-naphthoflavone (ANF).

179 estosterone (TST), and alpha-naphthoflavone (ANF).

180 ral population responses for auditory nerve (ANF) input and SBC output to assess the influence of inh

181 udy demonstrates the construction of a novel ANF-RGC-In-gene-(669)WTAPELL(675) mouse model.

182 required for the anti-hypertrophic action of ANF.

183 bility that the anti-hypertrophic actions of ANF involved the mitogen-activated protein kinase signal

184 s required for the synergistic activation of ANF by Tbx5 and GATA4, but TBE2 is required for repressi

185 ly inhibited the transcriptional activity of ANF induced by myotrophin.

186 Anatomical alignment of ANF spike-initiating heminodes relative to excitatory in

187 The binding of ANF to the newly discovered binding site appears to affe

188 sed ERK activity, and the combined effect of ANF and PE appeared to be additive.

189 The observed effect of ANF on the kinetics of TST metabolism is due to the addi

190 ession of Hrt2 suppressed mRNA expression of ANF and other cardiac-specific genes in cultured cardiom

191 ted with increased ventricular expression of ANF and that cells expressing ANF are found in regions o

192 g 20 candidate genes examined, expression of ANF, BNP, MLC2V, N-myc, MEF2C, HAND1 and Msx2 was distur

193 ocytes with srcF527 stimulated expression of ANF, SkM-alpha-actin, and beta-MHC by 62-, 6.7-, and 50-

194 endogenous firing produces some fraction of ANF spikes, accounting for their unusual properties; the

195 ntent may underlie postnatal improvements of ANF excitability and discharge synchrony.

196 r/luciferase reporter gene) and induction of ANF mRNA (measured by RNase protection assay) were also

197 ngly, activation of JNK led to inhibition of ANF expression induced by MEK kinase 1 (MEKK1) and the h

198 of TST, 1-PB, and BCT on the interactions of ANF monitored by changes in fluorescence of CYP3A4(C58,C

199 A4 wild type displayed sigmoidal kinetics of ANF 5,6-oxide formation and 7-BFC debenzylation.

200 NR and ANF cooperativity, and a mechanism of ANF heteroactivation is presented that involves effects

201 h the concept that the structural modules of ANF-RGC are designed to respond to more than one yet dis

202 avity contribute to distinct orientations of ANF in the two active sites.

203 nding consensus sequences in the promoter of ANF, only T-box binding element 1 (TBE1) is required for

204 orded EPSCs revealed that most properties of ANF spike trains derive from the characteristics of pres

205 Statistical properties of ANF spike trains showed developmental changes that appro

206 ity to interact with varying molar ratios of ANF and TST.

207 by PITX2 isoforms through the regulation of ANF and PLOD1 gene expression and Nkx2.5 transcriptional

208 ay important roles in the down-regulation of ANF gene expression and in heart development.

209 (SRF), a direct transcriptional regulator of ANF expression.

210 nscription factor Tbx5, a known regulator of ANF, and an additional Tbx5-dependent gene, connexin 40

211 The physiological relevance of ANF is not clear, but given the large cellular concentra

212 ion domain of JMJ mediates the repression of ANF gene expression.

213 Stimulation of ANF expression by srcF527 was greater than by Ha-rasV12,

214 These findings advance our understanding of ANF phase locking by highlighting the role of peripheral

215 e where frequency-threshold tuning curves of ANFs undergo a shape transition.

216 Here we analyze phase-locked responses of ANFs from cats of both sexes.

217 nderstanding the differential sensitivity of ANFs to acoustic trauma.

218 Using responses to tones of ANFs from cats of both sexes, we show that, for a given

219 suggesting that a loss of chloride turns off ANF binding rather than reducing affinity for ANF.

220 nd Ras produce a large synergistic effect on ANF-luciferase gene expression, we conclude that Rho fun

221 aM kinase II and also blocked its effects on ANF reporter gene and protein expression.

222 Of these substrates only ANF has a specific effect, causing a considerable decrea

223 with P450eryF preloaded with either 1-PB or ANF showed a decrease in the affinities for 9-AP at both

224 lack of natriuretic response to high-plasma ANF under certain physiological and pathophysiological c

225 s (kb -34, -31, and -21) and at the proximal ANF promoter by ChIP assay using neonatal mouse cardiomy

226 ion mapped to the proximal 147 bp of the rat ANF promoter, a region lacking a consensus retinoid resp

227 ower for low- than for high-spontaneous-rate ANFs, implying a synapse-specific contribution to lowpas

228 termine whether CaM kinase II could regulate ANF gene expression, we transiently expressed each of th

229 , PITX2C and Nkx2.5 synergistically regulate ANF and PLOD1 expression through binding to their respec

230 ed the mechanism by which GSK3beta regulates ANF transcription.

231 Here, we show that JMJ represses ANF gene expression by inhibiting transcriptional activi

232 In contrast, Tbx20 represses ANF promoter activity and also inhibits the activation m

233 ed protein kinase cascade and that selective ANF activation of ERK is required for the anti-hypertrop

234 Seven ANF's corresponding to soybean agglutinin and Kunitz try

235 Low and high SR ANFs respond to sound differently, and both are importan

236 as N17Rac1 inhibited endothelin 1-stimulated ANF expression, indicating that the synergy between Rac1

237 Furthermore, betaAR-stimulated ANF transcription is predominantly mediated by activatio

238 ; however, while the SAPK cascade stimulated ANF expression, activation of the ERK cascade inhibited

239 osporin A partially inhibited ISO-stimulated ANF transcription, indicating that calcineurin only part

240 dominant negative Akt blocked ISO-stimulated ANF transcription.

241 Pacing stimulated ANF-promoter activity approximately 10-fold.

242 hat preferentially activates JNK, stimulates ANF reporter gene expression, while a dominant negative

243 In the present study, it was found that ANF binding to its receptor requires the presence of chl

244 6beta-hydroxylation by ANF, indicating that ANF binds at two sites within CYP3A4.

245 um-labeled NR and unlabeled M1, we show that ANF increases k(cat)/k(off) ~1.8-fold in favor of the k(

246 as mimicked by cGMP analogs, suggesting that ANF-induced ERK activation involves the guanylyl cyclase

247 Paired recordings showed that ANFs contacting the same inner hair cell could have diff

248 only PITX2C can synergistically activate the ANF promoter in the presence of Nkx2.5.

249 PITX2C isoforms differentially activate the ANF promoter.

250 Jun, a substrate for JNK, also activated the ANF promoter, and the combination of pacing and c-Jun wa

251 cardiomyocyte hypertrophy and activates the ANF gene, at least in part, by associating with the card

252 orescence of CYP3A4(C58,C64)-BADAN or by the ANF-induced spin transition revealed no competition by t

253 ivation of the reporter genes containing the ANF promoter-enhancer or containing the Nkx2.5 or GATA4-

254 mpared with the value of 2.2 +/- 0.3 for the ANF-induced spin transition, thus revealing an additiona

255 lement, strongly reduces expression from the ANF promoter.

256 entified two DNA-binding sites of JMJ in the ANF enhancer by gel mobility shift assays.

257 ions (planting/sowing season) influences the ANF's content.

258 irect and cooperative transactivation of the ANF and cx40 promoters by Tbx5 and the homeodomain trans

259 Surprisingly, PITX2A activation of the ANF and PLOD1 promoters is repressed by co-transfection

260 ne, it had no effect on the induction of the ANF and SK genes.

261 5 is one of the major transactivators of the ANF gene in the developing heart.

262 e the temporal and spatial regulation of the ANF gene in vivo using transgenic embryos.

263 quired for atrial-specific expression of the ANF gene.

264 quired for transcriptional activation of the ANF gene.

265 ity to yield up to 90-fold activation of the ANF promoter in LS8 cells.

266 ed in a strong synergistic activation of the ANF promoter in LS8 oral epithelial cells but not in oth

267 ed recombinant hormone-binding domain of the ANF receptor in the presence of 0.1 mol/L NaCl or other

268 nvolves the guanylyl cyclase activity of the ANF receptor.

269 inhibit wild type Csx/Nkx2.5 function on the ANF promoter in cultured neonatal cardiac myocytes, poss

270 While ZIC3 by itself had no effect on the ANF promoter, it could bind to and inhibit a cardiac alp

271 ergistically, similar to their effect on the ANF promoter.

272 ed for the effects of pacing or c-Jun on the ANF promoter.

273 a feedback-control mechanism regulating the ANF-receptor action and, hence, renal sodium excretion.

274 ian cell culture studies have shown that the ANF gene is regulated by combinatorial interactions betw

275 /Nkx2.5 transcriptional activity through the ANF promoter in 10T1/2 cells.

276 ocked p38-mediated ANF induction through the ANF SRE.

277 Thirty ANFs from 15 guinea pigs were intracellularly labeled af

278 This ANF SRE does not possess sequences typically required fo

279 This ANF-binding event in the case of the BADAN-modified enzy

280 Thus, ANF expression might function as the natural defense of

281 Thus, ANF has as an allosteric effect on a kinetic branch poin

282 mechanism for this apparent insensitivity to ANF is unknown.

283 the lack of peak clipping is due neither to ANF refractoriness nor to spike-rate adaptation on time

284 which share a similar expression pattern to ANF during development.

285 yielded a chimeric GC that was sensitive to ANF/ATP and to a lesser extent to GCAP1.

286 Compared to ANFs, reconstructions of natural stimuli based on SBC re

287 suggests that early sowing reduces the total ANF's content irrespective of genotypes and their growin

288 brane-targeted mutant of Rlf, transactivated ANF and myosin light chain-2 promoters but did not activ

289 r (measured by the activity of a transfected ANF promoter/luciferase reporter gene) and induction of

290 B-CaM kinase II to transactivate a truncated ANF promoter, containing a serum response element (SRE)

291 In the failing adult ventricle, ANF and BNP were up-regulated to the same extent in wild

292 lationship between the amount of ventricular ANF gene expression and the degree of hypertrophy as wel

293 stablishes that (669)WTAPELL(675) is a vital ANF signal transducer motif of the guanylate cyclase.

294 isotope analysis revealed that the ~50% WHG-ANF individual was non-local to the Brunn 2 area.

295 istic frequency (CF), the frequency at which ANFs are most sensitive, were elevated across the CF ran

296 gely nonoverlapping and were consistent with ANF and Sp5 projections, respectively: VGLUT1 was highly

297 in similar positions for pi-pi stacking with ANF.

298 The mammalian and Xenopus ANF promoters show remarkable sequence similarity, inclu

299 We have isolated the Xenopus ANF promoter in order to examine the temporal and spatia

300 tration of actin, similar reactions yielding ANF could occur in vivo when increased levels of reactiv