ライフサイエンスコーパス: PKA

1 PKA activation results in tumors that are more benign, e

2 PKA can drive internal calcium release and promote calci

3 PKA knockdown did not affect the Drp1-Mff interaction, b

4 PKA phosphorylation attenuates I(SK) rectification by re

5 PKA preferentially targeted two serine residues in TOMM3

6 PKA-dependent phosphorylation of Ser(495) directly impai

7 at adrenergic stimulation of BAT activates a PKA-dependent mitochondrial Ca(2+) extrusion via the mit

8 rotein of 25 kDa (SNAP-25/SN25), serves as a PKA substrate, implying a potential role of SN25 in regu

9 Taken together, these findings identify a PKA/HSL signaling pathway in luteal cells in response to

10 Both compartments readily dissolve in a PKA-dependent manner within minutes of glucose reintrodu

11 Overexpression of a PKA inhibitor blocked the effects of LH and forskolin on

12 ll than in PKA-intact cells, indicative of a PKA-dependent feedback mechanism.

13 onversely, GNAS (G-protein alpha subunit), a PKA activator that is genetically activated in a small s

14 We further show that a PKA fusion oncoprotein associated with an atypical liver

15 ich cAMP increases NCC phosphorylation via a PKA-dependent phosphorylation of I1 and subsequent inhib

16 suppressed cAMP activated protein kinase A (PKA) activities, resulting in reduced phosphorylation of

17 subcellular regulation of protein kinase A (PKA) activity is important for the motile behavior of ma

18 gated (CNG) channels or by protein kinase A (PKA) activity.

19 one (LH) via activation of protein kinase A (PKA) acutely stimulates luteal progesterone synthesis vi

20 ultiple kinases, including protein kinase A (PKA) and C (PKC).

21 lternative cAMP targets to protein kinase A (PKA) and Epac2 is abundant in the cerebellum.

22 ite, through its effectors protein kinase A (PKA) and exchange proteins directly activated by cAMP (E

23 ties to signaling via cAMP/protein kinase A (PKA) and protein kinase C (PKC).

24 e profiling, we identified protein kinase A (PKA) as an active kinase in small cell lung cancer (SCLC

25 amban (PLN) is targeted by protein kinase A (PKA) at Ser(16) and by Ca(2+)/calmodulin-dependent prote

26 the formation of a SMAD3/4-protein kinase A (PKA) complex that activates C-terminal Src kinase (CSK)

27 athway at the level of the protein kinase A (PKA) enzyme.

28 monophosphate (cAMP), and Protein Kinase A (PKA) exist in an oscillatory circuit characterized by a

29 Protein Kinase A (PKA) exists as a tetrameric holoenzyme which activates w

30 differential modulation of protein kinase A (PKA) in each class of spiny projection neuron(2).

31 Regulatory subunits of protein kinase A (PKA) inhibit its kinase subunits.

32 ated protein kinase (ROCK)/protein kinase A (PKA) inhibitor fasudil, a drug already tested on humans.

33 enes in the cAMP-dependent protein kinase A (PKA) pathway and PKA catalytic activity.

34 that lack a well-conserved protein kinase A (PKA) phosphorylation site, S551, showed longer non-rapid

35 IK-1 has several predicted protein kinase A (PKA) phosphorylation sites.

36 ontractile properties in a protein kinase A (PKA) phosphorylation-dependent manner.

37 ardiomyocytes is driven by protein kinase A (PKA) phosphorylation.

38 rs of adenylyl cyclase and protein kinase A (PKA) prevented the effects of Lgmn.

39 ors of adenylyl cyclase or protein kinase A (PKA) prevented the effects of Lgmn.

40 onstrate that Ras/MAPK and Protein Kinase A (PKA) signaling act downstream of AdoR and that Ras/MAPK

41 mulation of cAMP-dependent protein kinase A (PKA) signaling in cells inactivates CaMKK2 by phosphoryl

42 ing hormone (LH) activates protein kinase A (PKA) signaling in luteal cells, increasing delivery of s

43 ated by the cAMP-dependent protein kinase A (PKA) signaling pathway.

44 -responsive cAMP-dependent protein kinase A (PKA) signaling pathways also suggests enhanced responses

45 pendent on downstream cAMP/protein kinase A (PKA) signaling, which differs between the mOFC and lOFC.

46 s of adenylate cyclase and protein kinase A (PKA) signaling.

47 gic receptor (betaAR)/cAMP/protein kinase A (PKA) signalling pathway leads to enhanced Ca(V) 1.2 acti

48 phorylation of Ca(v)1.2, a protein kinase A (PKA) site using S1928A Ca(v)1.2 phosphomutant mice revea

49 AKAPs anchor protein kinase A (PKA) through PKA regulatory subunits, and we show that A

50 iew mechanisms that bestow protein kinase A (PKA) versatility inside the cell, appraise recent advanc

51 a and its interaction with protein kinase A (PKA), a known node in the beta-adrenergic signaling path

52 tivated the cAMP effector, protein kinase A (PKA), as determined by the PKA reporter, AKAR4-NES, and

53 rotein kinase II (CaMKII), protein kinase A (PKA), protein kinase C (PKC), and AMPA receptor genes th

54 nding protein that targets protein kinase A (PKA), RNAs, and other signaling enzymes to the outer mit

55 protein kinase (ROCK) and protein kinase A (PKA), we attempted to rescue Ophn1-dependent pathologica

56 vels are also regulated by protein kinase A (PKA), which phosphorylates SK2 in its C-terminal domain,

57 rescue mechanism involving Portein Kinase A (PKA)-mediated facilitation of chloride channel-7 (ClC-7)

58 stresses, as seen for the protein kinase A (PKA)-mediated general stress response in yeast, which is

59 lycemia is associated with protein kinase A (PKA)-mediated stimulation of L-type Ca2+ channels in art

60 sphorylation at Ser-845, a protein kinase A (PKA)-targeted site within its intracellular C-terminal t

61 amma subunits, PIP(3), and protein kinase A (PKA).

62 AMP-mediated activation of protein kinase A (PKA).

63 of cAMP and thus activates protein kinase A (PKA).

64 ter its phosphorylation by protein kinase A (PKA).

65 een the two CNB domains of protein kinase A (PKA).

66 mediated by cAMP-dependent protein kinase A (PKA).

67 c output via activation of protein kinase A (PKA).

68 ock protein 90 (HSP90) and protein kinase A (PKA).

69 ing of P2Y(11)/ P2Y(11)-like receptors, AC5, PKA and Ca(V)1.2 into nanocomplexes at the plasma membra

70 activates AC8 to generate cAMP and activate PKA.

71 nd exhibit nuclear localization of activated PKA.

72 JMJD3 at Thr-1044 by FGF21 signal-activated PKA increases its nuclear localization and interaction w

73 Additionally, PKA is rapidly and locally activated by mechanical stret

74 channel activity by beta-adrenergic agonists/PKA also requires this rigid linker and beta-binding to

75 o the intrinsic allosteric regulation of all PKA holoenzymes and could also explain why most disease

76 nsights into how the finely tuned allosteric PKA signaling network is disrupted by the oncogenic J-C

77 By altering PKA activity PKI can act as a molecular switch, driving

78 subunits, and we show that AKAP8L can anchor PKA through regulatory subunit Ialpha.

79 plexities of interaction between the AIP and PKA pathway.

80 e points to a connection between the AIP and PKA pathways.

81 We conclude that cMyBP-C binding and PKA-mediated phosphorylation can modulate actin dynamics

82 Also, cAMP and PKA (cAMP dependent protein kinase) activity were monito

83 iomolecular condensates enriched in cAMP and PKA activity, critical for effective cAMP compartmentati

84 are coupled with activation of the cAMP and PKA pathway, the exact roles of these 2 receptors in the

85 cyclase inhibitor 2',5'-dideoxyadenosine and PKA inhibitor KT5720 inhibited enhancement of phosphoryl

86 real-time relationship between dopamine and PKA in spiny projection neurons remains untested in beha

87 uce Ca(2+) mobilization, cAMP formation, and PKA/protein kinase D (PKD) activation, but not beta-arre

88 ased phosphorylation sites in PKA-intact and PKA-null cells both revealed a preference for basic amin

89 , palmitate, and TNF-alpha via NF-kappaB and PKA pathways.

90 dependent protein kinase A (PKA) pathway and PKA catalytic activity.

91 and activation of protein kinase D (PKD) and PKA, but not beta-arrestin recruitment or PAR(2) endocyt

92 ssion yeast MAPK-activated kinase (Srk1) and PKA (Pka1).

93 ) at Thr(17) beta-Adrenergic stimulation and PKA-dependent phosphorylation of Ser(16) acutely stimula

94 To determine how TORC1 and PKA cooperate to regulate cell growth, we performed temp

95 se, in the presence and absence of TORC1 and PKA inhibitors.

96 hough both Ube3a-mediated ubiquitination and PKA-induced phosphorylation reduce synaptic SK2 levels,

97 reporting the first cryo-EM structure of any PKA holoenzyme.

98 Two downstream effectors of cAMP are PKA and exchange protein directly activated by cAMP (Epa

99 , intermolecular disulfide formation between PKA type I regulatory subunits (PKA-RI) has been describ

100 derstanding the complex interactions between PKA and Ube3a in the regulation of SK2 synaptic levels m

101 demonstrate the dynamic relationship between PKA, HSL, and lipid droplets in luteal progesterone synt

102 he mitochondria, which was dependent on both PKA and HSL activation.

103 ing is significantly reversed only when both PKA and Epac pathways were inhibited together.

104 phosphorylation happens, CFTR activation by PKA binding is completely reversible.

105 ation in tonic current, which was blocked by PKA and PKC inhibition.

106 nctional effects on the channel conferred by PKA-dependent phosphorylation at serine-465.

107 BS-induced SK2 endocytosis is facilitated by PKA activation, SK2 recycling to synaptic membranes afte

108 Long-lived memory was mediated by PKA-regulated stress-responsive transcription factors an

109 ibitors of the protein kinase Akt but not by PKA inhibitors.

110 ing but is unsuitable for phosphotransfer by PKA, and CFTR mutants lacking phosphorylatable serines--

111 t importantly, it can be acutely reversed by PKA inhibitors, leading to recovery of KCa3.1 function a

112 post-synaptic plasticity describing CaMKII, PKA, and PKC pathways and their contribution to synaptic

113 pendence of the relative phase between cAMP, PKA, and Ca(2+).

114 eptor stimulation of cardiac inotropy, cAMP, PKA, L-type Ca(2+) current, Ca(2+) transients, and cell

115 effects on hippocampal cAMP-CREB-BDNF, cAMP-PKA-LIMK1-cofilin, and RhoA-ROCK2 pathways.

116 ceptor activation could be abolished by cAMP-PKA inhibitors.

117 he molecular machinery for feedforward, cAMP-PKA-calcium signaling.

118 de detailed molecular insights into how cAMP-PKA signaling inactivates CaMKK2 and reveals a pathway t

119 2, secreted from infected BMM s induces cAMP-PKA pathway by binding to the EP2/EP4 receptor of CD4(+)

120 vates adenylyl cyclases to produce more cAMP-PKA signaling.

121 y repressing the nutrient signaling Ras-cAMP-PKA pathway at the level of the protein kinase A (PKA) e

122 The cAMP-PKA and MAP kinase pathways are essential for plant infe

123 -2 protein expression, probably via the cAMP-PKA pathway.

124 eam G-protein coupled receptors through cAMP-PKA signaling.

125 metabolism was found to be regulated by cAMP/PKA (protein kinase A)- and proteasome-dependent signali

126 oid receptor coupling to the downstream cAMP/PKA intracellular cascade.

127 oid receptor coupling to the downstream cAMP/PKA intracellular cascades.

128 traffics them to the nucleus following cAMP/PKA-mediated lipolytic stimulation.

129 xamined whether amnesiac is involved in cAMP/PKA dynamics in response to dopamine and acetylcholine c

130 del for the dynamics of calcium-induced cAMP/PKA dynamics in dendritic spines.

131 easonably well-studied, calcium-induced cAMP/PKA dynamics, particularly with respect to frequency mod

132 ells where they triggered intracellular cAMP/PKA signals that attenuated mitochondrial metabolism at

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

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

135 on can be achieved by activation of the cAMP/PKA pathway, by either intracellular injection of cAMP o

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

137 tivates sAC which in turn activates the cAMP/PKA/CREB axis.

138 xpression through the inhibition of the cAMP/PKA/p-CREB pathway, or by blocking adenosine signaling d

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

140 identified serine-465 as the site conferring PKA-dependent effects on SK2 channel function.

141 Signaling events coupling PKA activation and aquaporin-2 regulation were largely u

142 ropism and the role of the adenylate cyclase/PKA/AKT-mediated signaling pathway in HCMV infection rev

143 Furthermore, disruption of dAKAP1-PKA complexes affected cell motility and mitochondrial m

144 In some cases, for example Dopamine-PKA-CREB and GABA-PKC-CREB signaling pathways, the bioty

145 ransiently high PKA activity, the downstream PKA target important for regulating the transmission fro

146 evealing serine-465 as the site that elicits PKA-dependent phosphorylation effects on SK2 channel fun

147 ther these results indicate that endothelial PKA activity mediates a critical switch from active spro

148 units (PKA-RI) has been described to enhance PKA's affinity for protein kinase A anchoring proteins,

149 mulate cAMP production resulting in enhanced PKA-dependent LTCC activity.

150 ignaling is predominantly, but not entirely, PKA-dependent. Upregulated sites in PKA-null cells inclu

151 These observations establish PKA as a locally regulated effector of cellular mechanot

152 Finally, PKA activation increases SK2 phosphorylation and ubiquit

153 Here, we show that Amnesiac is required for PKA activation resulting from coincidence detection, a m

154 y of a sex difference in the requirement for PKA in synaptic potentiation, we tested how PKA inhibiti

155 -expression of beta-adrenergic pathway genes PKA regulatory subunit type I, PKA regulatory subunit ty

156 getable signaling networks, such as the GNAS/PKA/PP2A axis in SCLC.

157 any cell types, yet the mechanisms governing PKA activity during cell migration remain largely unknow

158 ritical solvent-exposed residues at the GRTH/PKA interface (E165/K240/D237), on the control of GRTH p

159 ylation via glucose-responsive kinases GSK3, PKA, PKC, and CDK5.

160 emporally synchronized with transiently high PKA activity, the downstream PKA target important for re

161 results provide important insights into how PKA-mediated phosphorylation and 14-3-3 binding regulate

162 PKA in synaptic potentiation, we tested how PKA inhibition affects LTP.

163 We recently reported that type I PKA regulatory subunits (RIalpha) interact with phosphat

164 pathway genes PKA regulatory subunit type I, PKA regulatory subunit type II, and Ca(2+)/calmodulin-de

165 A has been deleted (CRISPR-Cas9) to identify PKA-independent responses to vasopressin.

166 In model organisms, it impairs PKA (protein kinase A) phosphorylation, increases calciu

167 Fasting-associated changes in PKA signaling are attenuated in transgenic mice constitu

168 nduced intermolecular disulfide formation in PKA-RI, only 1-nitrosocyclohexalycetate (NCA) and diamid

169 levels were an order of magnitude higher in PKA-null than in PKA-intact cells, indicative of a PKA-d

170 analysis of the phosphopeptides increased in PKA-null cells indicates that vasopressin activates one

171 bservations of electrostatic interactions in PKA substrate recognition mechanism and nucleus localiza

172 d also explain why most disease mutations in PKA regulatory subunits are dominant negative.

173 We conclude that Myo5b defects result in PKA stimulation that activates residual channels on the

174 ificantly decreased phosphorylation sites in PKA-intact and PKA-null cells both revealed a preference

175 ntirely, PKA-dependent. Upregulated sites in PKA-null cells include Ser256 of AQP2, which is critical

176 rder of magnitude higher in PKA-null than in PKA-intact cells, indicative of a PKA-dependent feedback

177 d thus potentially attributable to increased PKA activity.

178 al that LH, forskolin, and 8-Br cAMP-induced PKA-dependent phosphorylation of HSL at Ser563 and Ser66

179 induced Q pathway was restored by inhibiting PKA activity (Rp-8-Br-cAMPS).

180 activation of cAMP-dependent protein kinase (PKA) and subsequent cardiac protein phosphorylation.

181 activities of cAMP-dependent protein kinase (PKA) and the protein phosphatase 1 (PP1) and/or PP2A.

182 ere we report cAMP-dependent protein kinase (PKA) as the direct target of hydralazine.

183 here that the cAMP-dependent protein kinase (PKA) inhibitor H89 increases lysosomal V-ATPase activity

184 I (TORC1) and cAMP-dependent protein kinase (PKA) pathways.

185 and Cbeta) of cAMP-dependent protein kinase (PKA), a pleiotropic holoenzyme that regulates numerous f

186 nophosphate (cAMP)-dependent protein kinase (PKA), leading to activation of the PKA pathway, are the

187 C) subunit of cAMP-dependent protein kinase (PKA), replacing exon 1, this fusion protein, J-C subunit

188 ry subunit of cAMP-dependent protein kinase (PKA), RIalpha, undergoes liquid-liquid phase separation

189 activation of cAMP-dependent protein kinase (PKA).

190 vation of the cAMP-regulated protein kinase (PKA).

191 been shown to be dependent both on localized PKA activity and, more recently, on mechanical reciproci

192 We find that localized PKA activity in migrating cells rapidly decreases upon i

193 characterize J-C bound to RIIbeta, the major PKA regulatory (R) subunit in liver, thus reporting the

194 Phosphoproteomic analyses identified many PKA substrates and mechanisms of action.

195 mic damage in mice lacking the mitochondrial PKA scaffold AKAP1, apparently via opposing effects on D

196 Moreover, PKA activity is spatially and temporally correlated with

197 ns, extracellular levels of dopamine and net PKA activity in spiny projection neurons in the nucleus

198 hout affecting the canonical Wnt pathway nor PKA signaling.

199 tently, Nep1 inhibition also restores normal PKA activation in amn mutant flies.

200 membrane progesterone signaling and nuclear PKA in metastatic recurrence, and provide genomic bases

201 re prominently upregulated via activation of PKA (protein kinase A), essential molecular details rema

202 after exposure to NCA revealed activation of PKA and inhibition of phosphatase activity thus explaini

203 Activation of PKA by forskolin decreased the binding of USP7 and USP10

204 Mammary-specific activation of PKA in mouse models leads to aberrant differentiation an

205 in governing correct temporal activation of PKA required for erythrocyte invasion, whilst suppressin

206 Here, we report that the activation of PKA signaling pathway decreases the unitary conductance

207 pharmacological tool to induce activation of PKA.

208 K-1 current was not related to activation of PKA.

209 led P2Y receptor is an upstream activator of PKA mediating LTCC potentiation during diabetic hypergly

210 that both production of cAMP and activity of PKA are critical for erythrocyte invasion, whilst key de

211 d of calcium signaling, and the amplitude of PKA signaling, upon receiving a cAMP-driving stimulus.

212 in studies involving single cell analysis of PKA activity.

213 onin with tropomyosin, and limits binding of PKA to local sarcomere microdomains.

214 906, 907 and 910 positions) by a cascade of PKA, GSK3beta and CSKI kinases.

215 the response to CRISPR-mediated deletion of PKA, results from in vitro phosphorylation studies using

216 ce DRP1 as an important target downstream of PKA in steroidogenic luteal cells.

217 vity, modulating the extent, and duration of PKA-mediated signaling events.

218 This newly discovered function of PKA-RIalpha adds an additional layer of complexity to ou

219 ef2/phospho-ERK activation, independently of PKA/CREB signaling.SIGNIFICANCE STATEMENT ERK phosphoryl

220 -1) ), which was eliminated by inhibition of PKA (1 mumol L(-1) ).

221 Inhibition of PKA activity genetically, or pharmacologically by activa

222 Finally, inhibition of PKA activity inhibits mechanically guided migration, als

223 Modulations of PKA in spiny projection neurons that express type-1 and

224 sion of PKI and its subsequent repression of PKA dysregulates these signaling pathways, resulting in

225 kinases, including the catalytic subunit of PKA (PKAc).

226 ortance of both Calpha and Cbeta subunits of PKA during human development.

227 via an autocrine process, the sustaining of PKA activation-mediating memory, which subsequently is i

228 a regulator of autophagy, as novel target of PKA.

229 of cardiac myocytes induced translocation of PKA and phosphatases to the myofilament compartment as s

230 Knockdown of USP10 had an additive effect on PKA-dependent inhibition of NHE3.

231 ng through binding the CORD domain of Ci, or PKA, revealing separate inhibitory roles of these two co

232 ignaling in collecting duct cells is in part PKA-independent.

233 In particular, PKA activity is required for the propagation of SCLC ste

234 on of Rev-ErbA-alpha and induced a PI3K/PDK1/PKA-dependent signaling cascade.

235 ion, but was abolished after pharmacological PKA inhibition and thus potentially attributable to incr

236 DEP1 also harbors the primary PKA phosphorylation site, suggesting that an improved un

237 Mutation of the putative PKA phosphorylation sites did not change the inhibitory

238 ro phosphorylation studies using recombinant PKA, the response to the broad-spectrum kinase inhibitor

239 , decreasing glucose production and reducing PKA-mediated phosphorylation in primary mouse hepatocyte

240 ogical phenotypes by treatment with the ROCK/PKA inhibitor fasudil.

241 t stage in Ophn1-dependent XLID through ROCK/PKA inhibition.SIGNIFICANCE STATEMENT In this study we d

242 get of Cyclin B-Cdk1), and of BCL9L at S915 (PKA).

243 Acting through the repression of SOX4, PKA activation promotes tumor differentiation and repres

244 Hence, when studying PKA-mediated cAMP signaling with cAMP derivatives in a n

245 tivation of EP2 receptors and the subsequent PKA-dependent phosphorylation of alpha3GlyRs within the

246 -dependent protein kinase catalytic subunit (PKA).

247 tion between PKA type I regulatory subunits (PKA-RI) has been described to enhance PKA's affinity for

248 (AKAP79; AKAP150 in rodents), which targets PKA to GluA1.

249 nce of activation of two major cAMP targets: PKA and EPAC.

250 multiplexed DREADD/PSAM chemogenetics, that PKA-induced restoration of synapses triggers an excitati

251 We conclude that PKA's regulatory subunits are cAMP-dependent signal tran

252 Ca(2+) imaging experiments established that PKA phosphorylation lessens rectification of I(SK) via r

253 We also found that PKA-mediated phosphorylation of the Thr(89) residue in H

254 Our results indicate that PKA maintains repressive control over MAPK signaling as

255 Here, we investigated the possibility that PKA is regulated by mechanical signaling during migratio

256 Thus, we propose that PKA phosphorylation of the DEP1 domain hampers P-Rex1 bi

257 Here, we report that PKA activation restores theta burst stimulation (TBS)-in

258 , CRISPR-mediated gene editing revealed that PKA and AMPK are not required for the starvation-depende

259 ometry and peptide spot arrays revealed that PKA phosphorylates ATG16L1alpha at Ser268 and ATG16L1bet

260 tants lacking phosphorylatable serines--that PKA efficiently opens CFTR channels through simple bindi

261 Our findings suggest that PKA-dependent phosphorylation of serine 53 on the amino

262 These results suggest that PKA-mediated phosphorylation and PP1/PP2A-dependent deph

263 These results suggest that PKA-SIK signaling is involved in the regulation of sleep

264 The PKA-inhibitor (PKI) family members PKIalpha, PKIbeta, an

265 The PKA/proteasome-dependent signaling cascade was mediated

266 -N,N,N',N'-tetraacetic acid tetrakis and the PKA inhibitor N-[2-(p-bromocinnamylamino)ethyl]-5-isoqui

267 protein kinase A (PKA), as determined by the PKA reporter, AKAR4-NES, and induced phosphorylation of

268 ving an exposed basic loop that contains the PKA site.

269 data show that amnesiac is necessary for the PKA activation process that results from coincidence det

270 Computational modeling revealed how the PKA-mediated regulatory network could encode previous st

271 nt to explain concurrent fluctuations in the PKA activity of spiny projection neurons.

272 stimulates sulfenylation of cysteines in the PKA catalytic subunit by H(2)O(2) and a significant prop

273 r Amnesiac in establishing within the MB the PKA dynamics that sustain middle-term memory (MTM) forma

274 n kinase (PKA), leading to activation of the PKA pathway, are the genetic cause of Carney complex whi

275 n channel activity beyond termination of the PKA signal.

276 how in addition that the substitution of the PKA-targeted serine with a negatively charged residue wi

277 in CCI-induced neuropathic pain through the PKA-TRP-A1 pathway.

278 comparable kinetics and dynamic range to the PKA FRET reporter, AKAR3EV.

279 r sex, an effect that was insensitive to the PKA inhibitors (H-89, KT270) but that was blocked by the

280 Here, we examined whether the PKA phosphorylation sites of SIK1 and SIK2 are involved

281 AKAPs anchor protein kinase A (PKA) through PKA regulatory subunits, and we show that AKAP8L can anc

282 that is maintained by cAMP signaling through PKA and EPAC.

283 Thus, PKA binding promotes release of the unphosphorylated R d

284 Thus, PKA-dependent pathways in each class of spiny projection

285 eta, and PKIgamma bind with high affinity to PKA and block its kinase activity, modulating the extent

286 , and reversible through R-domain binding to PKA--and possibly also to other members of a large netwo

287 l approaches, and we found that they lead to PKA holoenzymes which are more sensitive to activation b

288 embrane fractions and activated signaling to PKA, and this canonical endogenous pathway was attenuate

289 ctly activated by cAMP (Epac), which, unlike PKA, is often linked to elevation of [Ca(2+)](i).

290 rocyte invasion, whilst suppressing untimely PKA activation during early intra-erythrocytic developme

291 otentiate vascular L-type Ca(2+) channel via PKA, but the underlying mechanisms are unclear.

292 in external nutrients, such as glucose, via PKA.

293 We hypothesize that LH via PKA differentially regulates the phosphorylation of DRP1

294 to elucidate whether THIK-1 is regulated via PKA, we expressed THIK-1 channels in a mammalian cell li

295 t the strength of transmission from SACs via PKA-mediated phosphorylation at T138.

296 d an altered path of tumor evolution whereby PKA curtails the emergence of aggressive subpopulations.

297 proteomics in collecting duct cells in which PKA has been deleted (CRISPR-Cas9) to identify PKA-indep

298 While PKA is a well-known regulator of physiological and oncog

299 Prkci (an atypical PKC) are consistent with PKA-independent regulation of these protein kinases.

300 was reversible by incubation of the VMs with PKA inhibitor H89 (1 mumol L(-1) ).