ライフサイエンスコーパス: H89

1 H89 and protein kinase A (PKA) inhibitor peptide prevent

2 H89 and protein kinase A (PKA) inhibitor peptide, a spec

3 H89 blocks MSK1 activity but does not inhibit ultraviole

4 H89 relieved the inhibition of cAMP on MAPK activity and

5 H89 treatment led to a rapid loss of Sec13-labeled ER ex

6 H89, a potent inhibitor of MSK1, strongly suppressed TPA

7 H89, an inhibitor of cAMP-dependent protein kinase, dose

8 reased to 63.3 +/- 3.4% in 10 micromol l(-1) H89 (to inhibit PKA), providing further evidence of acti

9 reactivity of specific residues in Helix 89 (H89) and expansion segment 31 (ES31).

10 Inhibitors of protein kinase A (H89) and mitogen-activated protein kinase (PD98059) did

11 -4H-chromen-4-one, but not protein kinase A (H89), completely blocked DAMGO-induced RGS19 protein acc

12 by specific inhibitors of protein kinase A (H89), p38-mitogen-activated protein kinase (SB203580), a

13 agents that inhibited protein kinase (PK) A (H89), PKC (GFX), mitogen-activated protein (MAP)/extrace

14 ortmannin, but not that of protein kinase A, H89, of Rho kinase, Y-27632, of mTOR, rapamycin, or of J

15 olgi formation from the ER after brefeldin A/H89 washout in HeLa cells, we found that scattered, golg

16 inhibition of sAC (KH7) and PKA activation (H89) led to larger CBF declines in normal cells, now com

17 amatically reduced distal promoter activity; H89 inhibited IBMX-stimulated CREB phosphorylation and p

18 In addition, H89 incubation results in a rapid increase in NRIF3 leve

19 The pharmacological agents H89 and cerulenin, which are inhibitors of endoplasmic r

20 These results identify a requirement for an H89-sensitive factor(s), potentially a novel protein kin

21 ) within 5 min without activating Akt, in an H89-sensitive manner.

22 The inhibitors KN-92 and H89 were able to block both pathways in mutant TRPC6 exp

23 ACOCF3, exogenous arachidonic acid (AA), and H89 (an inhibitor of PKA) on the 5 day action of TCDD.

24 PKA inhibitors KT5720, PKI, Rp-Br-cAMPS, and H89, but not by PKG inhibitors KT5823 or Rp-pCPT-cGMPS.

25 refeldin A (BFA) to cause Golgi collapse and H89 to block ER export.

26 NO donors and H89, an inhibitor of cAMP-dependent protein kinase incre

27 shed the activating effects of NO donors and H89.

28 diazocine-10-carboxylicacid hexyl ester] and H89 (N-[2-(p-bromo-cinnamylamino)-ethyl]-5-isoquinoline-

29 Cells were incubated with forskolin and H89 to activate or inhibit protein kinase A (a family of

30 d-spectrum protein kinase inhibitors, H7 and H89, stabilized REC tubes on BM matrix and inhibited sec

31 were able to duplicate the effects of H7 and H89.

32 ownstream kinase of ERKs and p38 kinase, and H89, a potential MSK1 inhibitor.

33 own using the specific inhibitors KT5823 and H89, respectively.

34 Further, NO- and H89-mediated increases in TNF-alpha promoter activity we

35 ors Rp-cAMPs (100 microm in the pipette) and H89 (1 microm) failed to reduce basal I(Ca) or to block

36 in (depletes intracellular Ca2+ stores), and H89 (protein kinase A inhibitor), that PDGF-stimulated s

37 Tarceva, NU6102, Gleevec, SB203580, balanol, H89, PP1).

38 Most interestingly, both H89 and MPI added to the perfusion medium dramatically r

39 ylation of ATF-2 by CL was sensitive to both H89 and SB202190, while phosphorylation of cAMP-response

40 e protein kinase A (PKA) inhibitor, H89, but H89 did not affect the fEPSPs in control tissue.

41 inase acting downstream of MEK1/2-ERK1/2, by H89 or knockdown of MSK1 expression also inhibited phosp

42 -related DNA fragmentation was aggravated by H89 treatment but reduced by SOD1.

43 ed by forskolin treatment, and attenuated by H89, consistent with PKA-mediated phosphorylation.

44 cAMP analog 8-bromo-cAMP, and was blocked by H89 or the adenylate cyclase inhibitor 9-(tetrahydro-2-f

45 This reversal is blocked by H89, an inhibitor of PKA.

46 ffect of 8CPT-cAMP was completely blocked by H89.

47 nocytes to endothelial cells was enhanced by H89 treatment or overexpression of FoxO1-AAA, similar to

48 logical inhibition of the Egr-1 induction by H89 (48%) and calmidazolium (35%), but not by mitogen-ac

49 imicked by 8-bromo-cAMP and was inhibited by H89 or SB203580.

50 f the S112/136A mutant was >90% inhibited by H89, a PKA inhibitor.

51 ations were induced by iron and inhibited by H89, as shown by immunoprecipitation-coupled Western blo

52 phosphorylation, which was also inhibited by H89, suggesting increased [Ca(2+)](i) preceded PKA for g

53 Neither PKA inhibition by H89 nor cAMP induction by forskolin or dibutyrl-cAMP alt

54 lin mimics the action; (2) PKA inhibition by H89 reverses the neuropeptide-induced inhibition; and (3

55 lement-binding protein was inhibited only by H89.

56 thermore, blocking protein kinase A (PKA) by H89 completely abrogated the inductive effects of tumor-

57 Moreover, Bad/14-3-3 was prevented by H89 treatment but promoted by SOD1.

58 ly after tFCI and that they were promoted by H89 treatment but prevented by SOD1.

59 l-x(L) was prevented by SOD1 but promoted by H89 treatment.

60 P was delayed or inhibited, respectively, by H89, the inhibitor of protein kinase A.

61 mic heart were nearly completely reversed by H89 or MPI added to the perfusion medium.

62 ssion of GABA-evoked Ca2+ rises triggered by H89 (in the presence of TTX) recovered rapidly, suggesti

63 ific inhibitor of PKC, but was unaffected by H89, an inhibitor of protein kinase A.

64 nscription factors are largely unaffected by H89, whereas induction of IE genes is inhibited and its

65 Under these conditions, H89, but not H85, potentiated the cAMP accumulation indu

66 In contrast, H89 did not block the constitutive ER Golgi-intermediate

67 In contrast, H89 did not inhibit phosphorylation of eNOS-S(1179) indu

68 In contrast, H89 inhibited fen-beta(2)-AR stimulation of I(Ca,L), whi

69 ]-5-isoquinolinesulfonamide dihydrochloride (H89), or with the Golgi-disturbing agent brefeldin A, bl

70 ase with dideoxyadenosine or PKA with either H89 or RpcAMPs blocked kainate receptor-mediated actions

71 Akin to these in vitro findings, H89 prevented ROL- and Bt2cAMP-induced resolution of inf

72 n of NRIF3 protects breast cancer cells from H89-mediated apoptosis.

73 ed, and DIF-1 also protects these cells from H89-mediated apoptosis.

74 Furthermore, H89, a specific PKA inhibitor, blocked TNF-alpha-induced

75 eotide mutations and methylations in helices H89 and H91 confer resistance to orthosomycins and revea

76 A-tRNA-namely, ribosomal RNA (rRNA) helices H89, H91, and ribosomal proteins (rProtein) uL16-these s

77 stal histidine (H55) and proximal histidine (H89) were probed by the creation of site-specific mutati

78 nhibitors (SB203580, purvalanol B, imatinib, H89, and hymenialdisine), SCR provided excellent reprodu

79 ned the localization of betaCOP and Sec13 in H89-treated cells.

80 PKA inhibition (H89 or R(P)-adenosine-3',5'-cyclic monophosphorothioate

81 as blocked by the protein kinase A inhibitor H89 (N-(2-(p-bromocinnamylamino)-ethyl)-5-isoquinolinesu

82 as blocked by the protein kinase A inhibitor H89 and by removing extracellular Ca(2+).

83 rons and that the protein kinase A inhibitor H89 attenuated CGRP-induced CRE-dependent transcription

84 or H7 but not the protein kinase A inhibitor H89 blocked the response to Ang II.

85 function, and the protein kinase A inhibitor H89 blocks these actions.

86 unaffected by the protein kinase A inhibitor H89 but was reduced by the mitogen-activated protein (MA

87 rylation, and the protein kinase A inhibitor H89 failed to detectably inhibit the response to calcito

88 activity, and the protein kinase A inhibitor H89 led to a increase in G6PD activity in RINm5F cells.

89 Protein kinase A inhibitor H89 lowers beat frequency to that of wild-type sperm, su

90 However, the protein kinase A inhibitor H89 only partially reversed the inhibition of TNF-alpha

91 reatment with the protein kinase A inhibitor H89 or the anion exchange inhibitor 4,4'-diisothiocyano-

92 The protein kinase A inhibitor H89 prevented the 86Rb uptake response to SKF82958.

93 y reversed by the protein kinase A inhibitor H89, whereas H89 alone increased transport rates.

94 throcytes with the classical PKA-C inhibitor H89 leads to a block in parasite growth.

95 cetylation using both the chemical inhibitor H89 and RNA interference.

96 -activated protein kinase 1 or its inhibitor H89 had no effect on arsenite-induced phosphorylation of

97 d that the serine/threonine kinase inhibitor H89 abolishes membrane recruitment of Sar1, thereby prev

98 the cAMP-dependent protein kinase inhibitor H89 and the cystic fibrosis transmembrane conductance re

99 effects were blocked by the kinase inhibitor H89.

100 inhibited using the protein kinase inhibitor H89.

101 PKA blockade by the small molecule inhibitor H89 decreased the LY294002/LY303511-mediated increase in

102 ly, treatment of DCs with the MSK1 inhibitor H89 partially mimicked the effects of DMF on the DC sign

103 ked by cell treatment with the PKA inhibitor H89 and was not observed in PKA-transfected cells.

104 The PKA inhibitor H89 dihydrochloride did not affect the average mIPSC amp

105 s or WT cells treated with the PKA inhibitor H89 from glutamine deprivation.

106 The PKA inhibitor H89 had little or no effect on inflammatory mediators mo

107 atment of NC cultures with the PKA inhibitor H89 or 1-10 nm okadaic acid (OA), a serine/threonine PP2

108 Treatment of ECs with PKA inhibitor H89 or PI3K inhibitor LY294002 prevented the AdE4+-media

109 by coinfusion with either the PKA inhibitor H89 or Rp-CAMPS.

110 A (PKA) and is blocked by the PKA inhibitor H89 or small interfering RNA knockdown of PKA.

111 tment of HEK293 cells with the PKA inhibitor H89 or the PKC inhibitor GF109203X, individually or in c

112 The PKA inhibitor H89 potentiated LTB4 generation by control granulocytes

113 ated trauma-hemorrhage rats by PKA inhibitor H89 prevented the E2-BSA attenuation of hepatic injury.

114 ts interaction with LSD1 while PKA inhibitor H89 represses them by suppressing H3K4 methylation level

115 Bath application of the PKA inhibitor H89 suppressed the early LTP induced by a single tetanus

116 The PKA inhibitor H89 was without effect on the 007-induced increase in Ra

117 ggregates was abolished by the PKA inhibitor H89, whereas the effect of GD1a was mimicked by the PKA

118 1 activation is ablated by the PKA inhibitor H89.

119 hich could be prevented by the PKA inhibitor H89.

120 was already attenuated by the PKA inhibitor H89.

121 d by intra-VTA infusion of the PKA inhibitor H89.

122 or treatment of HAEC with the PKA inhibitor H89.

123 be completely reversed by the PKA inhibitor H89.

124 he specific protein kinase A (PKA) inhibitor H89 (N-[2-(p-bromocinnamyl-amino)ethyl]-5-isoquinolinesu

125 The protein kinase A (PKA) inhibitor H89 blocks this effect, suggesting that this feedback in

126 The protein kinase A (PKA) inhibitor H89 completely blocks the TCDD-dependent effect on C/EBP

127 on with the protein kinase A (PKA) inhibitor H89 or (R(p))-cAMPS, but not with the inactive isomer H8

128 AMP-dependent protein kinase (PKA) inhibitor H89 reduced RGS9-1 labeling by more than 90%, while dibu

129 The protein kinase A (PKA) inhibitor H89, the TK inhibitor genistein, and the JAK2 inhibitor

130 A protein kinase A inhibitor (H89) also elicits apoptosis of breast cancer cells but n

131 yadenosine) or a protein kinase A inhibitor (H89) also significantly attenuated morphine-induced NR1

132 tor (dibutyryl cyclic AMP) nor an inhibitor (H89) of cyclic AMP-dependent protein kinase had any effe

133 nase inhibitor (LY294002), or PKA inhibitor (H89) blocks the nicotine-induced Bad phosphorylation tha

134 A protein kinase A (PKA) inhibitor (H89) was largely ineffective under the same conditions.

135 A protein kinase A (PKA) inhibitor (H89, 20 micromol/l) suppressed hypoxia-induced GLUT1 mRN

136 inhibited by the protein kinase A inhibitor, H89.

137 , PD169316 and SB202190, and MSK1 inhibitor, H89, but not by mitogen-activated protein kinase kinase

138 One inhibitor, H89, an isoquinolinesulfonamide that is commonly used as

139 Similarly, a pharmacological inhibitor, H89, killed epimastigotes at a concentration of 10 muM.

140 er was decreased by NO* and a PKA inhibitor, H89, and increased by a PKA activator, dibutyryl cAMP (B

141 otein expression, whereas the PKA inhibitor, H89, inhibited the stimulatory effect of PGE2 on gap jun

142 ter tFCI, we administered the PKA inhibitor, H89, into the mouse brain after tFCI.

143 The PKA inhibitor, H89, was a potent inhibitor of PACAP38-induced neurite o

144 , and could be blocked by the PKA inhibitor, H89.

145 MP-dependent protein kinase (PKA) inhibitor, H89 (10 microm).

146 els by the protein kinase A (PKA) inhibitor, H89, but H89 did not affect the fEPSPs in control tissue

147 the cAMP-dependent protein kinase inhibitors H89 and PKI.

148 nfirmed by the ability of the PKA inhibitors H89 (20 microm) and (R(p))-cAMP-S (1 mm) to block phosph

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

150 when treating cells with the PKA inhibitors H89 or KT5720 as well as in cells expressing phosphotran

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

152 ereas treatment of cells with PKA inhibitors H89, KT5720, and PKA Catalpha siRNA all enhanced this ce

153 The protein kinase A (PKA) inhibitors H89 and Rp-3', 5'-cyclic monophosphothioate triethylamin

154 e protein kinase A (PKA)-specific inhibitors H89 and PKI (peptide specific inhibitor), and Gi, as inc

155 in kinase A or adenylate cyclase inhibitors, H89 and di-deoxyadenosine, respectively, indicating a cA

156 Two PKA inhibitors, H89 and KT5720, inhibited immune complex (IC)-stimulated

157 Human PDE1A RNA and the PKA inhibitors, H89 and Rp-cAMPS, partially rescued phenotypes of pde1a

158 contrast, protein kinase A (PKA) inhibitors, H89 and [PKI(2-22)amide] attenuated the enhancement of t

159 ed by the protein kinase A (PKA) inhibitors, H89 and myristoylated PKI(14--22) amide, indicating part

160 (4-bromocinnamylamino)ethyl]-5-isoquinoline (H89) or the p38 mitogen-activated protein kinase (MAPK)

161 (4-bromocinnamylamino)ethyl]-5-isoquinoline (H89).

162 (4-bromocinnamylamino)ethyl]-5-isoquinoline (H89)] and extracellular signal-regulated kinase (ERK)-de

163 (4-bromocinnamylamino)ethyl]-5-isoquinoline (H89; a protein kinase A inhibitor) stimulated cAMP accum

164 namylamino)ethyl]-5-isoquinolinesulfonamide (H89) shows that this assay can be successfully used to m

165 amyl)amino)ethyl]-5-isoquinolinesulfonamide (H89).

166 KT5823, H89, or artificial cerebrospinal fluid (ACSF; control) w

167 Thus, L85/H89/F191 and F85/F89/R191 are dominant in subtype B and

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

169 e state by treatment with the small molecule H89 or expression of its GTP-locked form, intact Golgi m

170 protein kinase A (cAMP/PKA) by either 5 mum H89 or 1 microm KT5720 in LMN myocytes mimicked the effe

171 activity were effectively reversed by 50 nm H89 or 50 nm myristoylated peptide inhibitor (MPI), spec

172 NO*, H89, and Bt2cAMP were found to produce reciprocal protei

173 heterologous promoter from responding to NO, H89 and Bt(2)cAMP.

174 In contrast, neither forskolin nor H89, a protein kinase A inhibitor, had a significant eff

175 t structures outside the ER, the addition of H89 to BFA-treated cells caused ER accumulation of all G

176 To further investigate the effect of H89 on COPII we developed a COPII recruitment assay with

177 l of CF cells with the expected exception of H89, which does not prevent dissociation of the fluoresc

178 Based on the known functions of H89 during translation, we propose that SBP2 allows Sec

179 The dose response of H89 inhibition of PMN adhesion correlated with its inhib

180 drug combination, as well as by Ro 318220 or H89, potent inhibitors of MSK1/MSK2.

181 but not by PD123319 (an AT-2R antagonist) or H89 (a protein kinase A (PKA) inhibitor).

182 nisms did not contribute to the forskolin or H89 effects on MCT1 kinetic function as determined with

183 s with wortmannin (PI 3-kinase inhibitor) or H89 (protein kinase A (PKA) inhibitor) but not ICI182780

184 A pathway inhibitors, suramin, MDL12330A, or H89 suppressed bile acid-mediated PEC replication.

185 by perfusing the heart with staurosporine or H89.

186 Results: (i) An inhibitor of PKA (H89) reduces tonicity-dependent increases in transactiva

187 m of PKC (LY333531), protein kinase A (PKA) (H89), and phosphotidylinositol (PI) 3 kinase (wortmannin

188 es showed that a selective inhibitor of PKA, H89, inhibited shear-dependent phosphorylation of eNOS-S

189 se G (PKG; KT5823) or protein kinase A (PKA; H89).

190 Inhibitors of the PKA catalytic subunits (H89 and PKA inhibitor peptide 14-22) failed to abrogate

191 Inhibitors of the PKA catalytic subunits (H89 and PKI(14-22) peptide) failed to abrogate the inhib

192 ssay with permeabilized cells and found that H89 potently inhibited binding of exogenous Sec13 to ER

193 Here, we report that H89, a selective inhibitor of the nucleosomal response,

194 , adjacent to either the IIICS domain or the H89 splice variant that contains the amino-terminal sequ

195 y towards H3/HMG-14 is uniquely sensitive to H89 inhibition.

196 nhibition of protein kinase A activity using H89 reduced Bt(2)cAMP-induced StAR protein.

197 By using H89 (N-[2-(p-bromo-cinnamylamino)-ethyl]-5-isoquinoline-

198 Inhibition of MSK1 using H89 and small interfering RNA knockdown both reduced RSV

199 Inhibition of PKA using H89 increased cell spreading on collagen gel in an EGF-d

200 f both cAMP-dependent effector pathways; (v) H89 and dominant negative Epac 279E block cAMP-inhibitor

201 the protein kinase A inhibitor H89, whereas H89 alone increased transport rates.

202 Dibutyryl-cAMP inhibits, whereas H89 restores, activation of Rac-GTPase and abolishes mor

203 To test whether H89 might act at the level of either the coatomer protei

204 ocking the activity of protein kinase A with H89, or by blocking the activity of protein kinase C wit

205 ein kinase A (PKA) activity was blocked with H89, or when the protein kinase C (PKC) activity was blo

206 o ERK activation could be distinguished with H89, an inhibitor of protein kinase A, and beta-arrestin

207 Rat lacrimal gland acini were incubated with H89, an inhibitor of protein kinase A, before the additi

208 P-dependent protein kinase A inhibition with H89 and NO synthase inhibition with l-nitroarginine meth

209 endritic spines, whereas PKA inhibition with H89 prevented AMPA-induced internalization.

210 fferent responsiveness; blockade of PKA with H89 also eliminated the TNF amplification effect.

211 ark-to-spark delays; (3) inhibiting PKA with H89 retarded amplitude recovery and increased spark-to-s

212 ark-to-spark delays; (3) inhibiting PKA with H89 retarded amplitude recovery and increased spark-to-s

213 l, or inhibiting protein kinase A (PKA) with H89, prevented glucose-induced Erk-1/2 phosphorylation.

214 endothelial cells (HAEC), pretreatment with H89 (PKA inhibitor) or siRNA knockdown of PKA-alpha decr

215 d significantly reduced by pretreatment with H89 and GF-109203X.

216 Pretreatment with H89 or brefeldin A or incubation at 4 degrees C prevente

217 significantly reduced in cells treated with H89, a protein kinase A inhibitor.

218 Treatment with H89 (a protein kinase A inhibitor) blocked the heat shoc

219 Treatment with H89 and knockdown of PKAc in cells led to the inhibition

220 ed by pretreatment of cells with wortmannin, H89, or by small interfering RNA knockdown of PKA.