ライフサイエンスコーパス: guanylyl cyclase

1 extent, by the direct stimulation of soluble guanylyl cyclase.

2 a multidomain, membrane-associated receptor guanylyl cyclase.

3 h, among other functions, stabilizes soluble guanylyl cyclase.

4 but not natriuretic peptide (NP)-stimulated guanylyl cyclase.

5 ion of a competitive inhibitor of a receptor guanylyl cyclase.

6 vitro, demonstrating that it is a functional guanylyl cyclase.

7 ssion of NF-kappaB and activation of soluble guanylyl cyclase.

8 ein-coupled receptors, adenylyl cyclase, and guanylyl cyclase.

9 f cGMP in response to nitric oxide-activated guanylyl cyclase.

10 way and the subsequent activation of soluble guanylyl cyclase.

11 ndothelial nitric-oxide synthase and soluble guanylyl cyclase.

12 the hsp90 chaperone machinery and by soluble guanylyl cyclase.

13 of NO synthase and subsequent activation of guanylyl cyclase.

14 ndothelial nitric oxide synthase and soluble guanylyl cyclase.

15 te the catalytic activation of transmembrane guanylyl cyclases.

16 s (GCAPs) bind and regulate retinal membrane guanylyl cyclase 1 (RetGC1) but not natriuretic peptide

17 erization domain of a human retinal membrane guanylyl cyclase 1 (RetGC1) linked to autosomal dominant

18 Retinal membrane guanylyl cyclase 1 (RetGC1) regulated by guanylyl cyclas

19 nfers Ca(2+)-sensitive activation of retinal guanylyl cyclase 1 (RetGC1).

20 An inhibitor of soluble guanylyl cyclase, (1)H-(1,2,4)oxadiazolo(4,3-a)quinoxali

21 ated enzymes, adenylyl cyclase-5 and retinal guanylyl cyclase-1.

22 Guanylyl cyclase 2C (GUCY2C) is a marker expressed by co

23 In intestinal epithelial cells, guanylyl cyclase 2C (GUCY2C) is a transmembrane receptor

24 o uroguanylin in the CNS, which can activate guanylyl cyclase 2C (GUCY2C) receptors in the brain to r

25 ic actions, as the endogenous ligand for the guanylyl cyclase 2C receptor has revealed a new system i

26 B-type natriuretic peptide (BNP) is a guanylyl cyclase A (GC-A) agonist.

27 effects were blocked by inhibition of either guanylyl cyclase A receptor or cyclic guanosine monophos

28 Endogenous pGC-A (particulate guanylyl cyclase A receptor) activators were reported to

29 Atrial natriuretic peptide (ANP) binds guanylyl cyclase-A (GC-A) and natriuretic peptide recept

30 t was shown that NPs, via their cGMP-forming guanylyl cyclase-A (GC-A) receptor and cGMP-dependent ki

31 Atrial natriuretic peptide (ANP) via its guanylyl cyclase-A (GC-A) receptor participates in regul

32 Guanylyl cyclase-A (GC-A) signaling, a natriuretic pepti

33 rtension decreases urine output, and second, guanylyl cyclase-A (GC-A), the primary signaling recepto

34 Guanylyl cyclase-A (GC-A), the transmembrane cGMP-produc

35 with endothelial-restricted deletion of the guanylyl cyclase-A receptor for ANP.

36 HF serums were active and generated cGMP via guanylyl cyclase-A receptors; however, the 180-minute sa

37 Atrial natriuretic peptide (ANP) binds guanylyl cyclase-A/natriuretic peptide receptor-A (GC-A/

38 Inhibition of the soluble guanylyl cyclase abolished the effect of L-arginine on g

39 Guanylyl cyclase activating protein 1 (GCAP-1), a Ca(2+)

40 Guanylyl cyclase activating protein 1 (GCAP1), a member

41 Guanylyl cyclase activating protein 1 (GCAP1), after sub

42 Two calcium-sensitive guanylyl cyclase activating proteins (GCAP1 and GCAP2) a

43 and cone photoreceptors by calcium-sensitive guanylyl cyclase activating proteins (GCAP1 and GCAP2) i

44 activity is modulated by the calcium-binding guanylyl cyclase activating proteins (GCAP1 and GCAP2).

45 etGC1 and RetGC2 isozymes using mice lacking guanylyl cyclase activating proteins GCAP1 and GCAP2 and

46 Guanylyl cyclase-activating protein 1 (GCAP-1) is an EF-

47 9C or E155G mutations of the retGC modulator guanylyl cyclase-activating protein 1 (GCAP-1), which pr

48 Guanylyl cyclase-activating protein 1 (GCAP1), a myristo

49 ackground light; similar effects are seen in guanylyl cyclase-activating protein knockout (GCAPs(-/-)

50 The guanylyl cyclase-activating protein, GCAP1, activates ph

51 clase (RetGC) activation via calcium-sensing guanylyl cyclase-activating proteins (GCAP), and RD3 tru

52 The photoreceptor-specific proteins guanylyl cyclase-activating proteins (GCAPs) bind and re

53 ane guanylyl cyclase 1 (RetGC1) regulated by guanylyl cyclase-activating proteins (GCAPs) controls ph

54 eceptors from degeneration by competing with guanylyl cyclase-activating proteins (GCAPs), which are

55 r segment and suppresses RetGC activation by guanylyl cyclase-activating proteins (GCAPs).

56 RetGC catalytic activity and stimulation by guanylyl cyclase-activating proteins (GCAPs).

57 icial effects of both nitric oxide-sensitive guanylyl cyclase activation and inhibition of the cGMP-d

58 ing, leading to NO production and subsequent guanylyl cyclase activation and K(ATP) channel opening i

59 al NMDARs and NOS stimulation and subsequent guanylyl cyclase activation that probably occurred in pe

60 important role in NO generation and soluble guanylyl cyclase activation under hypoxic conditions, wi

61 With the addition of nitrite, soluble guanylyl cyclase activation was significantly higher in

62 n but are well-tuned to the dynamic range of guanylyl cyclase activation.

63 tors (VPAC2 and NPR-C), inhibit adenylyl and guanylyl cyclase activities, and stimulate cAMP-specific

64 uced dephosphorylation of NPR2 decreases its guanylyl cyclase activity in growth plate chondrocytes i

65 y changes, but the absence of GCAP2 affected guanylyl cyclase activity in two ways; (a) the maximal r

66 mouse GCAP2 produced similar effects on the guanylyl cyclase activity in wild type retinas.

67 The guanylyl cyclase activity is modulated by the calcium-bi

68 xposed to green light, whereas inhibition of guanylyl cyclase activity negatively affects fungal phot

69 n kinase Ialpha on the phosphate content and guanylyl cyclase activity of NPR-A.

70 in 20 min, LH treatment results in decreased guanylyl cyclase activity of NPR2, as determined in the

71 Therefore, GCAP2 regulation of guanylyl cyclase activity quickens the recovery of flash

72 me activity, consistent with ATP stimulating guanylyl cyclase activity through an allosteric, phospho

73 y Ca(2+)-dependent binding of recoverin, (2) guanylyl cyclase activity via Ca(2+)-dependent GCAP prot

74 vity, DGK4 recombinant protein also revealed guanylyl cyclase activity, as inferred by sequence analy

75 CAP1 and GCAP2, confer Ca(2+) sensitivity to guanylyl cyclase activity, but the importance and the co

76 r catalytic spines within the PKDs increased guanylyl cyclase activity, increased sensitivity to natr

77 The protein exhibits robust light-dependent guanylyl cyclase activity, whereas a truncated form lack

78 eta1-sGC protein content, and impair soluble guanylyl cyclase activity.

79 igated how ATP binding to the PKD influenced guanylyl cyclase activity.

80 oso-N-acetyl-DL-penicillamine) and a soluble guanylyl cyclase agonist (YC-1) mimicked AMPA effect in

81 es an effector domain such as an adenylyl or guanylyl cyclase, all encoded in a single protein as a t

82 UCY1A3 encodes the alpha1 subunit of soluble guanylyl cyclase (alpha1-sGC), and CCT7 encodes CCTeta,

83 and GCalpha, a fusion protein composed of a guanylyl cyclase and a phospholipid transporter domain.

84 Although guanylyl cyclase and downstream cGMP are essential regul

85 signaling, was also inhibited by the soluble guanylyl cyclase and KATP channel blockers.

86 cAMP receptor protein (CRP) is linked to the guanylyl cyclase and when deleted is deficient in cyst d

87 total of 27 gcy genes encoding receptor-type guanylyl cyclases and of 7 gcy genes encoding soluble gu

88 erotrimeric G proteins but is independent of guanylyl cyclases and the previously identified cGMP-ind

89 s issue, report direct communication between guanylyl cyclases and the Rac-p21-activated kinase (PAK)

90 s, harbors a catalytic center diagnostic for guanylyl cyclases and the recombinant AtPNP-R1 is capabl

91 porters, nitric oxide (NO) synthase, soluble guanylyl cyclase, and ATP-sensitive potassium (KATP) cha

92 cked by inhibitors of nitric oxide synthase, guanylyl cyclase, and calcium/calmodulin.

93 phosphorylation and inactivation of the NPR2 guanylyl cyclase, and cGMP hydrolysis is increased by ac

94 ing pathway involving nitric oxide synthase, guanylyl cyclase, and cGMP-dependent protein kinase (PKG

95 e roles of endothelium-derived vasodilators, guanylyl cyclase, and potassium channels were examined i

96 Signaling is both soluble guanylyl cyclase- and phosphodiesterase 6-dependent but

97 not using the PI3 kinase/Akt/PKB pathway and guanylyl cyclases, AprA does not induce actin polymeriza

98 dely distributed across all kingdoms whereas guanylyl cyclases are generally thought to be restricted

99 g membrane-integral and soluble adenylyl and guanylyl cyclases, are central components in a wide rang

100 C-type natriuretic peptide activation of guanylyl cyclase B (GC-B), also known as natriuretic pep

101 ceptor for C-type natriuretic peptide (CNP), guanylyl cyclase B (GC-B, also known as Npr2 or NPR-B),

102 structure of human BNP to activate GC-A and guanylyl cyclase-B (GC-B), which is not reduced in heart

103 tor 3 and inactivating mutations in the NPR2 guanylyl cyclase both cause severe short stature, but ho

104 ependent vasodilation, which is dependent on guanylyl cyclase but not prostaglandins.

105 dependent, as well as nitric oxide (NO) and guanylyl cyclase, but not prostaglandin dependent.

106 naling proteins, including eucaryal receptor guanylyl cyclases, but its function remains obscure.

107 Blockade of soluble guanylyl cyclase by ODQ (1H-[1,2,4] oxadiazolo[4,3,-a]qu

108 l motility, through allosteric activation of guanylyl cyclases by autophosphorylated PAK.

109 ginine methyl ester) and blockade of soluble guanylyl cyclase (by ODQ; 1H-1,2,4-oxadiazolo[4,3-a]quin

110 Guanylyl cyclase C (GC-C) has been shown to be the prima

111 Guanylyl cyclase C (GC-C) is a multidomain, membrane-ass

112 Guanylyl cyclase C (GC-C) is expressed in intestinal epi

113 Guanylyl cyclase C (GC-C), an intestine-specific tumor s

114 Guanylyl cyclase C (GC-C), the receptor for diarrheageni

115 rgeting the intestinal cancer mucosa antigen guanylyl cyclase C (GCC) and its effect on inflammatory

116 tems, and the bacterial enterotoxin receptor guanylyl cyclase C (GCC), the principle source of cGMP i

117 ic tumors all express a unique surface-bound guanylyl cyclase C (GCC), which binds the diarrheagenic

118 ylin and uroguanylin, endogenous ligands for guanylyl cyclase C (GCC).

119 nuation of the colonic cell surface receptor guanylyl cyclase C (GUCY2C) that occurs due to loss of i

120 Guanylyl cyclase C (GUCY2C), a membrane-bound guanylyl c

121 enovirus (Ad5) combination regimen targeting guanylyl cyclase C (GUCY2C), a receptor expressed by int

122 endogenous ligands for the tumor suppressor guanylyl cyclase C (GUCY2C), disrupting a network of hom

123 Conversely, activating guanylyl cyclase C in human colon cancer cells delayed c

124 ntrol of cGMP levels and that membrane-bound guanylyl cyclases can be critically modulated by other r

125 gether with Ca(2+)-dependent acceleration of guanylyl cyclase, can successfully account for changes i

126 of a type I (microbial) rhodopsin domain and guanylyl cyclase catalytic domain.

127 g 8-bromo-cGMP, as well as by the NO-soluble guanylyl cyclase-cGMP signaling inhibitor thrombospondin

128 The guanylyl cyclase/cGMP signaling triggers opening of KATP

129 The nitric oxide-sensitive guanylyl cyclase/cGMP-dependent protein kinase type I si

130 The endogenous NO acts to stimulate guanylyl cyclase-coupled NO receptors in the axons, lead

131 ts in target cells by binding to specialized guanylyl cyclase-coupled receptors, resulting in cGMP ge

132 rough which NO generally acts is the soluble guanylyl cyclase-cyclic GMP (sGC-cGMP) pathway.

133 Activation of the guanylyl cyclase-cyclic GMP-protein-kinase-G system with

134 tion of retinal arterioles via activation of guanylyl cyclase; cyclooxygenase plays a relatively mino

135 cretes cGMP when developing cysts and that a guanylyl cyclase deletion strain fails to synthesize cGM

136 n modification, biologically through soluble guanylyl-cyclase-dependent modulation of the MMP-9/TIMP-

137 e identified a link between impaired soluble-guanylyl-cyclase-dependent nitric oxide signalling and m

138 levation of cGMP after activation of soluble guanylyl cyclase does not relax the muscle.

139 ion of the cyclase activity, we isolated the guanylyl cyclase domain from Escherichia coli with (GCwC

140 tivation of the C-terminal cGMP-synthesizing guanylyl cyclase domain.

141 , combining a type I rhodopsin domain with a guanylyl cyclase domain.

142 smembrane receptors containing intracellular guanylyl cyclase domains, such as GC-A and GC-B, also kn

143 eight different receptor-type, transmembrane guanylyl cyclases (encoded by gcy genes), which are expr

144 uanylyl cyclase C (GUCY2C), a membrane-bound guanylyl cyclase expressed in intestinal epithelial cell

145 segment of a natriuretic peptide receptor A guanylyl cyclase failed to bind GCAPs, but replacing its

146 nsory neurons (OSNs) expressing the receptor guanylyl cyclase GC-D, the cyclic nucleotide-gated chann

147 PSM2), RAP1GAP, and Gbeta5; cGMP modulators: guanylyl cyclase (GC) 1alpha1, GC1beta1, phosphodiestera

148 hat is lost when the predicted PEPR receptor guanylyl cyclase (GC) active site is mutated.

149 pr1 promoter activity and greatly stimulated guanylyl cyclase (GC) activity of the receptor protein i

150 activation of the intestinal receptor-enzyme guanylyl cyclase (GC) C, triggers an acute, watery diarr

151 Phosphodiesterase (PDE) and guanylyl cyclase (GC) enzymes are key components of the

152 RhoGC is a rhodopsin (Rho)-guanylyl cyclase (GC) gene fusion molecule that is centr

153 Soluble guanylyl cyclase (GC) is a heterodimer that is activated

154 and MyD88-dependent recruitment of platelet guanylyl cyclase (GC) toward the plasma membrane, follow

155 eptides and ATP activate and Go6976 inhibits guanylyl cyclase (GC)-A and GC-B.

156 hosphorylation is required for activation of guanylyl cyclase (GC)-A, also known as NPR-A or NPR1, by

157 gical effects in cells largely by activating guanylyl cyclase (GC)-coupled receptors, leading to cGMP

158 of cGMP from its receptor, the NO-sensitive guanylyl cyclase (GC1).

159 Guanylyl cyclases (GCs) catalyze the conversion of GTP t

160 ions of phosphodiesterase (PDE6) and retinal guanylyl cyclases (GCs), and mutations in genes that dis

161 uses PAK to directly activate transmembrane guanylyl cyclases (GCs), leading to increased cellular c

162 Guanylyl cyclases (GCs), which synthesize the messenger

163 to the activation of receptor enzymes called guanylyl cyclases (GCs).

164 inct set of four known chemoreceptors of the guanylyl cyclase (gcy) gene family.

165 rect inhibitors of an NRE-localized receptor-guanylyl-cyclase, GCY-8, which synthesizes cyclic guanos

166 After stimulation with nitric oxide, soluble guanylyl cyclase generates cGMP, which induces vasodilat

167 s alters expression of AFD-specific receptor guanylyl cyclase genes.

168 hyperphosphorylation occurs through soluble guanylyl cyclase/guanosine 3',5'-cyclic monophosphate si

169 The three Drosophila atypical soluble guanylyl cyclases, Gyc-89Da, Gyc-89Db, and Gyc-88E, have

170 We find that the Drosophila receptor guanylyl cyclase Gyc76C genetically interacts with Semap

171 Although guanylyl cyclases have been implicated in cell migration

172 on by the ligand NPPC, NPR2, the predominant guanylyl cyclase in follicular somatic cells, produces c

173 nated BlgC, was found to have photoactivated guanylyl cyclase in vitro.

174 cyclases and of 7 gcy genes encoding soluble guanylyl cyclases in the complete genome sequence of C.

175 BPIPP inhibited stimulation of guanylyl cyclases, including types A and B and soluble i

176 induced airway relaxation was resistant to a guanylyl cyclase inhibitor (ODQ) and a protein kinase G

177 -nitro-L-arginine methyl ester (L-NAME), the guanylyl cyclase inhibitor 1H- [1,2,4]oxadiazolo[4,3-a]q

178 Porcine leaflets exposed to the soluble guanylyl cyclase inhibitor ODQ increased osteocalcin and

179 mediated depolarizations were blocked by the guanylyl cyclase inhibitor ODQ indicating involvement of

180 nt with either a Ca(2+) channel blocker or a guanylyl cyclase inhibitor.

181 adiazolo-[4,3-a]quinoxalin-1-one) (a soluble guanylyl cyclase-inhibitor, Rp-8-(4-chlorophenylthio)-gu

182 In addition to L-NAME, the guanylyl cyclase inhibitors ODQ and thrombospondin-1 als

183 Ps(-/-)) rods, indicating that regulation of guanylyl cyclase is not necessary for at least a part of

184 In cones, calcium feedback to guanylyl cyclase is potentially a key step in phototrans

185 lation of cGMP synthesis by retinal membrane guanylyl cyclase isozymes (RetGC1 and RetGC2) in rod and

186 nthesis in photoreceptor by retinal membrane guanylyl cyclase isozymes (RetGC1 and RetGC2) to expedit

187 ugh H(2)S does not directly activate soluble guanylyl cyclase, it maintains a tonic inhibitory effect

188 wn cells and agonists for either adenylyl or guanylyl cyclase, it was found that PDE1B2 predominantly

189 ice that lack NO-GC specifically in SMCs (SM-guanylyl cyclase knockout [GCKO]), ICCs (ICC-GCKO), or b

190 NP is a critical discriminator of binding to guanylyl cyclase-linked but not clearance natriuretic pe

191 ndicating that NO-induced AMPK activation is guanylyl cyclase-mediated and calcium-dependent.

192 n of Foxp3 in MBP-primed T cells via soluble guanylyl cyclase-mediated production of cGMP.

193 in the granulosa cells by the transmembrane guanylyl cyclase natriuretic peptide receptor 2 (NPR2) i

194 natriuretic peptide (CNP), its receptor, the guanylyl cyclase natriuretic peptide receptor 2 (Npr2),

195 granulosa cells, where it is produced by the guanylyl cyclase natriuretic peptide receptor 2 (NPR2).

196 rial and brain natriuretic peptides activate guanylyl cyclase/natriuretic peptide receptor-A (GC-A/NP

197 ibrosis and dysfunction using Npr1 (encoding guanylyl cyclase/natriuretic peptide receptor-A, GC-A/NP

198 MCs) by acting on its receptor, NO-sensitive guanylyl cyclase (NO-GC).

199 the application of a nitric oxide-sensitive guanylyl cyclase (NO-sGC) receptor antagonist, a NOS inh

200 ow that one of these molecules, the receptor guanylyl cyclase Npr2, is required for bifurcation of th

201 ynthesis, L-NNA, and an inhibitor of soluble guanylyl cyclase, ODQ, greatly enhanced colonic contract

202 hermore, inhibition of the NO target soluble guanylyl cyclase or of the cGMP effector kinase protein

203 Inhibitors of soluble guanylyl cyclase or PKG decreased activity of the I425V

204 3-a]quinoxalon-1-one, a potent inhibitor for guanylyl cyclase, or 1,2-bis(2-aminophenoxy)ethane-N,N,N

205 that release nitric oxide, stimulate soluble guanylyl cyclase, or activate cGMP-dependent protein kin

206 all kingdoms of life, e.g. in human retinal guanylyl cyclase, our findings may be significant for ma

207 n suppressing Foxp3(+) Tregs via the soluble guanylyl cyclase pathway.

208 does not require the PI3 kinase/Akt/PKB and guanylyl cyclase pathways to induce chemorepulsion.

209 luding the insulin, TGF-beta, serotonin, and guanylyl cyclase pathways; however, the sensory processe

210 expression levels of particulate (membrane) guanylyl cyclases (pGC) and cGMP-specific phosphodiester

211 or repertoire of cilia-localized particulate guanylyl cyclases (pGC-G and pGC-A).

212 nic mutation carriers contained less soluble guanylyl cyclase protein and consequently displayed redu

213 3-kinase, endothelial nitric-oxide synthase, guanylyl cyclase, protein kinase G (PKG), and the mitoch

214 The effect of CORM-2 was not prevented by guanylyl-cyclase, protein kinase G, or thioredoxin inhib

215 hosphodiesterase 5 or stimulators of soluble guanylyl cyclase rapidly enhanced multiple proteasome ac

216 dly hypotensive and functions via a separate guanylyl cyclase receptor compared with CNP.

217 se (eNOS) by directly activating its soluble guanylyl cyclase receptor, rescued blood vessel function

218 the natural ligands for cell membrane-bound guanylyl cyclase receptors that mediate the effects of n

219 inhibitors of NO synthase (NOS) and soluble guanylyl cyclase, respectively, abolished tadalafil indu

220 5'-cyclic monophosphate ([cGMP]i) by soluble guanylyl cyclase, resulting in fast onset and long-lasti

221 xide that retrogradely activated presynaptic guanylyl cyclase, resulting in the presynaptic expressio

222 tors from degeneration by preventing retinal guanylyl cyclase (RetGC) activation via calcium-sensing

223 Retinal membrane guanylyl cyclase (RetGC) and Ca(2+)/Mg(2+) sensor protei

224 hat change the Ca(2+) sensitivity of retinal guanylyl cyclase (retGC) can result from an increase in

225 al for normal expression of retinal membrane guanylyl cyclase (RetGC) in photoreceptor cells, blocks

226 is an EF-hand protein that activates retinal guanylyl cyclase (RetGC) in photoreceptors at low free C

227 (2+) sensor protein that accelerates retinal guanylyl cyclase (RetGC) in the light and decelerates it

228 ein, GCAP1, activates photoreceptor membrane guanylyl cyclase (RetGC) in the light, when free Ca(2+)

229 in promotes accumulation of retinal membrane guanylyl cyclase (RetGC) in the photoreceptor outer segm

230 oding for the dimeric human retinal membrane guanylyl cyclase (RetGC) isozyme RetGC1 cause various fo

231 depend on Ca(2+)-regulated retinal membrane guanylyl cyclase (RetGC), comprised of two isozymes, Ret

232 Retinal guanylyl cyclase (RetGC)-activating proteins (GCAPs) reg

233 hodiesterase (PDE6) or regulation of retinal guanylyl cyclase (retGC).

234 d Ca(2+) sensor in vision, regulates retinal guanylyl cyclase (RetGC).

235 calcium sensor proteins for retinal membrane guanylyl cyclase (RetGC).

236 The GUCY2D gene encodes retinal membrane guanylyl cyclase (RetGC1), a key component of the photot

237 +) in its EF-hands, stimulates photoreceptor guanylyl cyclase, RetGC1, in response to light.

238 rs is supported by a pair of retina-specific guanylyl cyclases, retGC1 and -2.

239 utations in the AFD-expressed gcy-8 receptor guanylyl cyclase (rGC) gene result in defects in the exe

240 We show that AFD-specific receptor guanylyl cyclases (rGCs) are instructive for thermosensa

241 the observation that multiple receptor-type guanylyl cyclases (rGCs), encoded by the gcy genes, and

242 onstrate the effect of NO donors and soluble guanylyl cyclase (sGC) activators in differentiation of

243 tives have been studied as potential soluble guanylyl cyclase (sGC) activators.

244 Nitric oxide (NO) stimulates soluble guanylyl cyclase (sGC) activity, leading to elevated int

245 ivatives and tested their effects on soluble guanylyl cyclase (sGC) activity.

246 es that the functional properties of soluble guanylyl cyclase (sGC) are affected not only by the bind

247 dentified the alpha1-subunit gene of soluble guanylyl cyclase (sGC) as a novel androgen-regulated gen

248 nsertion is key during maturation of soluble guanylyl cyclase (sGC) because it enables sGC to recogni

249 es with the oxidation of the heme of soluble guanylyl cyclase (sGC) critically implicated in some of

250 Although soluble guanylyl cyclase (sGC) functions in an environment in wh

251 nine (NMMA); 300 or 500 microM) or a soluble guanylyl cyclase (sGC) inhibitor (1H-[1,2,4]oxadiazolo[4

252 ell volume that was abolished by the soluble guanylyl cyclase (sGC) inhibitor 1H-[1,2,4]oxadiazolo[4,

253 -arginine methyl ester; 30 mg/kg), a soluble guanylyl cyclase (sGC) inhibitor [1H-(1, 2, 4) oxadiazol

254 either a nitric oxide scavenger or a soluble guanylyl cyclase (sGC) inhibitor diminished the benefici

255 The enzyme soluble guanylyl cyclase (sGC) is a heterodimer composed of an a

256 Soluble guanylyl cyclase (sGC) is a key component of NO-cGMP sig

257 Diatomic ligand discrimination by soluble guanylyl cyclase (sGC) is paramount to cardiovascular ho

258 Soluble guanylyl cyclase (sGC) is the main receptor for nitric o

259 Soluble guanylyl cyclase (sGC) is the principal receptor for NO

260 Soluble guanylyl cyclase (sGC) is the receptor for nitric oxide

261 MP levels in this pathway, including soluble guanylyl cyclase (sGC) itself, the NO -activated form of

262 and cGMP in the above effects using soluble guanylyl cyclase (sGC) or adenylate cyclase (AC) specifi

263 Soluble guanylyl cyclase (sGC) plays an important role in cardio

264 of the alpha1 and beta1 subunits of soluble guanylyl cyclase (sGC) was directly and specifically reg

265 d neuronal systems via activation of soluble guanylyl cyclase (sGC), a heme-containing heterodimer.

266 ch encodes the alpha1 subunit of the soluble guanylyl cyclase (sGC), a key enzyme in the nitric oxide

267 They were tested for activation of soluble guanylyl cyclase (sGC), a key enzyme in the NO/cGMP sign

268 Soluble guanylyl cyclase (sGC), a key protein in the NO/cGMP sig

269 nal nitric oxide synthase (nNOS) and soluble guanylyl cyclase (sGC), and can be mimicked by the nitri

270 otein complexes with NMDA receptors, soluble guanylyl cyclase (sGC), and PSD95.

271 the major downstream effector of NO, soluble guanylyl cyclase (sGC), in the superficial dorsal horn o

272 the major downstream effector of NO, soluble guanylyl cyclase (sGC), is very limited.

273 through activation of its receptor, soluble guanylyl cyclase (sGC), leading to elevation of intracel

274 presence of inhibitors selective for soluble guanylyl cyclase (sGC), PKG, calmodulin, CaMKII or ERK1/

275 ural homology to the beta subunit of soluble guanylyl cyclase (sGC), suggesting a NO sensing function

276 homologous to the central region in soluble guanylyl cyclase (sGC), the main receptor for nitric oxi

277 ular mechanism of desensitization of soluble guanylyl cyclase (sGC), the NO receptor, has long remain

278 ly vasoactive through stimulation of soluble guanylyl cyclase (sGC), which produces the second messen

279 eased in cells that had a functional soluble guanylyl cyclase (sGC)-cGMP signaling pathway and was di

280 Nitric oxide (NO)-NO-sensitive (soluble) guanylyl cyclase (sGC)-cyclic guanosine monophosphate (c

281 renoceptors (beta(3)-ARs) coupled to soluble guanylyl cyclase (sGC)-dependent production of the secon

282 tivating its intracellular receptor, soluble guanylyl cyclase (sGC).

283 light source, to activate the enzyme soluble guanylyl cyclase (sGC).

284 organic nitrate to the activation of soluble guanylyl cyclase (sGC).

285 We compared the NO/soluble guanylyl cyclase (sGC)/cGMP pathway in human glioma tiss

286 glutamate NMDA receptors (NMDA-Rs), soluble guanylyl cyclase (sGC, the NO receptor), and PSD95 (a pr

287 tes a pool of oxidized and heme-free soluble guanylyl cyclase (sGC; see the related article beginning

288 her the classical, nitric oxide (NO)-soluble guanylyl-cyclase (sGC)-cGMP pathway could modulate Ca(2)

289 s, evolutionary diversification of primitive guanylyl cyclase signaling pathways allows GUCY2C to coo

290 chieved by activating the endogenous soluble guanylyl cyclase that produces cGMP.

291 at this toxin is a dual soluble adenylyl and guanylyl cyclase that results in intracellular cAMP and

292 peptide receptor B (NPR-B) are transmembrane guanylyl cyclases that catalyze the synthesis of cGMP in

293 olar concentrations of nitric oxide activate guanylyl cyclase to produce cGMP, which has diverse phys

294 canonical 5'-3' DNA polymerases and adenylyl/guanylyl cyclases, two enzyme families known to use a tw

295 its receptor on the intestinal brush border, guanylyl cyclase type C (GC-C).

296 To convert BlaC into a guanylyl cyclase, we constructed a model of the nucleoti

297 tion of NO species and activation of soluble guanylyl cyclase, where xanthine oxidoreductase is propo

298 Although soluble guanylyl cyclase (which generates cyclic guanosine monop

299 yclase, which synthesizes cGMP, or a mutated guanylyl cyclase, which synthesizes cAMP.

300 e conditional expression of either wild-type guanylyl cyclase, which synthesizes cGMP, or a mutated g