ライフサイエンスコーパス: cAMP

1 cAMP binding rotates cytoplasmic domains to favor openin

2 cAMP opens cyclic nucleotide-gated channels allowing a C

3 cAMP produced in Tregs is involved in their suppression

4 cAMP-dependent membrane binding required the high-affini

5 cAMP-enhanced repair of cisplatin-induced DNA damage was

6 cAMP/PKA signalling is compartmentalised with tight spat

7 cyclase in S. aureus and only detected 2',3'-cAMP but not 3',5'-cAMP in cellular extracts.

8 ificant hit located in phosphodiesterase 4D, cAMP-specif (PDE4D) and 26 SNPs with P-values < 1*10(-5)

9 D is essential to discriminate between 3',5'-cAMP and the native substrate AdoMet.

10 s and only detected 2',3'-cAMP but not 3',5'-cAMP in cellular extracts.

11 However, it remains unclear whether 3',5'-cAMP is universally present in the Firmicutes group of b

12 that searching for proteins that bind 3',5'-cAMP might provide new insight into this question.

13 3',5'-cyclic adenosine monophosphate (3',5'-cAMP) plays important physiological roles, ranging from

14 culosis, organisms known to synthesize 3',5'-cAMP, did not bind this signaling nucleotide.

15 icates that S. aureus does not produce 3',5'-cAMP, which would otherwise competitively inhibit an ess

16 n all three domains of life as a tight 3',5'-cAMP-binding protein.

17 A cAMP increase was noted within 5 minutes of photostimula

18 exposed to increased TSH, a TSHR agonist, a cAMP analog, or a TSHR-stimulating antibody.

19 ipram (ROL; a PDE4 inhibitor) and Bt2cAMP (a cAMP mimetic) drive caspase-dependent resolution of neut

20 e through ADORA2A and ADORA2B receptors in a cAMP/PKA pathway-dependent mechanism to induce V-ATPase-

21 Epac is a cAMP-activated guanine nucleotide exchange factor that m

22 am of the PDF receptor, the former through a cAMP-independent mechanism and the latter through a cAMP

23 dependent mechanism and the latter through a cAMP-PKA dependent mechanism.

24 action causes MuSC expansion by triggering a cAMP/phosphoCREB pathway that activates the proliferatio

25 vo We therefore propose that RAS2 acts via a cAMP-dependent pathway and exerts significant metabolic

26 y activates orexigenic AgRP(+) neurons via a cAMP-dependent pathway.

27 ic adenosine monophosphate-protein kinase A (cAMP-PKA)-dependent signaling pathway.

28 ted Cl(-) secretion and completely abolishes cAMP-activated whole cell currents.

29 f pth4 expression and that Pth4 can activate cAMP signaling mediated by Pth receptors.

30 ovel critical regulator of beta-adrenoceptor/cAMP signaling and cardiac contractility.

31 bules are predisposed to become cystic after cAMP stimulation.

32 epithelial cell cultures and intestine after cAMP agonists, cholera toxin, or heat-stable enterotoxin

33 yocytes and smooth muscle cells, cyclic AMP (cAMP) and subsequent calcium (Ca(2+)) fluxes are the bes

34 E: Although the second messenger cyclic AMP (cAMP) is physiologically beneficial in the heart, it lar

35 osis (Mtb) uses a complex 3', 5'-cyclic AMP (cAMP) signaling network to sense and respond to changing

36 Inhibition of cyclic AMP (cAMP)-specific phosphodiesterase 4 (PDE4) has been propo

37 moiety which increases host cell cyclic AMP (cAMP).

38 intracellular elements including cyclic AMP (cAMP).

39 ctor (BDNF)/TrkB and presynaptic cyclic AMP (cAMP)/PKA signaling.

40 al cortical concentrations of ATP, ADP, AMP, cAMP, creatinine phosphate and ATP:AMP ratio were increa

41 d dehydrogenase type 1 normalized Ca(2+) and cAMP responses.

42 uronal phosphoprotein 32 kDa [DARPP-32], and cAMP responsive element binding protein signaling [CREB]

43 ivation of a pathway involving Akt1/Akt2 and cAMP response element-binding protein.

44 cerol (2-AG), for [35S]GTPgammaS binding and cAMP inhibition (5-10 fold).

45 ugh simultaneous manipulation of calcium and cAMP signals mediated by TRPV1 and CB1R.

46 ved in olfactory classical conditioning, and cAMP signaling molecules are necessary and sufficient fo

47 s and via activation of adenylyl cyclase and cAMP-dependent protein kinase, but some alternative down

48 denosine monophosphate [cAMP], dopamine- and cAMP-regulated neuronal phosphoprotein 32 kDa [DARPP-32]

49 that cAMP-mediated signalling, dopamine- and cAMP-regulated neuronal phosphoprotein of 32 kDa feedbac

50 st targeted neurons expressing dopamine- and cAMP-regulated phosphoprotein (DARPP-32+), known to be m

51 tial nuclear localization during fasting and cAMP/cAMP-dependent protein kinase signaling, suggesting

52 GHRH also involved activation of Galphas and cAMP/PKA, and inhibition of increase in exchange protein

53 n selectivity, reversed polarity gating, and cAMP regulation in HCN channels.

54 se kinase-3, ribosomal S6 kinase, c-Jun, and cAMP response element binding protein.

55 expression in JG cells of control mice, and cAMP agonists regulated VEGF expression in cultured reni

56 n point to participation of the cGMP/PKG and cAMP/PKA/Epac (exchange protein directly activated by cA

57 ll line were infected with C. sakazakii, and cAMP levels and phosphorylation of PKA were measured.

58 a competitive mechanism in which TRIP8b and cAMP compete for the same binding site.

59 ed by partial competition between TRIP8b and cAMP.

60 lamines target the beta-adrenergic (beta-AR)/cAMP pathway to activate cytosolic lipases and induce th

61 e accelerated release and hydrolysis of ATP, cAMP, AMP, and NAD to adenosine.

62 AT) of PDE3B KO mice on a SvJ129 background, cAMP/protein kinase A (PKA) and AMP-activated protein ki

63 rster resonance energy transfer (FRET)-based cAMP biosensor, we confirmed that atropine inhibited ace

64 Using electrophysiology and a FRET-based cAMP assay, two compounds are identified as potent CB1 a

65 ome analysis suggested the interplay between cAMP and cGMP signalling as PKAc1 inactivation changes t

66 ant-negative PKAr isoform that does not bind cAMP triggers premature parasite egress from infected ce

67 feedback loop whereby glucocorticoids boost cAMP to maintain insulin secretion in the face of pertur

68 idated by homogeneous quantification of both cAMP and insulin from single pancreatic islets undergoin

69 f the exchange protein directly activated by cAMP (Epac) provokes inhibition of the phospholipase C b

70 n kinase A and exchange protein activated by cAMP (Epac) together predict the occurrence of LTP in re

71 tly activated by cAMP) directly activated by cAMP Epac pathways in the effects of ANP on beta-cell fu

72 r the exchange protein directly activated by cAMP were involved in this increase.

73 gnals by PGE2 Exchange proteins activated by cAMP were not required, but the effects were attenuated

74 Epac (exchange protein directly activated by cAMP) directly activated by cAMP Epac pathways in the ef

75 The transcriptomic changes caused by cAMP occurred in concert with 5hmC elevation in differen

76 tivity and subsequent stimulation of CFTR by cAMP-dependent protein kinase A.

77 ergy landscape for the modulation of HCN4 by cAMP, i.e. the primary cyclic nucleotide modulator of HC

78 ronal NMNAT2 levels are tightly regulated by cAMP signaling.

79 y apical vesicle recycling and stimulated by cAMP.

80 methyl-d-aspartate receptors and weakened by cAMP-PKA-potassium channel signaling in dendritic spines

81 tagamma subunits, rather than by a canonical cAMP mediated mechanism.

82 effects of Vps34 inhibition on the canonical cAMP response elicited by beta2AR activation.

83 ated the potential role of NDPK-C in cardiac cAMP formation and contractility.

84 dium reabsorption via increased tubular cell cAMP levels, we hypothesized the ET would also do so.

85 s for the understanding of compartmentalized cAMP signalling.

86 ips among the different PDEs that coordinate cAMP-signaling cascades in these cells.

87 expression is the transcription factor CREB (cAMP-responsive element binding protein).

88 Thus p-Creb/cAMP signaling is appropriate in NP and early nephron de

89 e change is caused by cocaine-exacerbated D1-cAMP/protein kinase A dopamine signaling in pyramidal ne

90 f t-LTP induction is caused by sensitized D1-cAMP/protein kinase A dopamine signaling in pyramidal ne

91 of cAMP using forskolin, dibutyryl-cAMP (db-cAMP), BAY60-6583 or Cicaprost induced rapid cytoskeleto

92 actility, whereas NDPK-C knockdown decreased cAMP levels.

93 h that may contribute to an NDPK-C-dependent cAMP reduction in HF.

94 o, GsD is expressed and allows CNO-dependent cAMP signaling and glycogen breakdown.

95 of PDE2A, by enhancing the hormone-dependent cAMP response locally, affects mitochondria dynamics and

96 PDE10A-dependent cAMP hydrolyzing activity and PDE10A mRNA were also asse

97 th respect to in vitro IP receptor dependent cAMP accumulation assays.

98 n kinase C-activating lipid, diacylglycerol, cAMP/Epac signaling blocks the bottleneck step of the co

99 Elevation of cAMP using forskolin, dibutyryl-cAMP (db-cAMP), BAY60-6583 or Cicaprost induced rapid cy

100 existence, within mitochondria, of different cAMP-Epac1 microdomains that control myocardial cell dea

101 g and memory rely on dopamine and downstream cAMP-dependent plasticity across diverse organisms.

102 Ectopic cAMP signaling is pathologic in polycystic kidney diseas

103 Furthermore, elevated cAMP inhibited mitogen-induced nuclear-translocation of

104 Elevating cAMP pharmacologically or optogenetically produced plast

105 Elevating cAMP to equivalent levels as appetitive conditioning als

106 enhanced in vitro, as evidenced by enhanced cAMP production or receptor plasma membrane localization

107 omplemented DeltacpdA strain showed enhanced cAMP levels in the presence of PknA, and this effect was

108 In vitro, TGR5 stimulation enhanced cAMP production, cell proliferation, and cyst growth by

109 e presence of noncognate Gq protein enhances cAMP stimulated by two Gs-coupled receptors, beta2-adren

110 rophage-derived IL-10 resulted in epithelial cAMP response element-binding protein (CREB) activation

111 n Escherichia coli, the transcription factor cAMP receptor protein (CRP) is responsible for much of t

112 ified and validated the transcription factor cAMP-responsive element binding protein (Creb1) and its

113 hown that both Ras and Rap1 are required for cAMP signaling to ERKs.

114 for cGMP accumulation and p-p38MAPK than for cAMP accumulation.

115 Stimulation of adenylyl cyclase to form cAMP induces hyphal morphogenesis.

116 f the holo-form at sites critical for gating cAMP binding.

117 We show that signaling of CyaA-generated cAMP blocks the oxidative burst capacity of neutrophils

118 ting response: glucocorticoid receptor (GR), cAMP responsive element binding protein 1 (CREB1), perox

119 ons in cardiomyocytes by coupling to both Gs/cAMP-dependent and Gs-independent/growth-regulatory path

120 ed receptor --> Gs --> adenylate cyclase --> cAMP --> neuritogenic cAMP sensor-Rapgef2 --> B-Raf -->

121 ed receptor --> Gs --> adenylate cyclase --> cAMP --> PKA --> cAMP response element-binding protein p

122 s --> adenylate cyclase --> cAMP --> PKA --> cAMP response element-binding protein pathway mediating

123 However, cAMP-dependent Ras signaling to ERKs is transient and ra

124 These data implicate cAMP signaling as a critical regulator of genomic stabil

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

126 this study, we interrogate the complexity in cAMP/PKA-MAPK/ERK1&2 crosstalk by using multi-parameter

127 inhibited acetylcholine-induced decreases in cAMP.

128 e model of dystonia, PDE10A, a key enzyme in cAMP and cGMP catabolism, is downregulated in striatal p

129 roducts were evaluated at the human GPR84 in cAMP and beta-arrestin assays.

130 Increase in cAMP levels may serve as a timing signal for respecifica

131 An increase in cAMP was demonstrated after infection, as well as an inc

132 c-di-GMP caused a persistent increase in cAMP, which still occurred in mutants lacking the adenyl

133 2/3 agonists on betaAR-mediated increases in cAMP accumulation are exclusively mediated by mGlu3.

134 han those effecting appreciable increases in cAMP levels for the majority of the compounds tested.

135 ositive modulators are predicted to increase cAMP concentration, suggesting that neuronal NMNAT2 leve

136 suggest that PDE4 inhibitors, which increase cAMP cascade activity, may have antidepressant effects.

137 hanistically, the absence of Cav-1 increased cAMP/PKA signaling in EC, as indicated by elevated phosp

138 ession of NDPK-C in cardiomyocytes increased cAMP levels and sensitized cardiomyocytes to isoprenalin

139 ost, but not EP4 agonist CAY10598, increased cAMP response in both cell lines.

140 While formoterol and clenbuterol increased cAMP, only formoterol increased the phosphorylation of A

141 ogenous incretin or GLP1R agonists increases cAMP generation, which stimulates glucose-induced beta-c

142 t the hypothesis that C. sakazakii increases cAMP and PKA activation in experimental NEC resulting in

143 ibutes to hepatic cystogenesis by increasing cAMP and enhancing cholangiocyte proliferation; our data

144 conditions the subsequent Forskolin-induced cAMP release reverses the transient increase of EGF-medi

145 Here, we show that high glucose induced cAMP response element-binding protein (CREB)-binding pro

146 ctive temperature prevented c-di-GMP-induced cAMP synthesis as well as c-di-GMP-induced stalk gene tr

147 h and biofilm formation, and also influences cAMP-regulated processes.

148 eased intensity and duration of D2-inhibited cAMP/cGMP signaling.SIGNIFICANCE STATEMENT In DYT1 trans

149 spectively of D1-stimulated and D2-inhibited cAMP/cGMP signals.

150 s a key mediator of COX-2 activity-initiated cAMP signaling in Neuro-2a and SH-SY5Y cells following 6

151 PGE2-initiated cAMP production in these cells was blocked by our recent

152 one regulatory (PKAr) subunits to integrate cAMP-dependent signals.

153 Similarly, increased intestinal cAMP and PKA phosphorylation were demonstrated in a rat

154 Intracellular cAMP, the production of which is catalyzed by the alpha-

155 s to be mediated by increasing intracellular cAMP levels, increasing synthesis of the G protein coupl

156 ization, and ligand-stimulated intracellular cAMP accumulation.

157 (PDE2) inhibitors increase the intracellular cAMP and/or cGMP activities, which may ameliorate cognit

158 This pathway did not involve cAMP, Galphas, or Galphai or the participation of the ot

159 One involves cAMP/protein kinase A-mediated activation of the Src hom

160 hough the increased gap junction coupling is cAMP-dependent, neither the protein kinase A nor the exc

161 Phosphodiesterase 4 (PDE4) is a key cAMP-metabolizing enzyme involved in the pathogenesis of

162 Type 4 phosphodiesterases (PDE4) are key cAMP-hydrolyzing enzymes, and PDE4 inhibitors are consid

163 ember B1 gene (DNAJB1) to the protein kinase cAMP-activated catalytic subunit alpha gene (PRKACA) has

164 usly stimulated intracellular Ca(2+) levels, cAMP activity, and GLP-1 secretion and improved glucose

165 Via the activation of Gi/o, they limit cAMP accumulation, diminish neurotransmitter release, an

166 he Rutabaga type I adenylyl cyclase, linking cAMP-dependent plasticity to behavioral modification.

167 rential kinetics and amplitudes of localized cAMP signals.

168 2 activation, NDPK-C may contribute to lower cAMP levels and the related contractile dysfunction in H

169 roteins interact and move within a cell make cAMP responses highly complex.

170 ine nucleotide exchange factor that mediates cAMP signaling in various types of cells, including beta

171 lic ATP to the key second messenger molecule cAMP.

172 ed a novel intracellular signaling molecule, cAMP-response element binding protein (CREB), which serv

173 Cyclic adenosine monophosphate (cAMP) and protein kinase A (PKA) are important mediators

174 tance of the cyclic adenosine monophosphate (cAMP) cascade in major depressive disorder (MDD) have no

175 f a PDE-PKAR-cyclic adenosine monophosphate (cAMP) complex (the termination complex).

176 elevation of cyclic adenosine monophosphate (cAMP) has emerged as a promising therapeutic approach to

177 Cyclic adenosine monophosphate (cAMP) is an important mediator of hormonal stimulation o

178 ntracellular cyclic adenosine monophosphate (cAMP) levels tune the voltage response, enabling sympath

179 oietin 1 and cyclic adenosine monophosphate (cAMP) to vary the Pd of the HUVECs monolayer towards flu

180 stidine, and cyclic adenosine monophosphate (cAMP) were found in urine samples of T2D subjects valida

181 at Tregs use cyclic adenosine monophosphate (cAMP)-dependent protein kinase A pathway to inhibit HIV-

182 ed pulses of cyclic adenosine monophosphate (cAMP).

183 ic, calcium, cyclic adenosine monophosphate [cAMP], dopamine- and cAMP-regulated neuronal phosphoprot

184 rtments, suggesting the presence of multiple cAMP/PKA signalling domains within the organelle.

185 adenylate cyclase --> cAMP --> neuritogenic cAMP sensor-Rapgef2 --> B-Raf --> MEK --> ERK pathway me

186 Here, we describe a novel cAMP/PKA signalling domain localised at mitochondrial me

187 MNADK deficiency reduced the activation of cAMP-responsive element binding protein-hepatocyte speci

188 ating ATF4 expression and that activation of cAMP/PKA and PI3K/Akt/mTORC1 mediates the effect of gluc

189 channels decreases the apparent affinity of cAMP for the CNBD.

190 en cell type, making the characterization of cAMP signaling compartments daunting.

191 s have shown that the basal concentration of cAMP in several cell types is about 1 muM.

192 he presence of a saturating concentration of cAMP.

193 based community maps of the kinase domain of cAMP-dependent protein kinase A allow for a molecular ex

194 Dysregulation of cAMP metabolism is a consistent finding in patients and

195 The effect of cAMP on Fe(II) and 5hmC was confirmed by adenylate cycla

196 e used to study the physiological effects of cAMP signaling, acute or chronic, in liver or any tissue

197 Here we investigated the effects of cAMP-induced cytoskeletal remodelling on the serum respo

198 Elevation of cAMP using forskolin, dibutyryl-cAMP (db-cAMP), BAY60-65

199 eveal that PDEs mediate active hydrolysis of cAMP bound to its receptor RIalpha by enhancing the enzy

200 of signaling through EP2/EP4-->induction of cAMP-->downregulation of IFN regulatory factor 1 express

201 the effects were attenuated by inhibition of cAMP-dependent protein kinase (PKA).

202 D2R-induced ADP is blocked by inhibitors of cAMP/PKA signaling, insensitive to pertussis toxin or be

203 e (GlcNAc), suggesting that a basal level of cAMP is sufficient for stimulation.

204 stimulate cAMP, or if normal basal levels of cAMP are required to maintain cellular health needed for

205 tation of cyr1Delta cells with low levels of cAMP enabled them to form hyphae in response to the indu

206 ing the cell to respond to dynamic levels of cAMP rather than steady-state levels.

207 Levels of cAMP, cell proliferation, and cyst growth in vitro were

208 Testing a panel of modulators of cAMP and cGMP signaling pathways, FASS-LTP identified va

209 untered during infection, so perturbation of cAMP signaling might be leveraged to disrupt Mtb pathoge

210 IL-10 production via the phosphorylation of cAMP response element-binding (CREB) protein on the IL-1

211 phosphoproteomes of the functional pools of cAMP/PKA/EPAC that are regulated by specific cAMP-PDEs (

212 n HCN channel in the absence and presence of cAMP at 3.5 A resolution.

213 eceptor signaling inhibits the production of cAMP in islets, which via CREB mediated pathways results

214 prisingly, the TRIP8b-dependent reduction of cAMP binding to the CNBD can largely be explained by par

215 e cyclase to achieve real-time regulation of cAMP and the PKA pathway.

216 define more compartmentalized regulation of cAMP, PKA, and EPAC, they have limited ability to link t

217 ne composition by CyaA-produced signaling of cAMP thus enables B. pertussis to evade the key innate h

218 t uncovered that HDAC2 is a direct target of cAMP response element-binding protein (CREB) that is act

219 B protein is central in the transcription of cAMP responsive genes, including those involved in long-

220 However, understanding of cAMP signaling pathways is hindered by the presence of a

221 investigated the effects of C. sakazakii on cAMP and PKA in vitro and in vivo.

222 re release, possibly engaging Store Operated cAMP Signaling (SOcAMPS) and activating Ca(2+) regulated

223 ulated kinase 1/2, ribosomal S6 kinase 1, or cAMP responsive element binding protein DNA-binding acti

224 exocytosis following intracellular Ca(2+) or cAMP elevation, thereby supplying the vasculature with f

225 KL2 cytoplasmic, irrespective of mitogens or cAMP.

226 ound an enduring reduction in phosphorylated cAMP-response element binding protein levels in the NAcS

227 chinery, an effect that is enhanced by prior cAMP-dependent accumulation of the protein at the plasma

228 ro, we assessed cholangiocyte proliferation, cAMP levels, and cyst growth in response to (1) TGR5 ago

229 However, our knowledge of how receptors, cAMP signaling enzymes, effectors, and other key protein

230 e calmodulin inhibitors W-7 and W-13 reduced cAMP levels, and W-7 reduced cyst growth, suggesting tha

231 c acid tetrakis(acetoxymethyl ester) reduced cAMP levels in PC1-knock-out cells.

232 uorescence and electron microscopy reflected cAMP-induced reorganization of intercellular contacts.

233 ta demonstrate that learning produces robust cAMP-dependent plasticity in intrinsic MB neurons, which

234 nd tested their activity in the HEK293-RXFP1 cAMP assay and the human hepatic cell line LX-2.

235 ear perturbs efficient chemotaxis in shallow cAMP gradients, without affecting the abundance of the m

236 Channel regulation is also compromised since cAMP-dependent PKA activity is enhanced, increasing the

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

238 These compounds stimulate cAMP levels and raise mature let-7 levels to suppress le

239 clear whether hyphal inducers must stimulate cAMP, or if normal basal levels of cAMP are required to

240 ially expressing D1 receptors that stimulate cAMP/cGMP synthesis.

241 and this PGI2 increase appeared to stimulate cAMP/PKA pathways, contributing to the enhanced lipolysi

242 ased intensity and duration of D1-stimulated cAMP/cGMP signaling; conversely, the increase of PDE10A

243 We found that 2-PAA stimulated cAMP synthesis and enhanced gap junction coupling in a c

244 one and neurotransmitter receptor-stimulated cAMP generation.

245 2R activation elicits the ADP by stimulating cAMP/PKA signaling.

246 compounds were equally potent in stimulating cAMP signaling in the mouse hippocampal cell line HT-22

247 nist of the V2R activation pathways studied: cAMP production, beta-arrestin interaction, and MAP kina

248 ted unfolding of two protein-ligand systems: cAMP-bound regulatory subunit of Protein Kinase A (RIalp

249 34 inhibition also attenuates the short-term cAMP response, and its effect begins several minutes aft

250 It is widely accepted that cAMP regulates gene transcription principally by activat

251 We found that cAMP activates cyclic nucleotide-gated (CNG) channels an

252 ve high-resolution microscopy, we found that cAMP elevation caused rapid binding of Epac2A to the bet

253 Previously, we found that cAMP-induced growth arrest of PC12 and NS-1 cells requir

254 We show that cAMP mediates inhibition of histamine-evoked Ca(2+) sign

255 cyr1Delta) to form hyphae has suggested that cAMP signaling is essential for hyphal growth.

256 pressed mRNAs, bioinformatics suggested that cAMP-mediated signalling, dopamine- and cAMP-regulated n

257 This suggests that cAMP signaling may serve to modulate intrinsic MB respon

258 The cAMP-elevating, Gs protein-coupled A2a adenosine recepto

259 e beta-adrenergic receptor and activates the cAMP-PKA-dependent pathway, caused a significant increas

260 n of the adenylate cyclase in vitro, and the cAMP analogue 8-bromo-cyclic AMP partially rescued the c

261 ophores can enhance agonist efficacy for the cAMP inhibition mediated by Gi/o-proteins, while reducin

262 adenylyl cyclase isoforms that generate the cAMP signal in the cytosol.

263 55 regulates genes such as pde-4 to keep the cAMP levels low in VD.

264 olf, which is critical for activation of the cAMP pathway in the striatal projection neurons.

265 tment through, for example, induction of the cAMP pathway.

266 te (cGMP) leading to increased levels of the cAMP response element binding protein (CREB), a transcri

267 nscription levels of specific members of the cAMP Response Element Binding protein gene family.

268 n part via the PKA-mediated induction of the cAMP response element-binding protein (CREB) signaling p

269 yclic nucleotide-binding domain (CNB) of the cAMP sensor, EPAC1.

270 nd by promoting the dephosphorylation of the cAMP- responsive transcriptional coactivators (CRTCs).

271 e that TRIP8b competes with a portion of the cAMP-binding site or distorts the binding site by making

272 Critical role of the cAMP-PKA pathway in hyperglycemia-induced epigenetic act

273 opy to study the effect of modulation of the cAMP-PKA-dependent pathway on ICAM-4 receptor activation

274 dence is provided for the involvement of the cAMP-protein kinase A pathway in gating the recovery.

275 Several components of the cAMP/PKA cascade are located to different mitochondrial

276 h-promoting substrates and activation of the cAMP/pkA signaling pathway play a key role in spontaneou

277 ng the adenylate cyclases ACG or ACR, or the cAMP phosphodiesterase RegA.

278 ACA produces the cAMP pulses that coordinate Dictyostelium morphogenetic

279 th necessary and sufficient for reducing the cAMP-dependent regulation of HCN channels.

280 We apply this method to study the cAMP binding domain A (CBD-A) of Protein kinase A.

281 es for specific drug discovery targeting the cAMP signaling pathway.

282 epressive disorder (MDD) have noted that the cAMP cascade is downregulated in MDD and upregulated by

283 lso produced plasticity, suggesting that the cAMP generated during conditioning affects odor-evoked r

284 We have shown previously that the cAMP-enhancing compounds rolipram (ROL; a PDE4 inhibitor

285 ollectively, these data demonstrate that the cAMP-PKA pathway plays a key role in epigenetic regulati

286 one marrow-derived macrophages, PGE2 via the cAMP/protein kinase A pathway is potently inducing IL-1b

287 This cAMP-driven synaptic potentiation requires the activatio

288 eoclast differentiation and function through cAMP/PKA and Wnt/beta-catenin pathways.

289 eins, activates downstream signaling through cAMP and plays important roles in skeletal development b

290 Thus, cAMP-independent signals contribute to the induction of

291 tion of Kv1.1 expression was attributable to cAMP elevations in the PFC secondary to reduced phosphod

292 of many different substrates contributes to cAMP-dependent regulation of these cells.

293 ingly different response of VSMCs and ECs to cAMP elevation.

294 ractions to create a switch-like response to cAMP.

295 ts, resulting in improved glucose tolerance, cAMP production, and insulin secretion as well as protec

296 Finally, dimers bound to either one or two cAMP molecules had similar DNA affinities, indicating th

297 Using cAMP measurements and a transcriptional reporter assay,

298 ST3 and PKA that creates a mechanism whereby cAMP mediates PP2A disinhibition.

299 rmational change of the CNBD associated with cAMP regulation and a competitive mechanism in which TRI

300 Treatment with cAMP-enhancing agents, forskolin/rolipram (F/R), mitigat