ライフサイエンスコーパス: PKA inhibitor

1 T-2R antagonist) or H89 (a protein kinase A (PKA) inhibitor).

2 ior treatment of cells with H-89, a specific PKA inhibitor.

3 The antagonist effects were occluded by a PKA inhibitor.

4 y of Slo-a, an effect that was reversed by a PKA inhibitor.

5 ry domain similar to that of the heat-stable PKA inhibitor.

6 nist, 8Br-cAMP, and was inhibited by H-89, a PKA inhibitor.

7 ally attenuated by pretreatment with H-89, a PKA inhibitor.

8 er basal conditions and in the presence of a PKA inhibitor.

9 112/136A mutant was >90% inhibited by H89, a PKA inhibitor.

10 ein kinase (PKA), and was blocked by H-89, a PKA inhibitor.

11 of G6PD with NOX, which was inhibited by the PKA inhibitor.

12 that is more stable and is a more effective PKA inhibitor.

13 were performed in the absence or presence of PKA inhibitors.

14 mouse platelets is inhibited by both PKG and PKA inhibitors.

15 in kinase A (PKA) activators and occluded by PKA inhibitors.

16 erine 10, based on inhibition exclusively by PKA inhibitors.

17 or forskolin and was inhibited by the AC and PKA inhibitors.

18 d inhibition of specific PKA activity by the PKA inhibitors.

19 icin damage is also significantly blocked by PKA inhibitors.

20 ctivator N(6)-Phe-cAMP and prevented by both PKA inhibitors.

21 cally dependent when pre-treated with PKC or PKA inhibitors.

22 othelial alignment, was similarly blocked by PKA inhibitors.

23 by a specific cAMP-dependent protein kinase (PKA) inhibitor.

24 P analog, and blocked by a protein kinase A (PKA) inhibitor.

25 T were blocked by cAMP and protein kinase A (PKA) inhibitors.

26 t kinase P70S6K was significantly reduced by PKA inhibitor 14-22 amide and by the mitogen signal-regu

27 In Pkd2cKO cells pretreated with the PKA inhibitor 14-22 amide, myristolated (1 muM) and in m

28 inhibitory peptide, or the protein kinase A (PKA) inhibitor 14-22 amide.

29 Another PKA inhibitor 4-cyano-3-methylisoquinoline only partly r

30 ts of cPKA were blocked by co-application of PKA inhibitor (6-22) amide (PKI).

31 lso increased [Ca2+]i in the presence of the PKA inhibitor 8-bromoadenosine-3',5'-cyclic monophosphor

32 mide I (Bis-I, 10 microM six rats)], PKG and PKA inhibitor (A-3, 1 mM, six rats), or the serine-threo

33 thermore, pre-treatment with Rp-8-Br-cAMP, a PKA inhibitor, abolished the effects of 8-Br-cAMP.

34 ced IGF-I gene activation, while cytoplasmic PKA inhibitor additionally caused the removal of C/EBPde

35 CGRP-induced currents were reduced by the PKA inhibitors adenosine 3',5'-cyclic monophosphorothioa

36 The specific PKA inhibitor, adenosine 3',5'-cyclic monophosphothioate

37 Addition of PKA inhibitors after purinergic stimulation only partial

38 Preincubation with PKA inhibitors also blocked the shift in mobility of the

39 A myristoylated PKA inhibitor, amide 14-22, inhibited excystation with a

40 ulated by isoproterenol in the presence of a PKA inhibitor and GTP-gamma-S in LDS but not VEDS cardio

41 ted that beta1-AR recycling was inhibited by PKA inhibitors and by mutations in the PDZ that interfer

42 d forskolin was also completely inhibited by PKA inhibitors and SB202190, indicating that these effec

43 8-fold), and this response was eliminated by PKA inhibitors and SB202190.

44 cted T150 phosphorylation was not blocked by PKA inhibitors and was not induced by PKA activation, an

45 ellular stimulation by forskolin (blocked by PKA inhibitor) and by the co-immunoprecipitation of p38

46 y pertussis toxin (G(i) inhibitor) and H-89 (PKA inhibitor), and was insensitive to depletion of endo

47 ted in response to elevated cAMP, blocked by PKA inhibitor, and essential for scaffold-receptor assoc

48 1 S845 phosphorylation could be blocked by a PKA inhibitor, and GluA1 T840 dephosphorylation could be

49 inhibitor of protein kinase A, myristoylated PKA inhibitor, and the adenylyl cyclase inhibitor SQ-225

50 y of the mutant receptor, whereas a specific PKA inhibitor antagonizes this increase.

51 H-89, a cyclic AMP-dependent protein kinase (PKA) inhibitor, antagonizes the enhancing effect of isop

52 Although a large number of PKA inhibitors are available, there are no reported EPAC

53 Injection of WIPTIDE (a PKA inhibitor) at 24 hr after PKACS reduced hyperalgesia

54 s raised overnight in BDNF were treated with PKA inhibitors, BDNF-mediated protection did not end, de

55 Treatment with PKA inhibitors before or in conjunction with BDNF treatm

56 However, in each unit, PKA inhibitors blocked only one of the two effects (eith

57 Application of a protein kinase A (PKA) inhibitor blocked the ability of D1 receptor activa

58 , pretreatment of HMC with protein kinase A (PKA) inhibitors blocked both Cdc42 activation and beta(1

59 Furthermore, specific protein kinase A (PKA) inhibitors blocked IL-1beta and PGE(2)-induced MUC5

60 When added to the pipette solution, H-89, a PKA inhibitor, blocked ATP and 8-Br-cAMP induced run-up

61 Furthermore, H89, a specific PKA inhibitor, blocked TNF-alpha-induced lipolysis and t

62 H-89, a protein kinase A (PKA) inhibitor, blocked the effect of forskolin.

63 ses S1412 phosphorylation that is blocked by PKA inhibitors but not by PI3-kinase/Akt inhibitors.

64 -stimulated p70s6k activity was repressed by PKA inhibitors but not by wortmannin or microinjection o

65 -kinase inhibitor) or H89 (protein kinase A (PKA) inhibitor) but not ICI182780 (estrogen receptor blo

66 This effect is not blocked by PKA inhibitors, but is blocked by inhibition of Kv1.2 en

67 nding, and the inhibition of PKA activity by PKA inhibitor can partially recover the reduced HNF-4alp

68 icular (i.c.v.) injection of either a PKC or PKA inhibitor completely reversed the expression of 5- t

69 omponent was occluded by a protein kinase A (PKA) inhibitor, consistent with our previous demonstrati

70 PKA inhibitor decreased CREB function in the CeA of NP r

71 cell migration was inhibited by ERK, but not PKA inhibitors, defining a functional link between PGE(2

72 TP is differentially sensitive to CaMKII and PKA inhibitors depending on the history of the synapse.

73 The cAMP-dependent PKA inhibitor did not prevent the taurocholate effect.

74 Protein kinase C (PKC) but not PKA inhibitor diminished the influence of hRFRP-1 on the

75 Although bath application of PKA inhibitor drugs (KT5720, Rp-8CPT-cAMP-S) blocked LTP

76 Administration of PKA inhibitor during T3 treatment of mice and rats as we

77 In contrast, injection of protein kinase A (PKA) inhibitors either before or after these hyperalgesi

78 PKA inhibitors elevate Kv1.2 surface levels, suggesting

79 ated with MKP3(DUSP6) inhibitors blocked and PKA inhibitors enhanced dephosphorylation of recombinant

80 n of PGE2 production with AACOCF3 or H-89, a PKA inhibitor, enhanced EGF-induced Erk-2 activity.

81 The pre-treatment with PKC or PKA inhibitors failed to attenuate or block the signs of

82 n of an inhibitor of protein kinase A (PKA), PKA inhibitor fragment (6-22) amide.

83 Pretreatment of the cells with the PKA inhibitor H-89 abolished the effect of the agonist o

84 The PKA inhibitor H-89 abrogates the effect of beta1 integri

85 The PKA inhibitor H-89 blocked both of these effects.

86 The fact that PKA inhibitor H-89 blocked these SCH442416 effects sugge

87 Treatment with the PKA inhibitor H-89 caused redistribution of C/EBPdelta t

88 The MEK inhibitor U0126 and/or the PKA inhibitor H-89 greatly enhanced the efficacy of the

89 In MIN6 beta-cells, the PKA inhibitor H-89 prevented Ca(2+)-dependent phogrin ph

90 enosine and 8-Br-cAMP, whereas the selective PKA inhibitor H-89 reversed the activation of Cdc42.

91 d CICR in response to exendin-4, whereas the PKA inhibitor H-89 was ineffective when tested at a conc

92 abrogated by treatment with 3 microm of the PKA inhibitor H-89, it is concluded that for INS-1 cells

93 KA activity, as shown in treatments with the PKA inhibitor H-89.

94 racellular Ca2+ stores, as revealed with the PKA inhibitor H-89.

95 n transfected Bal17 B cells treated with the PKA inhibitor H-89.

96 These actions were blocked with the specific PKA inhibitor H-89.

97 stitutively active RhoA or by treatment with PKA inhibitor H-89.

98 ression by PGE2 were blocked by the specific PKA inhibitors H-89 (30 microM) or SQ 22536 (500 microM,

99 Treatments of glioma cells using the PKA inhibitors H-89 and KT5720, overexpression of a PKA

100 KA) because of the lack of inhibition by the PKA inhibitors H-89 and KT5720.

101 activation of protein kinase A (PKA), as the PKA inhibitors H-89 and Rp-8Br-cAMPS abrogated cAMP inhi

102 ription stage, although experiments with the PKA inhibitors H-89 and Rp-cAMP or the PKG inhibitor KT5

103 surface NKCC2 and that the protein kinase A (PKA) inhibitor H-89 blocks this effect.

104 EC50 of <3 microm, and the protein kinase A (PKA) inhibitor H-89 enhanced ERK phosphorylation.

105 or PD98059, but not by the protein kinase A (PKA) inhibitor H-89.

106 this effect was blocked by protein kinase A (PKA) inhibitors H-89 and PKI, suggesting a dependence on

107 ls were treated with PGE2, protein kinase A (PKA) inhibitors H-89 or SQ 22536, protein kinase C (PKC)

108 We now report that protein kinase A (PKA) inhibitors (H-89, KT-5720, and myristoylated PKA in

109 n, pioglitazone plus atorvastatin plus H-89 (PKA inhibitor), H-89, or vehicle for 8 h.

110 erase activity in a dose-dependent manner; a PKA inhibitor, H-89, also blocked the induction by PTH a

111 Moreover bath application of PKA inhibitors, H-89, KT5720 and an inhibitory peptide t

112 and was attenuated by the protein kinase A (PKA) inhibitor, H-89 (20 microM).

113 ylation was blocked by the protein kinase A (PKA) inhibitor, H-89, and mimicked by the PKA activator,

114 he PKC activator, PMA; and protein kinase A (PKA) inhibitor, H-89; as well as the adenylate cylase ac

115 (pALDH3.5CAT) were enhanced 3-4-fold by the PKA inhibitor H8 but not by the PKC inhibitor H7 (>20 mi

116 ibitor calphostin C or the protein kinase A (PKA) inhibitor H8.

117 ffect was blocked by cell treatment with the PKA inhibitor H89 and was not observed in PKA-transfecte

118 The PKA inhibitor H89 dihydrochloride did not affect the ave

119 ct kin(-) cells or WT cells treated with the PKA inhibitor H89 from glutamine deprivation.

120 The PKA inhibitor H89 had little or no effect on inflammator

121 Treatment of NC cultures with the PKA inhibitor H89 or 1-10 nm okadaic acid (OA), a serine

122 Treatment of ECs with PKA inhibitor H89 or PI3K inhibitor LY294002 prevented t

123 S were negated by coinfusion with either the PKA inhibitor H89 or Rp-CAMPS.

124 protein kinase A (PKA) and is blocked by the PKA inhibitor H89 or small interfering RNA knockdown of

125 Pretreatment of HEK293 cells with the PKA inhibitor H89 or the PKC inhibitor GF109203X, indivi

126 The PKA inhibitor H89 potentiated LTB4 generation by control

127 in E2-BSA-treated trauma-hemorrhage rats by PKA inhibitor H89 prevented the E2-BSA attenuation of he

128 by reducing its interaction with LSD1 while PKA inhibitor H89 represses them by suppressing H3K4 met

129 Bath application of the PKA inhibitor H89 suppressed the early LTP induced by a

130 The PKA inhibitor H89 was without effect on the 007-induced

131 fibronectin aggregates was abolished by the PKA inhibitor H89, whereas the effect of GD1a was mimick

132 to block Raf-1 activation is ablated by the PKA inhibitor H89.

133 e cAMP pathway was already attenuated by the PKA inhibitor H89.

134 dobutamine, which could be prevented by the PKA inhibitor H89.

135 ntly attenuated by intra-VTA infusion of the PKA inhibitor H89.

136 n of PKA-alpha or treatment of HAEC with the PKA inhibitor H89.

137 pression could be completely reversed by the PKA inhibitor H89.

138 tivation was confirmed by the ability of the PKA inhibitors H89 (20 microm) and (R(p))-cAMP-S (1 mm)

139 (PKA) activation, as demonstrated using the PKA inhibitors H89 and myristoylated PKI(6-22) amide.

140 s are abolished when treating cells with the PKA inhibitors H89 or KT5720 as well as in cells express

141 Binding was reduced with PKA inhibitors H89 or Rp-8-Br-cAMPS.

142 cell fusion, whereas treatment of cells with PKA inhibitors H89, KT5720, and PKA Catalpha siRNA all e

143 n-2-amine] or the specific protein kinase A (PKA) inhibitor H89 (N-[2-(p-bromocinnamyl-amino)ethyl]-5

144 The protein kinase A (PKA) inhibitor H89 blocks this effect, suggesting that t

145 The protein kinase A (PKA) inhibitor H89 completely blocks the TCDD-dependent

146 Preincubation with the protein kinase A (PKA) inhibitor H89 or (R(p))-cAMPS, but not with the ina

147 cAMP-dependent protein kinase (PKA) inhibitor H89 reduced RGS9-1 labeling by more than

148 The protein kinase A (PKA) inhibitor H89, the TK inhibitor genistein, and the

149 The protein kinase A (PKA) inhibitors H89 and Rp-3', 5'-cyclic monophosphothio

150 D98059), PI3 kinase inhibitor (LY294002), or PKA inhibitor (H89) blocks the nicotine-induced Bad phos

151 A protein kinase A (PKA) inhibitor (H89) was largely ineffective under the s

152 A protein kinase A (PKA) inhibitor (H89, 20 micromol/l) suppressed hypoxia-i

153 the eNOS promoter was decreased by NO* and a PKA inhibitor, H89, and increased by a PKA activator, di

154 ns, and Cx43 protein expression, whereas the PKA inhibitor, H89, inhibited the stimulatory effect of

155 Bad pathway after tFCI, we administered the PKA inhibitor, H89, into the mouse brain after tFCI.

156 The PKA inhibitor, H89, was a potent inhibitor of PACAP38-in

157 ed by 8-Br-cAMP, and could be blocked by the PKA inhibitor, H89.

158 Two PKA inhibitors, H89 and KT5720, inhibited immune complex

159 Human PDE1A RNA and the PKA inhibitors, H89 and Rp-cAMPS, partially rescued phen

160 by the cyclic AMP-dependent protein kinase (PKA) inhibitor, H89 (10 microm).

161 d to control levels by the protein kinase A (PKA) inhibitor, H89, but H89 did not affect the fEPSPs i

162 In contrast, protein kinase A (PKA) inhibitors, H89 and [PKI(2-22)amide] attenuated the

163 d largely inhibited by the protein kinase A (PKA) inhibitors, H89 and myristoylated PKI(14--22) amide

164 tive PKA with targeted nuclear expression of PKA inhibitor had no effect on the subcellular location

165 These PKA inhibitors had no effect on the PAH induction of the

166 -8220, a PKC inhibitor, and 2 microM H-89, a PKA inhibitor, had no effect in unlesioned controls and

167 ted with TGFbeta and this was inhibited by a PKA inhibitor, (ii) PKA was co-immunoprecipitated from c

168 Furthermore, we found that a PKA inhibitor impaired ES cell proliferation, tumor grow

169 neurons in culture, we show that dialysis of PKA inhibitors in the presynaptic neuron blocks synaptic

170 ',5'-cyclic monophosphothioate (Rp-cAMPS), a PKA inhibitor, increased the period to 145 % of baseline

171 This effect was blocked by 30 microM H89, a PKA inhibitor, indicating that the observed effect was a

172 antagonized by a specific protein kinase A (PKA) inhibitor, indicating that the signaling pathway in

173 inhibit PKG, as these PKG inhibitors but not PKA inhibitors inhibit a different cGMP-induced intracel

174 H-89 and KT5720, two structurally different PKA inhibitors, inhibited LTD by more than 70% without a

175 (GFP)-tagged cAMP-dependent protein kinase (PKA) inhibitor, inhibits the ability of the permeant cAM

176 Moreover, infusing a PKA inhibitor into postsynaptic cells produced synaptic

177 ld tolerance was only partly reversed by the PKA inhibitor KT-5720 at a dose previously cited by othe

178 on of IBa by ISO was partially reversed by a PKA inhibitor, KT 5720, or a PKC inhibitor, calphostin C

179 Injecting the PKA inhibitor KT5720 before crowding prevented this tran

180 ssion was prevented by pretreatment with the PKA inhibitor KT5720 but not with the protein kinase G i

181 ced the level of phosphorylated PKA, and the PKA inhibitor KT5720 decreased, whilst the adenylate cyc

182 The selective PKA inhibitor KT5720 prevented the isoprenaline-induced

183 hibitor bisindolylmaleimide I (Bis I) or the PKA inhibitor KT5720.

184 desensitization in a manner sensitive to the PKA inhibitor KT5720.

185 oxide (NO) donor glyco-SNAP1 is inhibited by PKA inhibitors KT5720, PKI, Rp-Br-cAMPS, and H89, but no

186 The additional of a PKA inhibitor (KT5720) significantly ameliorated these e

187 Hindbrain injection of a PKA inhibitor, KT5720, significantly attenuated MTII-ind

188 of LCA were blocked by the protein kinase A (PKA) inhibitor, KT5720 (0.5-1.0 microm) and the K(ATP) c

189 rginase was abolished by a protein kinase A (PKA) inhibitor, KT5720, and was down-regulated by tyrosi

190 ffects were prevented by a protein kinase A (PKA) inhibitor, KT5720, or by mutation of a single conse

191 Pretreatment with the protein kinase A (PKA) inhibitor, KT5720, prevented the protective effect

192 Either ADORA2A or ADORA2B antagonists or the PKA inhibitor mPKI blocked these effects.

193 Both of these effects are prevented by the PKA inhibitor, myristoylated PKI.

194 was also inhibited by the protein kinase A (PKA) inhibitor, myristoylated PKI, but was not dependent

195 io-cAMP and blocked by pretreatment with the PKA inhibitor myrPKI(14-22).

196 y between PKA and PKI in the presence of the PKA inhibitor N-[2-(p-bromocinnamylamino)ethyl]-5-isoqui

197 ase inhibitor zaprinast (20 microm) plus the PKA inhibitor N-[2-(p-bromocinnamylamino)ethyl]-5-isoqui

198 esponse to PKA activation was blocked by the PKA inhibitor N-[2-p-bromocinnamyl-amino) ethyl]-5-isoqu

199 d this was reversed by the protein kinase A (PKA) inhibitor N-[2-((p-bromocinnamyl)amino)ethyl]-5-iso

200 lerythrine, but not by the protein kinase A (PKA) inhibitor N-[2-(4-bromocinnamylamino)ethyl]-5-isoqu

201 dideoxyadenosine, with the protein kinase A (PKA) inhibitor N-[2-(p-Bromocinnamyl-amino)ethyl]-5-isoq

202 Conversely, the protein kinase A (PKA) inhibitor N-[z-(p-bromocinnamylamino)ethyl]-5-isoqu

203 -4-fold by addition of the protein kinase A (PKA) inhibitors, N-(2-(methylamino)ethyl)-5-isoquinoline

204 Neither specific PKA inhibitors nor inactive control inhibitors have effe

205 al cultures was blocked by protein kinase A (PKA) inhibitor, occluded by PKA activator, and prevented

206 Application of a protein kinase A (PKA) inhibitor onto the SCN at Zeitgeber time (ZT) 10 on

207 leotide (alphaODN) specific for PKG, but not PKA inhibitor or mismatched ODN.

208 lls expressing GFP chimeras of either PKI (a PKA inhibitor) or a mutant PKA regulatory subunit relati

209 thelial cells (HAEC), pretreatment with H89 (PKA inhibitor) or siRNA knockdown of PKA-alpha decreased

210 kinase inhibitor, H-89, a protein kinase A (PKA) inhibitor, or tetradecylglycidate, a CPT-1 inhibito

211 ed adhesion was reversed by treatment with a PKA inhibitor, overexpression of PRKAR1beta, or expressi

212 euregulin-ErbB signaling was confirmed using PKA inhibitors, pathway-selective cAMP analogs, and natu

213 ibition was unaffected by cell dialysis with PKA inhibitor peptide (5 microM), and the PKA inhibitor

214 ntrolled by multiple classes of receptors, a PKA inhibitor peptide (PKIalpha) was developed and expre

215 itors of the PKA catalytic subunits (H89 and PKA inhibitor peptide 14-22) failed to abrogate the inhi

216 by Ang II was abolished by a combination of PKA inhibitor peptide 5-24 (5 microM) and PKC inhibitor

217 ylation was prevented by the addition of the PKA inhibitor peptide in the in vitro kinase assay.

218 ; 1 microM), and abolished by inclusion of a PKA inhibitor peptide in the pipette solution.

219 te(cBIMPS) and was inhibited by the specific PKA inhibitor peptide PKAI5-24.

220 tentiation in cells loaded with the specific PKA inhibitor peptide PKI(6-22) failed to be maintained.

221 This study used a novel PKA inhibitor peptide to inhibit PKA activity to test th

222 In PKA inhibitor peptide transgenic mice, chronic isoproter

223 e, whereas in vivo expression of an inactive PKA inhibitor peptide variant was not inhibitory.

224 In the presence of PKA inhibitor peptide, the inhibitory effect of Ang II w

225 lso blocked in B cells expressing a specific PKA inhibitor peptide, whereas in vivo expression of an

226 , is stimulated by cAMP, and is inhibited by PKA inhibitor peptide-(5-24), indicating that it is PKA.

227 The protein kinase A (PKA) inhibitor peptide [PKI(6-22)amide] blocked enhancem

228 H89 and protein kinase A (PKA) inhibitor peptide prevented rescue of breast cancer

229 H89 and protein kinase A (PKA) inhibitor peptide, a specific PKA inhibitor, preven

230 MPS and reduced or eliminated by the peptide PKA inhibitor PKI (5-24) amide.

231 tracellular injection of the highly specific PKA inhibitor PKI several days after nerve crush.

232 yl cyclase stimulator forskolin and with the PKA inhibitor PKI suggest that Ca(2+)/CaM-activated CaN

233 either exogenous alkaline phosphatase or the PKA inhibitor PKI(5-24).

234 aptic intracellular perfusion of the peptide PKA inhibitor PKI(6-22) amide.

235 However, the PKA inhibitor PKI-(14-22)-amide only partially reversed

236 nol also reduces inhibition of Calpha by the PKA inhibitor PKI.

237 ced protection, hearts were treated with the PKA inhibitors PKI and H-89.

238 forskolin, and a specific protein kinase A (PKA) inhibitor PKI 14-22-amide failed to block the effec

239 unit of T. cruzi (TcPKAc), a gene encoding a PKA inhibitor (PKI) containing a specific PKA pseudosubs

240 rbed flow in vivo, whereas inhibiting PKA by PKA inhibitor (PKI) injection enhanced PAK activation an

241 ist ICI118,551 or by inducible expression of PKA inhibitor (PKI) or of BCL2-associated death promoter

242 kage of PKA activity in COS-1 cells with the PKA inhibitor (PKI) prevented the 8-bromo-cAMP-mediated

243 ibitors H-89 and KT5720, overexpression of a PKA inhibitor (PKI), and in vitro PKA kinase assays show

244 ment of GCs with the PKA-selective inhibitor PKA inhibitor (PKI), the MEK inhibitor PD98059, or the r

245 KG) based on the findings that the selective PKA inhibitor, PKI, abolished the effects of SNAP and CN

246 ses the proteolytic processing of CI and the PKA inhibitor, PKI, blocks the processing.

247 HO cells expressing wild type GPIb-IX with a PKA inhibitor, PKI, reduced Ser(166) phosphorylation and

248 o-7874 or Go-6976, or with the myristoylated PKA inhibitor, PKI-(14-22)-amide failed to develop any t

249 t of noscapine in HLFs, as assessed with the PKA inhibitor, PKI.

250 osphorylation was also inhibited by specific PKA inhibitors, PKI and H-89.

251 oid in the presence of the protein kinase A (PKA) inhibitor, PKI.

252 d the current, and this was prevented by the PKA inhibitor, PKI14-22.

253 A PKA inhibitor present during priming abrogates the block

254 denosine 3',5'-cyclic monophosphothionate, a PKA inhibitor, prevented ATPgammaS or PDBu activation of

255 kinase A (PKA) inhibitor peptide, a specific PKA inhibitor, prevented rescue of T cells by PTX, 8-bro

256 ting whether pre-treating mice with a PKC or PKA inhibitor prior to pellet implantation would prevent

257 Rather, PKA inhibitors prolonged Rap1 activation, as did express

258 PKA inhibitors resulted in a twofold increase in the num

259 Furthermore, PKA inhibitors reverse cGMP-induced inhibition of thromb

260 A6, JAK2, STAT5, JNK1, or p38 siRNA and cAMP-PKA inhibitor reversed the repression of CRBP-I/RARalpha

261 We have previously reported that PKC or PKA inhibitors reversed morphine antinociceptive toleran

262 protein kinase C (PKC) or protein kinase A (PKA) inhibitors reversed morphine antinociceptive tolera

263 ion and apoptosis, which were blocked by the PKA inhibitor Rp diastereomers of cAMP (Rp-cAMP).

264 Application of the competitive PKA inhibitor Rp-8-CPT-cAMPS at the time of axotomy fail

265 ts were centrally infused with the selective PKA inhibitor Rp-adenosine 3',5'-cyclic monophosphothioa

266 , D1/D5 dopaminerdic antagonist SCH23390, or PKA inhibitor Rp-cAMP and unaffected by PKC inhibitor Go

267 Interestingly, infusion of the PKA inhibitor Rp-cAMP into the CeA provoked anxiety-like

268 /D5 dopaminergic antagonist SCH23390, of the PKA inhibitor Rp-cAMP or of the PKC inhibitor Go6976, an

269 ed by beta-adrenoreceptor antagonists or the PKA inhibitor rp-cAMP, indicating transduction via the a

270 th PKA inhibitor peptide (5 microM), and the PKA inhibitor Rp-cAMPS (100 microM) did not reduce IK,AT

271 Bilateral intra-amygdalar infusions of the PKA inhibitor Rp-cAMPS (18 microg per side) given immedi

272 cellular protein kinase A with the selective PKA inhibitor Rp-cAMPS also disrupted acquisition, sugge

273 The beta-receptor blocker propranolol or PKA inhibitor Rp-cAMPS blocks the effects of isoproteren

274 ntra-amygdala, or intra-PAG infusions of the PKA inhibitor Rp-cAMPS on naloxone-precipitated withdraw

275 Bilateral intra-NAc infusions of the PKA inhibitor Rp-cAMPS reduced baseline cocaine self-adm

276 n of cholinergic stimulation by the specific PKA inhibitor Rp-cAMPS.

277 The PKA inhibitors Rp-cAMPs (100 microm in the pipette) and

278 ing cells was inhibited by protein kinase A (PKA) inhibitors Rp-8-CPT-cAMP and H-89.

279 In THP-1 cells pretreated with a PKA inhibitor, Rp isomer of adenosine 3',5'-cyclic phosp

280 kolin activation, but still sensitive to the PKA inhibitor, Rp-8-CPT-cAMPS.

281 cells were incubated in the presence of the PKA inhibitor, Rp-cAMP.

282 er, concomitant infusions of TSA with either PKA inhibitor, Rp-cAMPS, into CA1 or cAMP analog, 8Br-cA

283 AMP-induced sensitization was blocked by the PKA inhibitors, Rp-cAMP (1 mM) and H-89 (100 microM).

284 in the presence of the structurally distinct PKA inhibitors, Rp-cAMPS or KT5720.

285 orbol myristate acetate were not affected by PKA inhibitors, suggesting that a different kinase(s) is

286 horylation, and this effect was prevented by PKA inhibitors, suggesting the involvement of PKA in ROL

287 A PKA inhibitor targeted to the ER surface (termed p4PKIg)

288 ion of PKA, and persisted in the presence of PKA inhibitors, the KATP channel blocker tolbutamide, an

289 ontaneous Ca(2+) release can be curtailed by PKA inhibitor treatment.

290 ide (NO*) and cAMP-dependent protein kinase (PKA) inhibitors up-regulate tumor necrosis factor alpha

291 , however, were not blocked when addition of PKA inhibitors was delayed as little as 15 min after BDN

292 Treatment with PKA inhibitors was sufficient to stimulate apoptosis in

293 isted for an extended period (>30 min) after PKA inhibitor washout.

294 lodynia was reversed if adenylate cyclase or PKA inhibitors were administered spinally 24 hr, but not

295 In other experiments PKC and PKA inhibitors were co-administered together to determin

296 ta(2)AR agonists, cAMP-elevating agents, and PKA inhibitors were used to show that beta(2)AR stimulat

297 because similar inhibition was observed with PKA inhibitors, whereas enhancing PKA activity increased