ライフサイエンスコーパス: cAMP

1 cAMP and glutathione were depleted.

2 A cell membrane-permeable form of 2',3'-cAMP and 3'-AMP mimicked the potentiating effects of IAA

3 se (CNPase; an enzyme that metabolizes 2',3'-cAMP into 2'- and 3'-AMP), effects of IAA/DNP on exosome

4 re, in part, mediated by intracellular 2',3'-cAMP.

5 iac fibroblasts, consistent with PDE10A as a cAMP/cGMP dual-specific PDE.

6 e conductance regulator) gene that encodes a cAMP-dependent anion channel vital for proper Cl(-) and

7 the msmeg_4207 gene and is a substrate for a cAMP-regulated protein lysine acyltransferase (KATms; MS

8 is phosphorylated in the dark at Ser21 in a cAMP-dependent manner and dephosphorylated in the light.

9 ted by its downstream receptor (d5-HT7) in a cAMP-dependent manner.

10 amplitude of PKA signaling, upon receiving a cAMP-driving stimulus.

11 tly blocks RIalpha LLPS and induces aberrant cAMP signaling.

12 intracellular ATP levels, with accompanying cAMP accumulation lost in sAC-/- cells.

13 s are coupled to Galphas/olf, which activate cAMP signaling.

14 Inhibition of the beta-adrenoreceptor-cAMP signaling pathway prevented the induction of traini

15 channel in the presence of the full agonist cAMP, but not with the partial agonist cGMP.

16 Also, cAMP and PKA (cAMP dependent protein kinase) activity we

17 P [Epac proteins (Epac 1-2)] are alternative cAMP targets to protein kinase A (PKA) and Epac2 is abun

18 the ubiquitous second messenger cyclic AMP (cAMP) is an activator of the Hypr GGDEF enzyme GacB from

19 f beta-cells to the elevation of cyclic AMP (cAMP) levels and reduced proliferation of beta-cells in

20 (PTX) insensitive inhibition of cyclic AMP (cAMP) levels in mammalian cells, suggesting coupling to

21 hat are responsive to changes in cyclic AMP (cAMP)-dependent signaling, consistent with metabolic act

22 multaneously monitored astrocytic Ca(2+) and cAMP and demonstrate that astrocytic second messengers a

23 e secretion-regulating messengers Ca(2+) and cAMP in mouse alpha-cells.

24 senescence; and fibrosis, angiogenesis, and cAMP/phospho-ERK expression.

25 vascular endothelial growth factor-A/C, and cAMP/ERK expression was performed.

26 zymes integrate signals from a chemokine and cAMP to specify the spatiotemporal mobilization of Ca(2+

27 The CREB-dependence and cAMP independence of this process suggests a manner in w

28 and DRD2 in neurons expressing dopamine- and cAMP-regulated phosphoprotein of 32 kDa (DARPP32) or tyr

29 lated full-length Dicer, through EP2/EP4 and cAMP.

30 sensitivity through GPR160-dependent ERK and cAMP response element-binding protein (CREB).

31 e of two key second messengers, c-di-GMP and cAMP, in this process.

32 As both low oxygen and cAMP are known to play a central role in placental funct

33 stin2 translocation, ERK phosphorylation and cAMP inhibition.

34 ibit uncoupled mitochondrial respiration and cAMP-induced lipolytic activity.

35 ften cluster together with their targets and cAMP regulatory proteins to form discrete cAMP signaloso

36 and IRAG are independent of trafficking and cAMP binding, and they are specific to the HCN4 isoform.

37 hese interactions affected both voltage- and cAMP-dependent gating of HCN2 channels.

38 vides a functional link between voltage- and cAMP-dependent mechanisms of HCN channel gating.

39 15 was a partial agonist in vitro (hA(3)AR, cAMP inhibition, 31% E(max); mA(3)AR, [(35)S]GTP-gamma-S

40 (PDE) break down cyclic nucleotides such as cAMP and cGMP, reducing the signaling of these important

41 ipid-raft domains responsible for attenuated cAMP signaling.

42 d glial cells, n-3 PUFA treatment attenuated cAMP accumulation in LCLs.

43 Because cAMP effector proteins often cluster together with their

44 matotroph adenomas, we studied links between cAMP signaling and DNA damage.

45 wnregulation is not involved in the biphasic cAMP response.

46 We suggest that this biphasic cAMP response allows the TSHR to mediate responses at lo

47 xclusion of D(1) R from lipid rafts, blunted cAMP response, impaired sodium transport, and increased

48 TP-10 treatment elevated both cAMP and cGMP levels in cardiac myocytes and cardiac fib

49 SCNA pathway analysis, we observed that both cAMP and Fanconi anemia DNA damage repair pathways were

50 results reveal that LH, forskolin, and 8-Br cAMP-induced PKA-dependent phosphorylation of HSL at Ser

51 Treatment with the cAMP analogue Br-cAMP to mimic cAMP rise at maturation onset rescued meio

52 In contrast, 8-bromo-cAMP administration had no effect on natriuresis or AT(2

53 The exchange protein activated by cAMP (EPAC) is a promising drug target for a wide diseas

54 Exchange proteins directly activated by cAMP (EPAC) play a central role in various biological fu

55 and exchange proteins directly activated by cAMP (Epac).

56 f3 encodes an exchange protein, activated by cAMP 1 (EPAC-1), a guanine nucleotide exchange factor th

57 tide exchange proteins directly activated by cAMP [Epac proteins (Epac 1-2)] are alternative cAMP tar

58 EPAC (exchange protein directly activated by cAMP).

59 es which are more sensitive to activation by cAMP than are the wild-type proteins.

60 sphorylation of its regulatory (R) domain by cAMP-dependent protein kinase catalytic subunit (PKA).

61 guanine nucleotide exchange protein Epac by cAMP.

62 ysosomes via connexin 43 (Cx43) and gated by cAMP-EPAC-RAP1-PP2A signaling.

63 o underlie CAP1 dephosphorylation induced by cAMP.

64 mbrane potential (RMP) that is maintained by cAMP signaling through PKA and EPAC.

65 results from total-flux feedback mediated by cAMP-Crp signalling but also requires inhibition by the

66 ry proteins which result in elevated calcium-cAMP signaling over a long lifespan can additionally dri

67 rly in life weaken the regulation of calcium-cAMP signaling and are associated with increased risk of

68 Thus, calcium-cAMP signaling must be tightly regulated, e.g., by agent

69 ne (TG15) had a ~15-fold increase in cardiac cAMP-PDE activity and a ~30% decrease in cAMP content an

70 resulting in a ~50-fold increase in cardiac cAMP-PDE activity caused a ~50% decrease in fractional s

71 ticles/mouse) had a ~50% increase in cardiac cAMP-PDE activity, which did not modify basal cardiac fu

72 y regulated, e.g., by agents that catabolize cAMP or inhibit its production (PDE4, mGluR3), and by pr

73 P and also interfered with the host cellular cAMP and MEK/ERK cascade pathways.

74 monitored by measuring reduction in cellular cAMP levels.

75 ecisely locate and measure compartmentalized cAMP, and this allows us to estimate the range of effect

76 successfully used to probe compartmentalized cAMP signaling in eukaryotic cells.

77 erases (PDEs) have been suggested to confine cAMP to distinct cellular compartments.

78 by activating the Galpha(s)/adenylyl cyclase/cAMP pathway.

79 by AG could be prevented by dibutyryl cyclic-cAMP or 3-isobutyl-1-methylxanthine and the somatostatin

80 opy, we show that, contrary to earlier data, cAMP at physiological concentrations is predominantly bo

81 In addition, nor-BNI and DB-cAMP also rescued cell cycle abnormalities in progranuli

82 nor-BNI) and dibutyryl-cAMP, sodium salt (DB-cAMP) as two phenotypic modulators of progranulin defici

83 production at low doses of TSH and decreased cAMP production at high doses (>1 mU/ml).

84 es at lower levels of TSH and that decreased cAMP production at high doses may represent a mechanism

85 beta-arrestin 2 did not affect the decreased cAMP production at high TSH doses, we studied the roles

86 endritic cells was associated with decreased cAMP, IL-6 and IL-12.

87 cities. Of interest, measured IBMX-dependent cAMP levels were an order of magnitude higher in PKA-nul

88 rtic SMCs resulted in increased IP-dependent cAMP production and consecutive facilitation of SMC rela

89 mine dihydrochloride (nor-BNI) and dibutyryl-cAMP, sodium salt (DB-cAMP) as two phenotypic modulators

90 nd cAMP regulatory proteins to form discrete cAMP signalosomes, proteomics and phosphoproteomics anal

91 hibitory synapses is dependent on downstream cAMP/protein kinase A (PKA) signaling, which differs bet

92 u-opioid receptor coupling to the downstream cAMP/PKA intracellular cascade.

93 u-opioid receptor coupling to the downstream cAMP/PKA intracellular cascades.

94 AMP and PKA activity, critical for effective cAMP compartmentation.

95 arge cytosolic astrocytic Ca(2+) elevations, cAMP changes were not detectable.

96 t blocks PI3K/Akt signaling, through the ERK/cAMP-responsive element-binding protein/c-Jun pathway.

97 Exogenous cAMP partially restored the mutant appressorium, but not

98 partially recovered by addition of exogenous cAMP.

99 kinases converge on the transcription factor cAMP response element-binding protein (CREB) to enhance

100 The transcription factor cAMP response element-binding protein (CREB1) has been s

101 ether they activate the transcription factor cAMP-responsive element-binding protein 1 (CREB).

102 The transcription factors, cAMP-response element-binding protein (CREB) and heat-sh

103 However, measured rates of fast cAMP diffusion and slow PDE activity render cAMP compart

104 ess the molecular machinery for feedforward, cAMP-PKA-calcium signaling.

105 Examining transport of a new fluorescent cAMP probe, Bock and coworkers observe "buffered diffusi

106 s and traffics them to the nucleus following cAMP/PKA-mediated lipolytic stimulation.

107 ess likely to couple to adenylyl cyclase for cAMP production.

108 They also reveal a novel role for cAMP-dependent phosphorylation of GRK1 in regulating the

109 cuting the dephosphorylation downstream from cAMP, whereas preventing CAP1 from accessing its kinase

110 e demonstrate that a nonconserved functional cAMP-responsive element in BDNF promoter IXa in humans r

111 as a molecular switch, driving GPCR-Galphas-cAMP signaling toward activation of EPAC-RAP1 and MAPK,

112 the MAPK pathway downstream of GPCR-Galphas-cAMP signaling, we show that the expression levels of PK

113 Collectively, this non-genomic cAMP signaling modality contributes to one-third of the

114 oncoproteins that drive constitutively high cAMP signaling pathway output in susceptible cell types

115 provide detailed molecular insights into how cAMP-PKA signaling inactivates CaMKK2 and reveals a path

116 d a proof-of-concept strain that illustrates cAMP-chemotaxis with four fluorescent reporters coded by

117 iac cAMP-PDE activity and a ~30% decrease in cAMP content and fractional shortening associated with a

118 h no statistically significant difference in cAMP levels at 1 and 100 mU/ml TSH.

119 to form biomolecular condensates enriched in cAMP and PKA activity, critical for effective cAMP compa

120 unting of D(5) R agonist-induced increase in cAMP production and decrease in Na(+) transport, effects

121 elial cells, we postulated that increases in cAMP, a critical cellular "second messenger," may be lin

122 dcy10-dependent (sAC-dependent) increases in cAMP, activation of protein kinase A, and cytoprotection

123 we examined whether amnesiac is involved in cAMP/PKA dynamics in response to dopamine and acetylchol

124 ex vivo show that Opn5 POA neurons increase cAMP when stimulated with violet light.

125 ril blunted the ability of GLP-1 to increase cAMP levels in coronary vascular cells in vitro.

126 olysis and glucose oxidation and to increase cAMP levels is dependent on MTPalpha.

127 Increased cAMP levels have been found in vitro in both animal mode

128 budesonide, and progesterone each increased cAMP levels within 3 minutes without phosphodiesterase i

129 is the first to find evidence for increased cAMP activity in areas of fibrous dysplasia in vivo.

130 (R)-rolipram to indirectly measure increased cAMP pathway activation in human disease.

131 co-knockdown of G(i)/G(o) proteins increased cAMP levels stimulated by 100 mU/ml TSH from 55% to 73%

132 Stimulation of TSHR leads to increasing cAMP production that has been reported as a monotonic do

133 -shaped dose-response curve" with increasing cAMP production at low doses of TSH and decreased cAMP p

134 y tumors are driven by oncogenes that induce cAMP signaling.

135 edox states are vital toward agonist-induced cAMP formation and subsequent CREB and G-protein-depende

136 insulin exhibit impaired beta(2) AR-induced cAMP accumulation and airway relaxation.

137 half-maximum inhibition of dopamine-induced cAMP accumulation in cells coexpressing D(1)-receptor an

138 ve and agonist-sensitive activity to inhibit cAMP production and downstream beta-cell function, with

139 etion in patients with acromegaly, inhibited cAMP and GH and reversed DNA damage induction.

140 mmune cells from inhibition by intracellular cAMP and (b) prevent immunosuppressive transcription of

141 High intracellular cAMP levels and ERK1/2 activation were observed in human

142 thways, resulting in increased intracellular cAMP, and enhanced activation of EPAC and MAPK.

143 Direct measurements of intracellular cAMP ex vivo show that Opn5 POA neurons increase cAMP wh

144 zed cells where they triggered intracellular cAMP/PKA signals that attenuated mitochondrial metabolis

145 sp40) member B1 (DNAJB1) with protein kinase cAMP-activated catalytic subunit alpha (PRKACA) and by d

146 We also tested if raising cGMP, like cAMP, can promote the degradation of mutant proteins tha

147 nist (determined by measuring MDCK cell line cAMP accumulation), producing 57% of AVP's maximal activ

148 cyclases (ACs) drives oscillations of local cAMP levels to be precisely in-phase with Ca(2+) oscilla

149 assemble liquid droplets to further localize cAMP signaling.

150 n vivo experiments indicate that CIRL lowers cAMP levels in both mechanosensory submodalities.

151 alter the balance of activation of two major cAMP targets: PKA and EPAC.

152 phorylation, chemotaxis, and G(i/o)-mediated cAMP inhibition.

153 onstrate biphasic regulation of TSH-mediated cAMP production involving coupling of the TSH receptor (

154 The second messenger cAMP is an important determinant of synaptic plasticity

155 plication of IBMX or of the second messenger cAMP via the patch pipette had no effect on THIK-1 curre

156 e abundant than the free cellular messengers cAMP, cGMP, H(+) , and Ca(2+) .

157 n of Galphai and inhibits second messengers (cAMP).

158 ment with the cAMP analogue Br-cAMP to mimic cAMP rise at maturation onset rescued meiotic maturation

159 HEK293 cells to induce Ca(2+) mobilization, cAMP formation, and PKA/protein kinase D (PKD) activatio

160 vated PAR(2) to induce calcium mobilization, cAMP formation, and activation of protein kinase D (PKD)

161 H promoter recruited the epigenetic modifier cAMP-response element-binding protein-binding protein/p3

162 lly regulated in fat by agents that modulate cAMP levels, by cold exposure, and by pharmacological st

163 these results suggest that FgCdc25 modulates cAMP and MAPK signalling pathways and further regulates

164 Cyclic-3',5'-adenosine monophosphate (cAMP) is an ancient second messenger but organizing sign

165 1) to reduce cyclic adenosine monophosphate (cAMP) levels in mice and in GPR151-expressing cell lines

166 es the 3',5'-cyclic adenosine monophosphate (cAMP) pathway-associated G-protein, G(s)alpha.

167 se the 3',5'-cyclic adenosine monophosphate (cAMP) production.

168 gh increased cyclic adenosine monophosphate (cAMP) response element binding (CREB)/CREB binding prote

169 enger 3', 5'-cyclic adenosine monophosphate (cAMP) signaling and suppressed stemness features of ovar

170 lls, Ca(2+), cyclic adenosine monophosphate (cAMP), and Protein Kinase A (PKA) exist in an oscillator

171 AR1A) of the cyclic adenosine monophosphate (cAMP)-dependent protein kinase (PKA), leading to activat

172 s messenger, cyclic adenosine monophosphate (cAMP).

173 The cyclic AMP (adenosine monophosphate; cAMP)-hydrolyzing protein PDE4B (phosphodiesterase 4B) i

174 activates adenylyl cyclases to produce more cAMP-PKA signaling.

175 This study reveals a new cAMP-dependent signaling pathway for cocaine-induced beh

176 Presence of a nonmetabolizable cAMP analog during culture period counteracted the effec

177 NCS-Rapgef2 is a novel cAMP effector, expressed in neuronal and endocrine cells

178 neurons (MSNs), Muntean et al. used a novel cAMP sensor to track cAMP dynamics and report a coordina

179 n upon direct binding of cyclic nucleotides (cAMP and/or cGMP), but the allosteric mechanism by which

180 ocyte specifically induced substance (OASIS)/cAMP responsive element-binding protein 3-like 1 (CREB3l

181 we demonstrate that the octopamine-Octbeta1R-cAMP pathway processes both aversive and appetitive lear

182 e basal voltage dependence in the absence of cAMP.

183 arious brain functions through activation of cAMP-dependent pathways.

184 naling cascade, which leads to activation of cAMP-dependent protein kinase (PKA) and subsequent cardi

185 also known as AKT) depended on activation of cAMP-responsive element-binding protein (CREB) for induc

186 ed that it is regulated by the activities of cAMP-dependent protein kinase (PKA) and the protein phos

187 lls in a manner dependent on the activity of cAMP-hydrolyzing phosphodiesterase 3 (PDE3).

188 ndence of HCN4 in response to the binding of cAMP.

189 IBMX inhibits breakdown of cAMP and thus activates protein kinase A (PKA).

190 two catalytic subunits (Calpha and Cbeta) of cAMP-dependent protein kinase (PKA), a pleiotropic holoe

191 or variants, spatial compartmentalization of cAMP signaling and new downstream signaling targets invo

192 uid phase separation (LLPS) as a function of cAMP signaling to form biomolecular condensates enriched

193 4 (PDE4), which catalyzes the hydrolysis of cAMP.

194 holoenzyme which activates with increase of cAMP and plays an important role in many physiological p

195 sensitivity to opioid-mediated inhibition of cAMP and promote hyperactivity of nociceptors by enhanci

196 (15 mm K(+); -45 mV), reducing inhibition of cAMP signaling by mu-opioid receptor agonists DAMGO and

197 n ovarian CSC mediated through inhibition of cAMP signaling.

198 agonists using agonist-induced inhibition of cAMP.

199 Inhibitors of cAMP-phosphodiesterase 4 (PDE4) exert a number of promis

200 athway, by either intracellular injection of cAMP or DREADD-Gs stimulation.

201 Excessive levels of cAMP-calcium signaling can have a number of detrimental

202 Compiling a dynamic map of cAMP nanodomains in defined cell types would establish a

203 ove fruitful in generating a detailed map of cAMP signalosomes and reveal new details of compartmenta

204 s per second time-lapse FLIM measurements of cAMP levels using an Epac-based fluorescent biosensor in

205 This work unveils a novel mechanism of cAMP compartmentation utilized for localized tuning of a

206 We functionally localized modifiers of cAMP signaling, the photo-activated adenylyl cyclase bPA

207 t its expression is induced by modulators of cAMP levels in isolated adipocytes.

208 consistent with the downstream production of cAMP and contractile responses.

209 ensitivity of adenylyl cyclase production of cAMP to inhibitory Galphai proteins in DRGs.

210 ai of adenylyl cyclase and its production of cAMP, independent of alterations in G protein-coupled re

211 These data show that biphasic regulation of cAMP production is mediated by G(s) and G(i)/G(o) at low

212 lack of LTB(4) -mediated down-regulation of cAMP, subsequent failure to induce Death-Inducing Signal

213 the composition, function, and regulation of cAMP-signaling nanodomains in health and disease is esse

214 Remarkably, ceramide-induced RIP of cAMP response element-binding protein 3-like 1 (CREB3L1)

215 Stimulation of cAMP in C57BL/6 mouse primary pituitary cultures using f

216 r effector systems, including stimulation of cAMP production and inhibition of G protein inward recti

217 We found that remote stimulation of cAMP signaling in DMS dMSNs activates Fyn and promotes t

218 ticoid showed similarly rapid stimulation of cAMP, implying that responses are initiated at the cell

219 JB1 is fused to the catalytic (C) subunit of cAMP-dependent protein kinase (PKA), replacing exon 1, t

220 reveal that the type I regulatory subunit of cAMP-dependent protein kinase (PKA), RIalpha, undergoes

221 ppression was associated with suppression of cAMP in INS-1 cells.

222 chanisms underlying subcellular targeting of cAMP-generating adenylyl cyclases and processes regulate

223 ream signaling and the downstream targets of cAMP involved in these events remain poorly understood.

224 ) prevent immunosuppressive transcription of cAMP response element- and hypoxia response element-cont

225 thods: beta-adrenergic agonistic activity on cAMP generation (dedicated dataset generated for this st

226 N) production, which was largely depended on cAMP signalling.

227 rentiation and GH secretion are dependent on cAMP activation and we previously showed DNA damage, ane

228 Estradiol had small effects on cAMP levels but G protein estrogen receptor antagonists

229 ects of abrogating NCS-Rapgef2 expression on cAMP-dependent ERK->Egr-1/Zif268 signaling in cultured n

230 signaling as well as a negative feedback on cAMP concentration.

231 lish phosphodiesterase activity can organize cAMP nanodomains, while Zhao and coworkers find that pro

232 restin2 recruitment, ERK1/2 phosphorylation, cAMP inhibition) and in vivo (anxiety-like behaviors, ca

233 tic interaction and imaging studies pinpoint cAMP signaling as a key downstream effector for Octbeta1

234 Also, cAMP and PKA (cAMP dependent protein kinase) activity were monitored b

235 alogs exhibited improved functional potency (cAMP, beta-arrestin 2), metabolic stability, and aqueous

236 on a Ca(2+)-induced increase in presynaptic cAMP that is mediated by Ca(2+)-sensitive adenylyl cycla

237 effectively with adenylyl cyclase to produce cAMP, and this is reversed by antidepressant treatment.

238 Because raising cAMP enhances 26S proteasome activity and the degradatio

239 Raising cGMP, like raising cAMP, stimulated the degradation of short-lived cell pro

240 but by repressing the nutrient signaling Ras-cAMP-PKA pathway at the level of the protein kinase A (P

241 tered in metastases, including mTOR, CDK/RB, cAMP/PKA, WNT, HKMT, and focal adhesion.

242 rine to stimulate beta-adrenergic receptors, cAMP production, and protein kinase A activity to augmen

243 umors and Caki-1 cells, V2R agonists reduced cAMP and ERK1/2 activation, while dDAVP treatment had th

244 gene silencing in Caki-1 cells also reduced cAMP and ERK1/2 activation.

245 ing cascade through which Gi-protein reduces cAMP levels and attenuates protein kinase A and protein

246 inimal PDZ-RhoGEF fragment can down-regulate cAMP signaling, suggesting that this effector competes w

247 cAMP diffusion and slow PDE activity render cAMP compartmentalization essentially impossible.

248 s: both occur together and similarly require cAMP signaling in the antennal lobe inhibitory local int

249 s and liver expression of fasting-responsive cAMP-dependent protein kinase A (PKA) signaling pathways

250 ated with n-3 PUFAs, the cAMP antagonist, RP-cAMPs did not block n-3 PUFA CREB activation.

251 inly associated with the P13K-AKT signaling, cAMP signaling and cell cycle process.

252 Here, we investigate slow cAMP-induced activation in purified SthK channels using

253 This is reminiscent of the slow, cAMP-induced activation reported for the hyperpolarizati

254 oach, we studied the contribution of spatial cAMP signaling in controlling cilia length.

255 Our study reveals that spatiotemporal cAMP signaling is under precise control of nanometer-siz

256 To explain signaling specificity, cAMP-degrading phosphodiesterases (PDEs) have been sugge

257 nergic axonal activity and gradual sustained cAMP increases.

258 The rutabaga-adenylyl cyclase synthesizes cAMP in a Ca(2+)/calmodulin-dependent manner, serving as

259 oprecipitation experiments demonstrated that cAMP response elements binding protein regulates the exp

260 Here, we find that cAMP synthesis in response to elevated glucose and the s

261 ht-activated phosphodiesterase LAPD, and the cAMP biosensor mlCNBD-FRET to the cilium.

262 n used to identify additional players in the cAMP-signaling cascade.

263 As in mammals, the cAMP/PKA pathway plays a key role in memory formation.

264 ssfully to study the in vivo activity of the cAMP cascade.

265 We found that loss of the cAMP response element-binding protein (CREB) transcripti

266 pha mutation results in dysregulation of the cAMP signaling cascade, leading to upregulation of phosp

267 owth factors, cytokines, and elements of the cAMP-generating system as potential biomarkers for depre

268 oration can be achieved by activation of the cAMP/PKA pathway, by either intracellular injection of c

269 Forskolin, an activator of the cAMP/PKA pathway, increased wild-type Kv7.5 but not wild

270 D39 expression through the inhibition of the cAMP/PKA/p-CREB pathway, or by blocking adenosine signal

271 assays by showing that they can predict the cAMP-signaling potencies of AM and AM2/IMD chimeras.

272 astrocytes were treated with n-3 PUFAs, the cAMP antagonist, RP-cAMPs did not block n-3 PUFA CREB ac

273 Our results suggest that the cAMP-Fyn axis in the DMS dMSNs is a molecular transducer

274 e when cAMP levels are monitored through the cAMP sensor.

275 In cells CFTR is activated through the cAMP signaling pathway, overstimulation of which during

276 or via a novel pathway initiated through the cAMP-activated guanine nucleotide exchange factor NCS-Ra

277 measuring real-time cAMP dynamics using the cAMP difference detector in situ assay in a variety of i

278 a(v)1.5 (Na(v)1.5(+/)) and mice in which the cAMP-dependent regulation of hyperpolarization-activated

279 Treatment with the cAMP analogue Br-cAMP to mimic cAMP rise at maturation o

280 ) channels probably by interference with the cAMP/cAMP-dependent protein kinase pathway, resulting in

281 e whether Fyn's actions are mediated through cAMP signaling, DMS dMSNs were infected with GalphasDREA

282 wnstream G-protein coupled receptors through cAMP-PKA signaling.

283 assessed for AR subtype selectivity through cAMP accumulation assays.

284 diesterase inhibitors by measuring real-time cAMP dynamics using the cAMP difference detector in situ

285 cal concentrations is predominantly bound to cAMP binding sites and, thus, immobile.

286 phodiesterase two dependent negative cGMP-to-cAMP cross-talk.

287 ean et al. used a novel cAMP sensor to track cAMP dynamics and report a coordinated effort of adaptat

288 mooth muscle cells that eventually triggered cAMP/PKA-dependent relaxation of airways.

289 ion of short-lived cell proteins, but unlike cAMP, also markedly increased proteasomal degradation of

290 induction of PRC by sildenafil depends upon cAMP and the transcription factor CREB.

291 irochaeta thermophila, activates slowly upon cAMP increase.

292 y reveal the molecular basis for the I942 vs cAMP mimicry and competition, but also suggest that the

293 exhibit blunted responses to octopamine when cAMP levels are monitored through the cAMP sensor.

294 tes both Ser307 and Ser309 residues, whereas cAMP signaling induces dephosphorylation at the tandem s

295 It is unclear whether cAMP generated by beta-adrenergic receptors (betaARs) is

296 d we apply it to the HCN4 ion channel, whose cAMP-binding domain is an archetypal conformational swit

297 ta holoenzyme: It is easier to activate with cAMP, and the cooperativity is reduced.

298 ion is widely accepted to be associated with cAMP-mediated activation of protein kinase A (PKA).

299 her, treatment of mouse pituitary cells with cAMP pathway agonists in vitro and in vivo elicited biom

300 ed chloride secretory response together with cAMP-mediated inhibition of Poly I:C-stimulated IFNbeta