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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

45 tes negligible binding cooperativity between ANF and TST.

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

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

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

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

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

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

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

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

54 In contrast, ANFs colabeled predominantly with VGLUT1.

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

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

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

58 iption repressor Hey2, similar to endogenous ANF expression.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

77 up-regulates the atrial natriuretic factor (ANF) gene, but does not affect skeletal alpha-actin or m

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

101 mbryonic gene for atrial natriuretic factor (ANF).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

117 NF binding rather than reducing affinity for ANF.

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

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

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

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

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

123 on a neighboring subunit is responsible for ANF formation.

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

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

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

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

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

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

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

131 statistics and endogenous firing in immature ANFs.

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

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

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

135 drenergic stimulation lead to an increase in ANF gene transcription.

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

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

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

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

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

141 Kinase-inactive GSK3beta increased ANF transcription.

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

143 block the ability of activated Ras to induce ANF and myosin light chain-2 reporter gene expression.

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

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

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

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

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

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

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

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

152 4 MAPK failed to block phenylephrine-induced ANF expression, although Ras-induced gene expression was

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

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

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

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

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

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

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

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

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

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

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

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

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

166 ing that calcineurin only partially mediates ANF transcription.

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

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

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

170 2.7 A resolution with alpha-naphthoflavone (ANF) bound in the active site cavity.

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

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

173 ic allosteric effector alpha-naphthoflavone (ANF).

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

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

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

177 enylephrine-stimulated MAPK activity but not ANF reporter gene expression.

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

179 required for the anti-hypertrophic action of ANF.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

212 nderstanding the differential sensitivity of ANFs to acoustic trauma.

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

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

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

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

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

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

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

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

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

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

223 ed the mechanism by which GSK3beta regulates ANF transcription.

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

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

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

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

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

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

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

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

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

233 dominant negative Akt blocked ISO-stimulated ANF transcription.

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

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

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

237 6beta-hydroxylation by ANF, indicating that ANF binds at two sites within CYP3A4.

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

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

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

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

242 PITX2C isoforms differentially activate the ANF promoter.

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

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

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

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

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

248 lement, strongly reduces expression from the ANF promoter.

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

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

251 side of the proximal 3 kilobase pairs of the ANF 5'-flanking region.

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

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

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

255 5 is one of the major transactivators of the ANF gene in the developing heart.

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

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

258 quired for transcriptional activation of the ANF gene.

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

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

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

262 nvolves the guanylyl cyclase activity of the ANF receptor.

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

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

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

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

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

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

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

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

271 Thirty ANFs from 15 guinea pigs were intracellularly labeled af

272 This ANF SRE does not possess sequences typically required fo

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

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

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

276 mechanism for this apparent insensitivity to ANF is unknown.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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