ライフサイエンスコーパス: cGMP

1 cGMP binding produces global conformational changes that

2 cGMP binds both the 3'- and 5'-end vG4s and forms two fi

3 cGMP is rapidly hydrolyzed, possibly via "substrate chan

4 cGMP-AMP (cGAMP) synthase (cGAS) is a cytosolic DNA sens

5 cGMP-specific phosphodiesterases (PDEs), which degrade c

6 Type 1 cGMP-dependent protein kinases (PKGs) play important rol

7 dy, we tested the ability of cGMP and type 2 cGMP-dependent protein kinase (PKG2) to activate forkhea

8 , Palphabetagamma(2), and Palphabetagamma(2)-cGMP) with a quantitative cross-linking/mass spectrometr

9 ant cells and catalyzes the formation of 2'3'cGMP-AMP (cGAMP), which in turn triggers interferon (IFN

10 3) cGMP- and Ca(2+)-mediated inhibition of NHE3 was impaire

11 2',5'/3',5'-cGMP-AMP (cGAMP) is a second messenger produced in respo

12 and FoxO target genes were unaffected by 8Br-cGMP challenge in vitro.

13 t of human colonic biopsy specimens with 8Br-cGMP also activated catalase and manganese superoxide di

14 Treatment of colon explants with 8Br-cGMP also activated FoxO target gene expression at both

15 A cGMP-activated phosphodiesterase (AtCN-PDE1) was respons

16 NPRA) receptor and, in turn, by activating a cGMP-dependent pathway.

17 falciparum Its life cycle is regulated by a cGMP-dependent protein kinase (PfPKG), whose inhibition

18 ans, the AWC neurons are thought to deploy a cGMP signaling cascade in the detection of and response

19 roadmap can be used to efficiently develop a cGMP-compliant formulation and improve the translation o

20 ria parasite Plasmodium falciparum encodes a cGMP-dependent protein kinase G (PfPKG) that is critical

21 GEP1 interacts with GCalpha, a cGMP synthesizing enzyme in gametocytes.

22 ur major aspects for MAM implementation in a cGMP environment for both new and existing products: ris

23 ol (QC) testing of therapeutic proteins in a cGMP environment.

24 oposed, in which PKGIalpha is activated in a cGMP-independent fashion via oxidation of Cys(43), resul

25 NO also appears to function in a cGMP-independent manner, via S-nitrosation (SNO), a redo

26 the medicinal chemistry efforts focused on a cGMP-dependent protein kinase (PKG) inhibitor scaffold,

27 al transduction cascade, here we optimized a cGMP-based luciferase assay that reports on heterologous

28 yed from the receptor guanylate cyclase to a cGMP-gated channel that serves as a perfect chemo-electr

29 tion or environmental acidification, while a cGMP-phosphodiesterase inhibitor circumvents egress repr

30 se G intracellular cascade consistent with a cGMP-dependent switch from short- to long-term memory ob

31 However, NP/GC-A/cGMP signaling protects podocyte integrity under patholo

32 ce of CNG channel alone also caused abnormal cGMP accumulation.

33 attractant peptide, via receptor activation, cGMP synthesis and decay.

34 tween Cys117 and Cys195 in the high affinity cGMP-binding site.

35 onist cAMP, but not with the partial agonist cGMP.

36 s involves the activation of cyclic GMP-AMP (cGMP-AMP) synthase (cGAS) and generation of the cyclic d

37 ) mice treated with GC inhibitor, A71915 and cGMP-dependent protein kinase (cGK) inhibitor, (Rp-8-Br-

38 ory domain, PfD, in its apo, cGMP-bound, and cGMP analog-bound states, we elucidated its inhibition m

39 rase beta (PDEbeta) hydrolyses both cAMP and cGMP and is essential for blood stage viability.

40 enzyme that catalyzes hydrolysis of cAMP and cGMP and is highly expressed in tissues that regulate en

41 f dystonia, PDE10A, a key enzyme in cAMP and cGMP catabolism, is downregulated in striatal projection

42 TP-10 treatment elevated both cAMP and cGMP levels in cardiac myocytes and cardiac fibroblasts,

43 Testing a panel of modulators of cAMP and cGMP signaling pathways, FASS-LTP identified vardenafil

44 sis suggested the interplay between cAMP and cGMP signalling as PKAc1 inactivation changes the phosph

45 eak down cyclic nucleotides such as cAMP and cGMP, reducing the signaling of these important intracel

46 activation of the NPR2 guanylyl cyclase, and cGMP hydrolysis is increased by activation of the PDE5 p

47 tandardize the development, formulation, and cGMP translation of molecular fluorescent tracers.

48 guanine metabolites, such as dGMP, GMP, and cGMP, as well as guanine-derivative drugs.

49 y decreased NPRA mRNA and protein levels and cGMP accumulation in cultured mesangial cells and attenu

50 MDA effect is mediated solely via the NO and cGMP signaling pathway.

51 ), BNP (brain-type natriuretic peptide), and cGMP, and decreased plasma endothelin-1 compared with PH

52 as required by the European Pharmacopeia and cGMP guidelines.

53 d understanding of the major regulations and cGMP practices governing microbiological testing in the

54 nucleotide building blocks of DNA, RNA, and cGMP and that cancer cells possess elevated GTP levels,

55 of a key regulatory domain, PfD, in its apo, cGMP-bound, and cGMP analog-bound states, we elucidated

56 functional reorganization of the beta(3)-AR/cGMP signalosome happens in heart failure and should be

57 d subcellular compartmentation of beta(3)-AR/cGMP signals underpinning this protection in health and

58 on in PKGIalpha, inducing the same effect as cGMP binding, namely kinase activation and thus vasorela

59 Allosteric kinase inhibitors, such as cGMP analogs, offer enhanced selectivity relative to com

60 Furthermore, attenuated cGMP signals led to impaired phosphodiesterase two depen

61 Basal cGMP level is strictly controlled by the opposing action

62 rster Resonance Energy Transfer (FRET)-based cGMP biosensor combined with scanning ion conductance mi

63 fluorescence resonance energy transfer-based cGMP biosensor cGi500, NO-induced elevation of cGMP was

64 d two tandem GAF domains, one of which binds cGMP noncatalytically.

65 atriuretic defect in SHR, we infused 8-bromo-cGMP.

66 inhibitor decreased sGC activity measured by cGMP production following stimulation with an NO donor.

67 iapoptotic effects were at least mediated by cGMP/PKG pathway.

68 nd activity of RyR2 were highly regulated by cGMP/PKG signaling.

69 has the unique property to be stimulated by cGMP, but primarily hydrolyzes cAMP.

70 +) channels of the BK type are stimulated by cGMP/cGMP-dependent protein kinase type I, and recent ex

71 dant than the free cellular messengers cAMP, cGMP, H(+) , and Ca(2+) .

72 ibroblasts, consistent with PDE10A as a cAMP/cGMP dual-specific PDE.

73 Changes in cAMP/cGMP levels, PKA/PKG and BDNF expression were also preve

74 ly expressing D2 receptors that inhibit cAMP/cGMP synthesis.

75 intensity and duration of D2-inhibited cAMP/cGMP signaling.SIGNIFICANCE STATEMENT In DYT1 transgenic

76 ively of D1-stimulated and D2-inhibited cAMP/cGMP signals.

77 expressing D1 receptors that stimulate cAMP/cGMP synthesis.

78 intensity and duration of D1-stimulated cAMP/cGMP signaling; conversely, the increase of PDE10A in th

79 nitive performance in AD are related to cAMP/cGMP-dependent pathways.

80 o known as Npr2 or NPR-B), increase cellular cGMP and cause skeletal overgrowth, but how these mutati

81 Moreover, cGK (cGMP-dependent protein kinase) activity was downregulate

82 ed synthesis of cGMP and activation of cGK1 (cGMP-dependent protein kinase 1) in cultured porcine val

83 evated cyclic guanosine monophosphate (cGMP)/cGMP-dependent protein kinase (PKG) signaling and upregu

84 hoprotein was increased in response to 8-CPT-cGMP treatment, but not when disulfide formation in PKGI

85 Cyclic cGMP-AMP synthase (cGAS) is a pattern recognition cytoso

86 in outer granulosa cells to rapidly decrease cGMP.

87 sing 967K or 1034F NPR-A displayed decreased cGMP production in response to ANP and BNP (all P<10(-6)

88 fic phosphodiesterases (PDEs), which degrade cGMP to guanosine monophosphate, play key role in contro

89 se and nitric oxide synthase (NOS)-dependent cGMP production.

90 their tissue-specific expression, different cGMP affinities, and isoform-specific protein-protein in

91 s (GCs), and mutations in genes that disrupt cGMP homeostasis leads to retinal degeneration in humans

92 d female transgenic mice wherein a disrupted cGMP-gated channel (CNG) gene can be repaired at the end

93 This substitution disrupts cGMP binding to the pocket, but it also unexpectedly cau

94 Our data strongly implicate two distinct cGMP-mediated cell death pathways, and suggest that ther

95 of nitric oxide synthase and the downstream cGMP kinase Foraging or PKG to restrict axon regrowth.

96 of GCAP1, is predicted to abnormally elevate cGMP production and Ca(2+) influx in photoreceptors in t

97 els prolongs rod survival caused by elevated cGMP in a PDE6 mutant mouse model.

98 photoreceptor cell death caused by elevated cGMP.

99 The channel/PDE5 tandem encodes cGMP turnover rates rather than concentrations.

100 A mutation in the human PRKG1 gene encoding cGMP-dependent protein kinase 1 (PKG1) leads to thoracic

101 ver, this pathway is regulated by endogenous cGMP/PKG2 signaling, and can be targeted using phosphodi

102 erved ejection fraction (HFpEF) by enhancing cGMP signaling and improving hemodynamics, but real-worl

103 Abeta42 reversed the DIO deficit in the eNOS/cGMP/PKG pathway and decreased endothelin-1.

104 om hibernation (GABARB1), breakdown of fats (cGMP-PK1), and vocalizations (FOXP2).

105 glutamine (RQ) substitution within the first cGMP-binding pocket in PKG1.

106 d selectivity for the 5'-vacancy, except for cGMP.

107 he C43S-mutant PKGIalpha has a higher Ka for cGMP.

108 ascular cells, ML290 was 10x more potent for cGMP accumulation and p-p38MAPK than for cAMP accumulati

109 ein is optimized for activity and primed for cGMP manufacture in preparation for upcoming clinical st

110 enching resonance energy transfer (QRET) for cGMP to monitor both sGC and PDE activities using high t

111 ge, this is the first synthetic receptor for cGMP, which also demonstrates a high preference to bind

112 contains a catalytic domain responsible for cGMP hydrolysis and two tandem GAF domains, one of which

113 It is known that CodY consists of a GAF (cGMP-stimulated phosphodiesterases, adenylate cyclases,

114 It participates in signaling by generating cGMP in response to nitric oxide (NO).

115 Cyclic GMP (cGMP) generated in the granulosa cells diffuses through

116 DE) enzymes are known to control cyclic GMP (cGMP) levels in the parasite, but the mechanisms by whic

117 e stable assembly of the retinal cyclic GMP (cGMP) phosphodiesterase (PDE6) holoenzyme.

118 subunit (Galpha(T).GTP) and the cyclic GMP (cGMP) phosphodiesterase 6 (PDE6), which stimulates cGMP

119 cal and basolateral secretion of cyclic GMP (cGMP) under baseline, unstimulated conditions.

120 xide, soluble guanylate cyclase, cyclic GMP (cGMP), and PKG.

121 endothelial NO synthase (eNOS), cyclic GMP (cGMP), and protein kinase G (PKG) activity independently

122 The parasite's cyclic GMP (cGMP)-dependent protein kinase (PKG) is essential at mul

123 ation but is unable to hydrolyze cyclic GMP (cGMP).

124 ransduction and vision because it hydrolyzes cGMP.

125 responsible for the UVA-induced decrease in cGMP in Arabidopsis.

126 and support the role of RyR2 upregulation in cGMP/PKG signaling-induced ER stress and photoreceptor d

127 Only formoterol increased cGMP.

128 In HCFs, ML290 increased cGMP accumulation but did not affect p-ERK1/2 and given

129 urine Na(+) excretion or renal interstitial cGMP in SHR.

130 conditions but did not enhance intracellular cGMP accumulation.

131 ides through the generation of intracellular cGMP, which interacts with specific enzymes and ion chan

132 peptide receptor A and reduces intracellular cGMP levels.

133 defect is abrogated by exogenous intrarenal cGMP, the renal cGMP pathway may represent a viable targ

134 ophy and exerts protective effects involving cGMP/cGK axis by repressing CDK blockers p21(Cip1) and p

135 s intracellular signaling pathways involving cGMP.

136 antigen display platforms and have launched cGMP manufacturing efforts to advance the SARS-CoV-2-RBD

137 e (Fe(3+)), is desensitized to NO and limits cGMP production needed for downstream activation of prot

138 REEP6 plays an essential role in maintaining cGMP homeostasis though facilitating the stability and/o

139 The current model is that PKG, a malarial cGMP-dependent protein kinase, triggers egress, activati

140 alue of approximately 0.2 microM and maximal cGMP formation at 10 microM.

141 Because the second messenger cGMP exerts a central role in LTP mechanisms, here we st

142 ter rate of turnover of the second messenger cGMP in darkness; and (3) an accelerated rate of decay o

143 riphosphate to an important second messenger cGMP.

144 entalize the flagellum: Within milliseconds, cGMP is relayed from the receptor guanylate cyclase to a

145 stigate whether the intradisulfide modulates cGMP binding, real-time imaging was performed in vascula

146 vels of AT(2)R downstream signaling molecule cGMP (cyclic guanosine 3',5' monophosphate) from 0.91+/-

147 llular cyclic guanosine 3',5'-monophosphate (cGMP) and subsequent vascular smooth muscle relaxation.

148 The cyclic guanosine-3',5'-monophosphate (cGMP)-dependent protein kinase (PKG) was identified >25

149 ne-permeable cyclic guanosine monophosphate (cGMP) analog on KATP channel activity and insulin secret

150 eceptors and cyclic guanosine monophosphate (cGMP) are implicated in the response to sexual cues, whi

151 lower basal cyclic guanosine monophosphate (cGMP) concentrations than in wild-type dogs, which could

152 senger 3',5'-cyclic guanosine monophosphate (cGMP) have been shown to protect from heart failure.

153 response for cyclic guanosine monophosphate (cGMP) in an aqueous solution.

154 eased plasma cyclic guanosine monophosphate (cGMP) in normal sheep (p < 0.05) while concurrently redu

155 ) hydrolyzes cyclic guanosine monophosphate (cGMP) leading to increased levels of the cAMP response e

156 yclase (sGC)-cyclic guanosine monophosphate (cGMP) pathway regulates diverse set of important physiol

157 The cyclic guanosine monophosphate (cGMP) specific phosphodiesterase type 5 (PDE5) plays an

158 e (cAMP) and cyclic guanosine monophosphate (cGMP), is preferentially expressed in neurons of CA1, th

159 nafil in the cyclic guanosine monophosphate (cGMP)-activated protein kinase G (PKG) axis.

160 egans in the cyclic guanosine monophosphate (cGMP)-bound open state.

161 #3 relies on cyclic guanosine monophosphate (cGMP)-gated channels and activity of the ASJ, AWB, and A

162 The elevated cyclic guanosine monophosphate (cGMP)/cGMP-dependent protein kinase (PKG) signaling and

163 le cells expressing 541S NPR-A produced more cGMP compared with cells expressing wild-type NPR-A (P<=

164 ts were independent of changes in myocardial cGMP content and were associated with upregulation of bo

165 Low myocardial cGMP-PKG (cyclic guanosine monophosphate-protein kinase

166 ite-directed mutagenesis, we show that 8-NBD-cGMP inhibits PfPKG not simply by reverting a two-state

167 Here, we show that 8-NBD-cGMP is an effective PfPKG antagonist.

168 red phosphodiesterase two dependent negative cGMP-to-cAMP cross-talk.

169 evidence point to impaired nitric oxide (NO)-cGMP bioavailability as playing a central role in each o

170 C is the major mediator of nitric oxide (NO)-cGMP signaling in cells that, upon NO binding, catalyzes

171 nylyl cyclase (sGC) is a key component of NO-cGMP signaling in mammals.

172 st free-living animals, the complexity of NO-cGMP-mediated signaling in Placozoa is greater to those

173 apies, an alternative strategy to restore NO-cGMP signaling is via inorganic nitrite.

174 is study strongly suggests that targeting NO-cGMP signaling pathways may be a novel therapeutic strat

175 oxide (NO) and a central component of the NO-cGMP pathway, critical to cardiovascular function.

176 nhibitory gamma-subunit and the noncatalytic cGMP to the GAFa domains of rod PDE6, as well as a stabl

177 mulation and p38MAPK phosphorylation but not cGMP accumulation or ERK1/2 phosphorylation although pri

178 eeded that of the natural cyclic nucleotides cGMP or cAMP.

179 In this study, we tested the ability of cGMP and type 2 cGMP-dependent protein kinase (PKG2) to

180 PKG1 to have high activity in the absence of cGMP via an unknown mechanism.

181 opt an active conformation in the absence of cGMP, similar to that of cGMP-bound WT enzyme.

182 e-5 (PDE5) inhibitor causing accumulation of cGMP, is frequently used for treatment of PH.

183 mic domain of BRI1 generates pmol amounts of cGMP per mug protein with a preference for magnesium ove

184 nal changes to GAFab induced upon binding of cGMP and the PDE6 inhibitory gamma-subunit (Pgamma).

185 oy this approach to show that the binding of cGMP to pacemaking ion channels is weakened by a slower

186 ose a scheme in which cooperative binding of cGMP, beginning at the CNB closest to the KD, transmits

187 Depletion of cGMP by deleting retinal guanylate cyclase 1 or inhibiti

188 Depletion of cGMP or deletion of Ryr2 equivalently inhibited unfolded

189 , whether the molecular events downstream of cGMP involve BK channels present in cardiomyocytes or in

190 s, it is likely that at least one element of cGMP signaling in plants has evolved differently to the

191 MP biosensor cGi500, NO-induced elevation of cGMP was detected in real-time in IHCs but not in OHCs.

192 We demonstrate that the increase of cGMP levels by the phosphodiesterase-5 inhibitors silden

193 ime- and concentration-dependent increase of cGMP levels.

194 similar to those elicited by an increase of cGMP, suggesting that intradisulfide formation is associ

195 receptor ligands) maintain the low level of cGMP in the oocyte.

196 quires a reduction in the cytosolic level of cGMP.

197 Increased levels of cGMP decrease BP by inducing natriuresis, diuresis, and

198 witches in response to dynamic modulation of cGMP levels in the parasite.

199 n kinase G with the subsequent production of cGMP, which prompts the stimulation of NADPH oxidase and

200 from this work demonstrate the regulation of cGMP/PKG signaling on RyR2 in the retina and support the

201 pH and PKAc1 act as balancing regulators of cGMP metabolism to control egress.

202 kers to the 8-position of the purine ring of cGMP or cAMP.

203 ncreased apical and basolateral secretion of cGMP relative to the level under static conditions but d

204 catalysis, the physiological significance of cGMP binding to the GAF domains of PDE6 is unknown.

205 (+/-) valves, and CNP triggered synthesis of cGMP and activation of cGK1 (cGMP-dependent protein kina

206 upon NO binding, catalyzes the synthesis of cGMP and subsequently activates protein kinase G (PKG).

207 to examine two distinct cellular targets of cGMP: the cGMP-gated (CNG) channels and protein kinase G

208 n in the absence of cGMP, similar to that of cGMP-bound WT enzyme.

209 cade; an increase in the rate of turnover of cGMP in darkness; and an increase in the rate of decay o

210 odule outputs were fitted to kinetic data on cGMP activity and early membrane potential changes measu

211 he homodimer and allosteric perturbations on cGMP binding.

212 ctional BRI1 kinase is essential for optimal cGMP generation.

213 itors increase the intracellular cAMP and/or cGMP activities, which may ameliorate cognitive deficits

214 t binding of cyclic nucleotides (cAMP and/or cGMP), but the allosteric mechanism by which this occurs

215 direct binding of cyclic nucleotide (cAMP or cGMP) to a cytoplasmic region of the channel.

216 lase (sGC), a key enzyme in the nitric oxide/cGMP signaling pathway.

217 g-term potentiation through the nitric oxide/cGMP/protein kinase G intracellular cascade consistent w

218 rs and are mediated through the nitric oxide/cGMP/protein kinase G pathway.

219 The ability of resveratrol to oxidize cGMP-dependent PKG1alpha (protein kinase 1alpha) was ass

220 us allosteric states (Palphabeta, Palphabeta-cGMP, Palphabetagamma(2), and Palphabetagamma(2)-cGMP) w

221 In these pathways, cGMP-AMP synthase (cGAS) and the pyrin and HIN domain fa

222 This occurs by two complementary pathways: cGMP production is decreased by dephosphorylation and in

223 On the other hand, FAT10 inhibits PDE6 cGMP hydrolyzing activity by noncovalently interacting w

224 ect on HSP90 binding, the modulation of PDE6 cGMP levels was impaired.

225 es the effector enzyme of phototransduction, cGMP phosphodiesterase 6 (PDE6).

226 ir function can be studied with sub-picomole cGMP sensitivity.

227 ers, quality-of-life (QOL) score, and plasma cGMP concentrations before and after sildenafil therapy.

228 OL score with sildenafil treatment by plasma cGMP level and by the PDE5A:E90K polymorphic status.

229 ved after sildenafil therapy, and the plasma cGMP concentration was significantly decreased.

230 the NIH current good manufacturing practice (cGMP) environment.

231 eld of current good manufacturing practices (cGMP) based on biopharmaceutical industry standards and

232 ost of current Good Manufacturing Practices (cGMP) production.

233 expression of a phosphodiesterase to prevent cGMP buildup.

234 t with current good manufacturing processes (cGMPs).

235 es the phosphorylation profile of a putative cGMP-phosphodiesterase.

236 assium-atpase) and phosphorylation of AT(2)R-cGMP downstream signaling molecules Src (Src family kina

237 s, we investigated whether agents that raise cGMP may also regulate protein degradation.

238 l protein degradation, and agents that raise cGMP may help combat the progression of neurodegenerativ

239 Raising cGMP, like raising cAMP, stimulated the degradation of s

240 In cells and cell extracts, raising cGMP also enhanced within minutes ubiquitin conjugation

241 We also tested if raising cGMP, like cAMP, can promote the degradation of mutant p

242 ease in the granulosa cells results in rapid cGMP diffusion out of the oocyte, initiating meiotic res

243 nct from atrial natriuretic peptide receptor-cGMP-PKG-RyR2 Ser-2808 signaling and independent of musc

244 A significant decrease in renal cGMP levels and cGK activity was observed in 0-copy mice

245 ated by exogenous intrarenal cGMP, the renal cGMP pathway may represent a viable target for the treat

246 to facilitate the stable assembly of retinal cGMP phosphodiesterase, PDE6.

247 The Cngb1 locus-encoded beta-subunit of rod cGMP-gated cation channel and associated glutamic acid r

248 interaction with HSP90 and modulate the rod cGMP PDE6 stability and activity.

249 a functional soluble guanylyl cyclase (sGC)-cGMP signaling pathway and was diminished upon small int

250 Aarsd1, STIP1, and Cdc37) and an active sGC-cGMP signaling pathway to promote heme insertion into im

251 Specific cGMP analogs are able to act as partial agonists of PfPK

252 We first showed that CRRL269 stimulated cGMP generation, suppressed plasma angiotensin II, and r

253 n and activity is critical for NO-stimulated cGMP production and vasodilation.

254 GEP1 disruption abolishes XA-stimulated cGMP synthesis and the subsequent signaling and cellular

255 phosphodiesterase 6 (PDE6), which stimulates cGMP hydrolysis, leading to hyperpolarization of the pho

256 these receptors and a change of subcellular cGMP compartmentation.

257 D) critical for activation of the C-terminal cGMP-synthesizing guanylyl cyclase domain.

258 than has been previously published and that cGMP acts as a weak partial SthK agonist.

259 Here, we report that cGMP-AMP synthase (cGAS), a DNA sensor, is a critical re

260 We showed that cGMP synthesis was significantly elevated by ERG in PCa

261 Taken together, our results suggest that cGMP acts as a modulator that enhances downstream signal

262 Our data suggest that cGMP positively regulates Abeta levels in the healthy br

263 The cGMP decrease in the granulosa cells results in rapid cG

264 with both the ligand-free, inactive and the cGMP-bound, active states.

265 RhoBTB1 augmented the cGMP response to nitric oxide by restraining the activit

266 e two distinct cellular targets of cGMP: the cGMP-gated (CNG) channels and protein kinase G (PRKG), a

267 s expressing a FRET-biosensor comprising the cGMP-binding sites of PKGIalpha.

268 ophosphate, play key role in controlling the cGMP level and the strength or length of the cGMP-depend

269 We have determined the cGMP-free crystallographic structures of PKG from Plasmo

270 hibit PfPKG, without losing affinity for the cGMP analog.

271 sociated variants affect NPR-A function, the cGMP response to ANP and BNP was measured in cells expre

272 , resulting in significant elevations in the cGMP/NP ratio in both states (p < 0.001 and p < 0.05, re

273 Moreover, the cGMP-induced enhancement of LTP and memory was disrupted

274 merized forms of protein kinase G and of the cGMP hydrolyzing phosphodiesterases 2 and 3.

275 cardial infarction, causes a decrease of the cGMP levels generated by these receptors and a change of

276 ioning or pharmacological stimulation of the cGMP pathway and by using direct modulators of BK.

277 lyl cyclase activation and inhibition of the cGMP-degrading phosphodiesterase-5, ischemic preconditio

278 cGMP level and the strength or length of the cGMP-dependent cellular signaling.

279 Concordantly, inhibition of the cGMP-dependent protein kinase G (PKG) blocks egress indu

280 ulin secretion point to participation of the cGMP/PKG and cAMP/PKA/Epac (exchange protein directly ac

281 tibodies or APP knock-out mice, prevents the cGMP-dependent enhancement of LTP and memory.

282 Genetic studies demonstrate that the cGMP-dependent protein kinase EGL-4 determines the times

283 onstrate that the extent of agonism by these cGMP derivatives relates to the degree of stabilization

284 cyte injury and prevents proteinuria through cGMP- and PKG-dependent binding of PPAR-gamma to the TRP

285 Signaling through cGMP has therapeutic potential in the colon, where it ha

286 nsitizes cyclic nucleotide gated channels to cGMP and causes photoreceptor cell death.

287 ing the C43S mutation was less responsive to cGMP-induced activation.

288 igates the potential contribution of RyR2 to cGMP/PKG signaling-induced ER stress and cone degenerati

289 ular conversion of guanosine triphosphate to cGMP (cyclic 3',5'-guanosine monophosphate) on binding o

290 A or elevated pH are required for triggering cGMP/PKG dependent gametogenesis.

291 Promising formulations were produced under cGMP conditions and advanced to a full-scale stability s

292 PDE9-I dose-dependently increased urinary cGMP in both states (both p < 0.001).

293 We demonstrate that using cGMP-specific antibody, sGC or PDE activity and the effe

294 sis is central to photoreceptor cells, where cGMP is the signal transducing molecule in the light res

295 Unlike related GAF-containing PDEs where cGMP binding allosterically activates catalysis, the phy

296 e in LTP mechanisms, here we studied whether cGMP affects Abeta levels and function during LTP.

297 To test whether cGMP could bypass the natriuretic defect in SHR, we infu

298 ity of BRI1 is modulated by the kinase while cGMP, the product of the guanylate cyclase, in turn inhi

299 In addition, treatment with cGMP significantly enhanced Ryr2 expression in cultured

300 e or Angeli's salt induced disulfides within cGMP-dependent protein kinase I-alpha (PKGIalpha), an in