ライフサイエンスコーパス: PDE

1 PDE activity is required for robust replication in myelo

2 PDE is caused by mutations in ALDH7A1, also known as ant

3 PDE is characterized by recurrent seizures that are resi

4 PDE levels of PDGF-AA, platelet glycoprotein VI, integri

5 PDEs controlling natriuretic-peptide-coupled cGMP remain

6 including activation of phosphodiesterase-1 (PDE-1), dampen the rise of cGMP.

7 Modulation of 2'-PDE represents a unique therapeutic approach for regulat

8 Systemic oral phosphodiesterase type 4 (PDE-4) inhibitors have been effective in the treatment o

9 ecting both humans and animals, encode 2',5'-PDEs capable of antagonizing RNase L.

10 With this system, we found that 2',5'-PDEs encoded by the human coronavirus HCoV-OC43 (OC43; a

11 iruses encode proteins with homologous 2',5'-PDEs that antagonize activation of innate immunity.

12 showed that 2',5'-phosphodiesterases (2',5'-PDEs) encoded by the prototypical Betacoronavirus, mouse

13 -CoV, encode 2',5'-phosphodiesterases (2',5'-PDEs) that antagonize the OAS-RNase L pathway, and we re

14 The consistent structural alignment of 57 PDE ligand binding site residues enables the systematic

15 Roflumilast cream contains a PDE-4 inhibitor that is being investigated for the topic

16 phosphodiesterase 3A (PDE3A) gene encodes a PDE that regulates cardiac myocyte cyclic adenosine mono

17 ls by deletion of the pdeA gene coding for a PDE promoted biofilm formation in Streptococcus mutans.

18 We show that pGpG inhibits a PDE-A from Pseudomonas aeruginosa.

19 We predict that levosimendan, a PDE inhibitor for heart failure, inhibits serine/threoni

20 es to show that the isolated EAL domain of a PDE from Escherichia coli (YahA) is in a fast thermodyna

21 ase A (PKA) R-subunit through formation of a PDE-PKAR-cyclic adenosine monophosphate (cAMP) complex (

22 specifically inhibited DisA but not YybT (a PDE) whilst TA was more promiscuous and inhibited both D

23 9,10-tetrahydrobenzo[a]pyrene (dG-N (2) -B[a]PDE) were not detected in any specimen, whereas N-(deoxy

24 8,9,10-tetrahydrobenzo[a]pyrene (dG-N(2)-B[a]PDE); the aromatic amine 4-aminobiphenyl (4-ABP), N-(deo

25 of cAMP signal amplification by accelerated PDE-mediated cAMP turnover.

26 ium spiny neuron-enriched and cGMP-activated PDE, in AMPAR trafficking.

27 me, thereby reducing the number of activated PDE molecules.

28 nd) form of Tr*, we found that Tr* activated PDE at a similar efficiency in rods and cones.

29 By activating PDE with known concentrations of the active (guanosine 5

30 Active PDE then hydrolyzes anti-inflammatory cAMP to facilitate

31 Additionally, PDEs encoded by OC43 and BEV rescue MHV(Mut) replication

32 we show that atropine acts as an allosteric PDE type 4 (PDE4) inhibitor.

33 atial model with interacting agent-based and PDE components).

34 larly on those proteins bearing both DGC and PDE modules, and for future optimization studies to targ

35 In a dual DGC and PDE-A reaction, excess pGpG extends the half-life of c-d

36 Elevated EDE and PDE levels of atherosclerosis-promoting proteins in CeVD

37 osphodiesterase-5 (PDE5) gene expression and PDE activity is significantly reduced in penile tissues

38 drug molecules, including COX, ACE, MAO, and PDE inhibitors, have been successfully [(18)F]-labeled i

39 In this study, PKAR and PDE from Dictyostelium discoideum (RD and RegA, respecti

40 , allowing optimization of PDE1B potency and PDE selectivity.

41 sfer (QRET) for cGMP to monitor both sGC and PDE activities using high throughput screening adoptable

42 ria typically encode many different DGCs and PDEs within their genomes.

43 a sophisticated interaction between DGCs and PDEs.

44 rgeted classes of cAMP modulators, GPCRs and PDEs.

45 y map cAMP gradients at the nanoscale around PDE molecules and the areas of resulting downstream acti

46 e monophosphate have been attempted, such as PDE-3 or PDE-5 inhibition (with negative or neutral resu

47 exogenously provided cholesterol augmented, PDE inhibitor-induced steroidogenesis, suggesting that t

48 ion may provide a further level of bacterial PDE regulation.

49 PDE6C increased the basal PDE activity and speeded the rate-limiting step for phot

50 tigated pharmacokinetic interactions between PDE-Is (cilostazol and sildenafil) and rifampin.

51 trations ranges overlapped partially between PDE patients and control groups.

52 ith a large fraction of cAMP being buffered, PDEs can create nanometer-size domains of low cAMP conce

53 ssociation from sGC, and cGMP degradation by PDE, exerted a dominant influence on cGMP accumulation r

54 nosine monophosphate is mainly hydrolyzed by PDE (phosphodiesterases) 5a and 9a.

55 The termination phase is initiated by PDEs actively targeting the protein kinase A (PKA) R-sub

56 control of nanometer-size domains shaped by PDEs that gate activation of downstream effectors.

57 P-mediated sequestration of the R-subunit by PDEs.

58 study, we identify PDE10A as the major cAMP PDE in mouse striatum and monitor PKA-dependent PDE10A p

59 ting for only a small fraction of renal cAMP PDE activity.

60 G15) had a ~15-fold increase in cardiac cAMP-PDE activity and a ~30% decrease in cAMP content and fra

61 lting in a ~50-fold increase in cardiac cAMP-PDE activity caused a ~50% decrease in fractional shorte

62 s/mouse) had a ~50% increase in cardiac cAMP-PDE activity, which did not modify basal cardiac functio

63 PKA/EPAC that are regulated by specific cAMP-PDEs (the PDE-regulated phosphoproteomes).

64 substructure analysis of the cocrystallized PDE ligands in combination with those in the ChEMBL data

65 Fifteen patients with molecularly confirmed PDE were detected using liquid chromatography-mass spect

66 Unlike related GAF-containing PDEs where cGMP binding allosterically activates catalys

67 its, this mechanism is able to use a cyclase/PDE enzyme pair to dynamically control a cyclic nucleoti

68 Herein, we demonstrate PDE-4 inhibition as a therapeutic strategy to ameliorate

69 show that calcium- and calmodulin-dependent PDEs (PDE1A and PDE1C) and PDE3A modulate the developmen

70 and inhibited the activity of EAL-dependent PDEs (PA2133, PvrR, and purified recombinant RocR) from

71 pG exert product inhibition on EAL-dependent PDEs, thereby increasing intracellular c-di-GMP in Delta

72 reus produces a second cytoplasmic DHH/DHHA1 PDE Pde2.

73 The role of different PDE isozymes, particularly PDE3A vs PDE3B, in the regula

74 n be defined by their responses to different PDE inhibitors.

75 ogy for understanding the roles of different PDEs in the regulation of cyclic nucleotide signaling.

76 ynergistic relationships among the different PDEs that coordinate cAMP-signaling cascades in these ce

77 ylation occurs unless at least two different PDEs are concurrently inhibited in these cells.

78 In Jurkat cells we find multiple, distinct PDE-regulated phosphoproteomes that can be defined by th

79 osphoproteome analyses of myocytes with each PDE selectively inhibited reveals substantial differenti

80 lated from the peritoneal dialysis effluent (PDE) of noninfected uremic patients.

81 ter benefits compared with inhibiting either PDE alone.

82 150 bp periodic downstream sequence element (PDE) following the typical pause location, strongly sugg

83 Programmed DNA elimination (PDE) plays a crucial role in the transitions between ger

84 levels via overexpression of genes encoding PDEs.

85 previously published pseudopodium-enriched (PDE) protein/phosphoprotein datasets to identify novel P

86 Pyridoxine-dependent epilepsy (PDE) is a rare autosomal recessive disease caused by mut

87 ividuals with pyridoxine-dependent epilepsy (PDE).

88 diagnosis of pyridoxine-dependent epilepsy (PDE).

89 ion-diffusion partial differential equation (PDE) models have been only occasionally used since they

90 ion-diffusion partial differential equation (PDE).

91 solution of a partial differential equation (PDE).

92 Partial differential equations (PDE) were built to model a radially symmetric reaction-d

93 The partial differential equations (PDEs) are derived using the extended Hamilton's principl

94 solution of partial differential equations (PDEs) is challenging because of the need to resolve spat

95 ric MHV system (MHV(Mut)) in which exogenous PDEs were expressed from an MHV backbone lacking the gen

96 osomes (EDEs) and platelet-derived exosomes (PDEs) were precipitated and enriched separately by immun

97 validated using the patient-derived explant (PDE) model.

98 e enzyme PDE10A is the most highly expressed PDE in striatal medium-sized spiny neurons (MSNs) with l

99 rea under the curve [AUC] = 0.926), even for PDE patients (AUC = 0.901, sensitivity = 0.857, specific

100 P6C (AASA-P6C) in all types of samples from PDE patients were markedly elevated.

101 ution in the HD dyad caused loss of c-di-GMP PDE activity and of two iron atoms.

102 d biochemical characterization of a c-di-GMP PDE, PdcA, 1 of 37 confirmed or putative c-di-GMP metabo

103 One class of c-di-GMP PDEs contains a characteristic HD-GYP domain.

104 converging to the solution of the governing PDE.

105 d on an analysis of the phosphodiesterase I (PDE I)-mediated size variation of a fluorescein-labeled

106 In PDE cortex, antiquitin immunofluorescence was greatly at

107 gative modulator of TLRs that we detected in PDE, inhibited PDE-induced, TLR2- or TLR4-mediated profi

108 ught to determine age-related differences in PDE activity and associated intracellular signaling resp

109 tribution of antiquitin, its distribution in PDE, and associated brain malformations.

110 l cells in the brain, and its dysfunction in PDE is associated with neuronal migration abnormalities

111 usly quantify multiple lysine metabolites in PDE, including alpha-aminoadipic semialdehyde (a-AASA),

112 the large diversity of chemical scaffolds in PDE ligands.

113 bsence (with GTPgammaS) of Tr* inactivation, PDE activation required more light (and was therefore le

114 ant of MHV (ns2(H126R)) encoding an inactive PDE fails to antagonize RNase L activation and replicate

115 ne is limited by counter-adaptions including PDE upregulation.

116 tion of pGpG in the orn strain could inhibit PDE-As, increasing c-di-GMP concentration.

117 r of TLRs that we detected in PDE, inhibited PDE-induced, TLR2- or TLR4-mediated profibrotic response

118 cAMP levels, PDE activity, and phospholamban phosphorylation (pPLB) w

119 games for which the behavior of the limiting PDE is not known.

120 ent phosphodiesterase PDE-1 and co-localizes PDE-1 with molecular sensors for CO(2) at dendritic ends

121 data suggest that whereas PDE4 is the major PDE isoform involved in the regulation of global intrace

122 Our results using PDE8 as a model PDE, reveal that PDEs mediate active hydrolysis of cAMP

123 RmdB from S. venezuelae is a monofunctional PDE that hydrolyzes c-di-GMP to 5'pGpG.

124 Most PDE patients also suffer from neurodevelopmental deficit

125 Whereas most PDEs have accessory domains that are involved in the reg

126 mising drug target with the emergence of new PDE inhibitors and a novel PKA target protein, HSP20, wh

127 o imaging data were also fit well by the new PDE model, with estimates of the dissociation constant (

128 ce of well-established and potentially novel PDE-dependent mechanisms that regulate cGMP under physio

129 cellular levels of cAMP by cyclic nucleotide PDE inhibition both suppresses the immune response and i

130 we examined the efficiency of activation of PDE by activated Tr (Tr*).

131 Processing of BdlA leads to activation of PDE DipA, which results in a net reduction of c-di-GMP a

132 Histologic analysis of PDE cortex revealed areas of abnormal radial neuronal or

133 residues enables the systematic analysis of PDE-ligand interaction fingerprints (IFPs), the identifi

134 E8-RIalpha complex represents a new class of PDE-based complexes for specific drug discovery targetin

135 In a comparison of PDE activation in the presence (with GTP) and absence (w

136 y regulating the splicing and degradation of PDE transcripts.

137 ed to an ongoing surge in the development of PDE inhibitors as lead compounds for trypanocidal drugs.

138 remaining difference in the effectiveness of PDE activation between rods and cones.

139 The lower effectiveness of PDE activation in carp cones is due partly to the fact t

140 Furthermore, we examine the effects of PDE-4 inhibition by pharmacologic treatment in the fragi

141 tions trigger a reduction in the fidelity of PDE compartmentalization.

142 ality of cAMP concentration as a function of PDE concentration are both altered by GIV levels.

143 We assessed the impact of PDE-Is on the duration of treatment in tuberculous mice.

144 We demonstrate that acute inhibition of PDE-4 by pharmacologic treatment in hippocampal slices r

145 pharmacological and genetic manipulation of PDE activity, we found that the rise in cAMP resulting f

146 brain tissue was utilized for measurement of PDE-associated metabolites and Western blot analysis.

147 mutant TNNT2 and epigenetic modifications of PDE genes in both DCM iPSC-CMs and patient tissue.

148 vel, it is not clear whether perturbation of PDE alone, under oxidative stress, is the best approach

149 gest that a disturbance in the regulation of PDE-coupled CNs linked to N-type Ca(2+) channels is an e

150 erstanding of the structural requirements of PDE binding that will be useful in future drug discovery

151 p54(nrb)/NONO in regulating the stability of PDE transcripts by facilitating the interaction between

152 )/NONO regulates the splicing of a subset of PDE isoforms.

153 Finder (ADFinder), an efficient detector of PDEs using high-throughput sequencing data.

154 to understand the regulation and function of PDEs in SMC pathogenesis of vascular diseases.

155 is the first instance, to our knowledge, of PDEs directly interacting with a cAMP-receptor protein i

156 This software will facilitate research of PDEs and all down-stream analyses.

157 en the I-site of DGCs and the active site of PDEs; this molecule represents a novel tool for mechanis

158 tely integrable hydrodynamic-type systems of PDEs - which provides explicit finite-size solutions, ma

159 icellular systems require solving systems of PDEs for release, uptake, decay and diffusion of multipl

160 difications, as well as the potential use of PDEs as disease biomarkers.

161 the Protein Data Bank (PDB) with a focus on PDE-ligand interactions.

162 PDE1 is the only PDE family activated by Ca(2+), which is reduced in PKD

163 Reducing ARCP-1 or PDE-1 activity promotes CO(2) escape by altering neurope

164 sphate have been attempted, such as PDE-3 or PDE-5 inhibition (with negative or neutral results), NO-

165 te that using cGMP-specific antibody, sGC or PDE activity and the effect of small molecules modulatin

166 0.39 nM, ~100-fold selectivity versus other PDE enzymes, clean cytochrome P450 profile, in vivo targ

167 0.49, and >5000-fold selectivity over other PDEs, fully attenuates MK-801-induced hyperlocomotor act

168 n but enhanced selectivity against the other PDEs.

169 OvC-PDE cultures retained the original tumour architecture a

170 OvC-PDE cultures were exposed to standard-of-care chemothera

171 We established an OvC-PDE dynamic culture in which tumour architecture and cel

172 a long-term OvC patient-derived explant (OvC-PDE) culture strategy in which architecture and cell typ

173 In addition, PdcA PDE activity is allosterically regulated by GTP, further

174 d ADORA2B signaling underlies reduced penile PDE activity by decreasing PDE5 gene expression in a HIF

175 binds the Ca(2+)-dependent phosphodiesterase PDE-1 and co-localizes PDE-1 with molecular sensors for

176 Phosphodiesterase (PDE) 10A is an enzyme involved in the regulation of cycl

177 Phosphodiesterase (PDE) enzymes are known to control cyclic GMP (cGMP) leve

178 s is presented of the 220 phosphodiesterase (PDE) catalytic domain crystal structures present in the

179 s RVs relies on its 2'-5'-phosphodiesterase (PDE) domain to counteract RNase L-mediated antiviral sig

180 rotein 2 (ns2) is a 2',5'-phosphodiesterase (PDE) that cleaves 2-5A, thereby antagonizing RNase L act

181 and that treatment with a phosphodiesterase (PDE) 4 inhibitor rolipram rescues the decrease in cAMP.

182 portion of p70 includes a phosphodiesterase (PDE) domain and an oligonucleotide/oligosaccharide bindi

183 hat produces c-di-AMP and phosphodiesterase (PDE) that degrades c-di-AMP.

184 lymphocytes (CRTh2), and phosphodiesterase (PDE)-4 inhibitors.

185 enzymes and hydrolyzed by phosphodiesterase (PDE) enzymes.

186 ghly homologous catalytic phosphodiesterase (PDE) domain.

187 s to activate 50% of cGMP phosphodiesterase (PDE).

188 /DHHA1) domain-containing phosphodiesterase (PDE) GdpP, S. aureus produces a second cytoplasmic DHH/D

189 ors of the cGMP-degrading phosphodiesterase (PDE) 5 have achieved blockbuster status in the treatment

190 ion of c-di-GMP-degrading phosphodiesterase (PDE) activity.

191 re, we show that the dual phosphodiesterase (PDE)7- glycogen synthase kinase (GSK)3 inhibitor, VP3.15

192 of clinically established phosphodiesterase (PDE) families.

193 and a C-terminal c-di-GMP phosphodiesterase (PDE) domain.

194 the nitric oxide (NO)-GMP-phosphodiesterase (PDE) pathway, the evaluation of nitrates, synthetic natr

195 our effort in identifying phosphodiesterase (PDE) 4B-preferring inhibitors for the treatment of centr

196 differential switching in phosphodiesterase (PDE) activity.

197 he expression of multiple phosphodiesterase (PDE) isoforms, including PDE2A, PDE3A, PDE3B, PDE4A, PDE

198 l 3',5'-cyclic nucleotide phosphodiesterase (PDE) inhibitors, concentrating on both experimental and

199 t combining inhibitors of phosphodiesterase (PDE) 3 and PDE4 provides greater benefits compared with

200 The effects of phosphodiesterase (PDE) 4 inhibitors on gene expression changes in BEAS-2B

201 On average around one phosphodiesterase (PDE) molecule is spontaneously active per mouse compartm

202 memory formation, but the phosphodiesterase (PDE) involved remains unknown.

203 RET approach and in vitro phosphodiesterase (PDE) activity assays, we show that atropine acts as an a

204 Phosphodiesterases (PDE-As) end signaling by linearizing c-di-GMP to 5'-phos

205 n of cAMP degradation by phosphodiesterases (PDE) likely has an important role, because cAMP is inact

206 cellular cAMP gradients, phosphodiesterases (PDE) mediate fundamental aspects of brain function relev

207 Cyclic nucleotide phosphodiesterases (PDE) break down cyclic nucleotides such as cAMP and cGMP

208 Phosphodiesterases (PDEs) are a family of enzymes that break down cGMP and c

209 Phosphodiesterases (PDEs) are a superfamily of enzymes that catalyze the bre

210 Phosphodiesterases (PDEs) are enzymes responsible for catalyzing hydrolysis

211 Phosphodiesterases (PDEs), enzymes that degrade 3',5'-cyclic nucleotides, ar

212 ynthesizing c-di-GMP and phosphodiesterases (PDEs) for degrading c-di-GMP.

213 nylyl cyclases (ACs) and phosphodiesterases (PDEs) since their discoveries 40 years ago, downstream c

214 ) and cAMP hydrolysis by phosphodiesterases (PDEs) (termination phase).

215 levels are regulated by phosphodiesterases (PDEs), with PDE4s predominantly responsible for cAMP deg

216 lases and degradation by phosphodiesterases (PDEs).

217 GPCRs) and attenuated by phosphodiesterases (PDEs).

218 yclic nucleotide coupled phosphodiesterases (PDEs) play a key role limiting the hydrolysis of cAMP an

219 tors, adenylyl cyclases, phosphodiesterases (PDEs)), and receptor tyrosine kinases involved in growth

220 GMP (c-di-GMP)-degrading phosphodiesterases (PDEs) and the chemosensory protein BdlA, with BdlA playi

221 cificity, cAMP-degrading phosphodiesterases (PDEs) have been suggested to confine cAMP to distinct ce

222 atalytic site of the EAL phosphodiesterases (PDEs).

223 e cAMP-degrading enzymes phosphodiesterases (PDEs) play a key role in shaping local changes in cAMP.

224 cAMP-degrading enzymes, phosphodiesterases (PDEs), localise to specific subcellular domains within w

225 d CdgC, and the c-di-GMP phosphodiesterases (PDEs) RmdA and RmdB, are poorly understood.

226 le, c-di-GMP hydrolysing phosphodiesterases (PDEs) have been identified as key targets to aid develop

227 Cyclic nucleotide phosphodiesterases (PDEs) catalyze the breakdown of cAMP, thereby regulating

228 ferent cyclic nucleotide phosphodiesterases (PDEs) have not yet been identified in most cell types.

229 sis by cyclic nucleotide phosphodiesterases (PDEs) is a critical determinant of the amplitude, durati

230 making cyclic nucleotide phosphodiesterases (PDEs) potential regulators of synaptic strength.

231 Cyclic nucleotide phosphodiesterases (PDEs), through degradation of cyclic nucleotides, play c

232 ety of cyclic nucleotide phosphodiesterases (PDEs), which play a critical role in the regulation of c

233 ted by cyclic nucleotide phosphodiesterases (PDEs).

234 effects of inhibition of phosphodiesterases (PDEs).

235 ylate cyclases (DGCs) or phosphodiesterases (PDEs) were screened for their involvement in low-tempera

236 al c-di-GMP synthases or phosphodiesterases (PDEs).

237 ctivity versus the other phosphodiesterases (PDEs).

238 cGMP-specific phosphodiesterases (PDEs), which degrade cGMP to guanosine monophosphate, pl

239 ded by c-di-GMP-specific phosphodiesterases (PDEs).

240 yclases and cdG-specific phosphodiesterases (PDEs).

241 the latter via specific phosphodiesterases (PDEs).

242 iPSC-CMs, we found that phosphodiesterases (PDEs) 2A and PDE3A were upregulated in DCM iPSC-CMs and

243 been recently shown that phosphodiesterases (PDEs) can catalyze dissociation of bound cAMP and thereb

244 be hydrolyzed by various phosphodiesterases (PDEs).

245 regulate the dynamic interplay between PKAR, PDE, and cAMP are unclear.

246 ysine metabolites were present in postmortem PDE cortex.

247 ADFinder can predict PDEs with relatively low sequencing coverage, detect mul

248 we identified that Orn serves as the primary PDE-B enzyme that removes pGpG, which is necessary to co

249 y activity, as well as SureChEMBL for recent PDE related patents, to provide a wider context for expl

250 of PDE1, the only family of Ca(2+)-regulated PDEs, also induced a mitogenic response to AVP in NHK ce

251 th BdlA playing a pivotal role in regulating PDE activity and enabling dispersion in response to a wi

252 of the intramolecular mechanisms regulating PDE function and trafficking is emerging, making these p

253 selectivity (>6000-fold) over other related PDEs but with a poor pharmacokinetic profile.

254 ole of cAMP hydrolysis and the most relevant PDEs in the pathogenesis of PKD, we examined cyst develo

255 The RVA PDE forms the carboxy-terminal domain of the minor core

256 vated form of sGC, and phosphodiesterase(s) (PDE).

257 inder is effective in predicting large scale PDEs.

258 between the exoribonuclease XRN2 and select PDE transcripts.

259 )/NONO led to increased expression of select PDE isoforms revealed that p54(nrb)/NONO regulates the s

260 he effect of specific inhibition of selected PDEs on cardiac myocyte hypertrophic growth.

261 ew insights into how conserved and selective PDE interaction hot spots can accommodate the large dive

262 tabases ChEMBL and PDB for fragments showing PDE inhibitory activity, as well as SureChEMBL for recen

263 tis in children worldwide, encodes a similar PDE.

264 demonstrate that inactivation of this single PDE gene is sufficient to impact multiple c-di-GMP-depen

265 asured rates of fast cAMP diffusion and slow PDE activity render cAMP compartmentalization essentiall

266 ent with PDE10A as a cAMP/cGMP dual-specific PDE.

267 FPs), the identification of subtype-specific PDE-ligand interaction features, and the classification

268 Conventional approaches to study PDE function typically rely on measurements of global cA

269 oncept for the utility of the model to study PDE pathophysiology and to test new therapeutics.

270 odiesterase 10A (PDE10A) is a dual substrate PDE that can hydrolyze both cGMP and cAMP.

271 s novel strategies to therapeutically target PDE function, including enhancing catalytic activity, no

272 molecules by yet unidentified enzymes termed PDE-Bs.

273 ontent, and significantly higher levels than PDEs of the endothelial proteins vascular cell adhesion

274 sults using PDE8 as a model PDE, reveal that PDEs mediate active hydrolysis of cAMP bound to its rece

275 It was recently shown that PDEs interact with PKAR to initiate the termination phas

276 Thus, we sought to identify the PDE-B enzyme(s) responsible for pGpG degradation.

277 ytes to endogenous components present in the PDE of noninfected patients.

278 gests a role for substrate channeling in the PDE-dependent dissociation and hydrolysis of cAMP bound

279 cally interpretable mechanistic forms of the PDE terms which provides new insights into the biologica

280 hat are regulated by specific cAMP-PDEs (the PDE-regulated phosphoproteomes).

281 l domain and the linker connecting it to the PDE domain are disordered in the reported crystal struct

282 of cyclic nucleotide degrading enzymes, the PDEs.

283 Therefore, PDE isoform expression and activity strongly influence g

284 These PDEs were selected because of their importance in cross-

285 Nearly 80% of these PDEs are predicted to depend on the catalytic function o

286 creasing the expression or activity of these PDEs may, therefore, retard the development of PKD.

287 ants tested, deletions of six DGCs and three PDEs were found to affect these phenotypes at low temper

288 Thus, PDE inhibitors also have clear clinical applications.

289 hod for learning optimized approximations to PDEs based on actual solutions to the known underlying e

290 In addition, total PDE- and PDE3-specific activities were not altered in pe

291 In contrast, higher total PDE and PDE3 activities in adult IDC patients treated wi

292 patients on PDE3i demonstrated higher total PDE-specific (74.6+/-13.8 pmol/mg per minute) and PDE3-s

293 -based approach coupled with treatment using PDE isozyme-selective inhibitors to characterize the pho

294 vance, in that this identifies and validates PDE-4 inhibition as potential therapeutic intervention f

295 ow that compared to the parental strain, VP3 PDE mutant RVs replicated at low levels in the small int

296 d endothelial nitric oxide synthase, whereas PDEs had significantly higher levels of platelet glycopr

297 study, we analyzed tissue from a child with PDE as well as control human and murine brain to determi

298 Therapies for some of these disorders with PDE inhibitors have been successful at increasing cGMP l

299 Modeling of these systems with PDE models with Bayesian priors is necessary for quantit

300 PD patients with disease duration <=2 years (PDE).