ライフサイエンスコーパス: protein kinase G

1 r-cGMP), and were prevented by inhibition of protein kinase G.

2 f activation of soluble guanylyl cyclase and protein kinase G.

3 by okadaic acid or KT-5823, an inhibitor of protein kinase G.

4 ling, stimulating phosphorylation changes by protein kinase G.

5 n effect not mimicked by protein kinase C or protein kinase G.

6 almodulin, NO synthase, guanylyl cyclase, or protein kinase G.

7 e receptors Npr1 and Npr2, and activation of protein kinase G.

8 nput to dorsal horn neurons through sGC-cGMP-protein kinase G.

9 via inducible NO synthase and activation of protein kinase G.

10 ynthesis/PDE-5-hydrolyzed pool signaling via protein kinase G.

11 The cGMP-dependent protein kinase G-1alpha (PKG-1alpha) is a downstream med

12 hat had been phosphorylated with recombinant protein kinase G-1alpha was analyzed by use of Fourier t

13 The autocatalytic cycle can be arrested by protein kinase G activated with 8-bromo-cyclic GMP and b

14 ISO yet rose nearly 5-fold with ANP, whereas protein kinase G activation (vasodilator-stimulated prot

15 inhibition, sustained elevation of cGMP, and protein kinase G activation.

16 nor S-nitroso-N-acetylpenicillamine, and the protein kinase G activator 8-bromo-cGMP, were significan

17 e bypassed by the addition of the downstream protein kinase G activator, 8-Br-cGMP.

18 Protein kinase A and protein kinase G activators fail to acutely down-regulat

19 greater detectable increases in cGMP but not protein kinase G activity and does not modulate beta-adr

20 This highlights the importance of myocyte protein kinase G activity as a protection for pathologic

21 ide synthase 3-coupled cGMP generation, with protein kinase G activity suppressed in both models.

22 Activation of Frizzled-2 suppressed protein kinase G activity while activating NF-AT-depende

23 inhibition (e.g., by sildenafil) stimulates protein kinase G activity, suppressing and reversing mal

24 yclic guanosine 5'-monophosphate levels, and protein kinase G activity.

25 n by CO involves reactive oxygen species and protein kinase G activity.

26 molecular remodeling, increasing myocardial protein kinase G activity.

27 BH4 did not enhance net protein kinase G activity.

28 results show that NHERF2, acting as a novel protein kinase G-anchoring protein, is required for cGMP

29 ons with anchoring proteins, and myosin is a protein kinase G-anchoring protein.

30 stimulation was suppressed by activation of protein kinase G and by buffering intracellular Ca2+.

31 the canonical cGMP pathway, possibly through protein kinase G and opening of mitochondrial K(ATP) cha

32 ily (the cAMP-dependent PKA, cGMP- dependent protein kinase G and phospholipid-dependent protein kina

33 reases CBF is less well defined but involves protein kinase G and possibly PKA.

34 named after family members protein kinase A, protein kinase G and protein kinase C).

35 vels, suggesting that it is mediated through protein kinase G and soluble guanylate cyclase.

36 croneme secretion is centrally controlled by protein kinase G and that this pathway is further augmen

37 nction, restored myocardial levels of active protein kinase G, and dephosphorylated NFATc1 and phosph

38 cells through CysLT1R and EP3 involving Gi, protein kinase G, and Erk and contributing to vascular i

39 that this synergism is mediated through Gi, protein kinase G, and Erk signaling.

40 -dependent protein kinases A, cGMP-dependent protein kinases G, and phospholipid-dependent protein ki

41 )oxadiazolo(4,3-a)quinoxalin-1-one (ODQ), or protein kinase G antagonist (Rp-8-Br-cGMPS).

42 of HT1376 cells increased cGMP and activated protein kinase G at doses that induce apoptosis, whereas

43 ntinociception might involve a NO-cyclic GMP-protein kinase G-ATP-sensitive potassium (K(ATP)) channe

44 how that atrial natriuretic peptide, through protein kinase G, attenuated both the amplitude and dura

45 Inhibitors of soluble guanylate cyclase and protein kinase G block this modulation.

46 Also, inhibition of protein kinase G blocked the increase in glycinergic sIP

47 a(2+) into intracellular stores but, through protein kinase G, both stimulates plasma membrane Ca(2+)

48 A role for protein kinase G but not protein kinase A downstream of

49 hibition was independent of nitric oxide and protein kinase G but was prevented by antioxidants and t

50 micked the BNP effect, whereas inhibition of protein kinase G by KT5823 (10(-6) mol/L) significantly

51 different mechanisms, and that activation of protein kinase G by NO-dependent stimulation of guanylyl

52 Inhibition of protein kinase G by Rp-8-Br-PET-cGMPS had no effect, ind

53 Chemical inhibition of protein kinase G by Rp-8-pCPT-cGMP, conversely, was show

54 These results indicate that NO and protein kinase G contribute to Drosophila's ability to r

55 from the surface of hepatocytes via NO/cGMP/protein kinase G-dependent activation and surface transl

56 rum albumin induced microneme secretion in a protein kinase G-dependent manner that correlated with i

57 d protein kinase through a nitric oxide/cGMP/protein kinase G-dependent mechanism.

58 inculin and talin expression occur through a protein kinase G-dependent pathway and therefore differ

59 echanical stimuli through a nitric oxide and protein kinase G-dependent pathway.

60 oduction needed for downstream activation of protein kinase G-dependent signaling and blood vessel di

61 a critical regulator of cGMP production and protein kinase G-dependent signaling.

62 n of TACE and iRhom2, which are also NO/cGMP/protein kinase G-dependent.

63 r levels of activated thiol-sensitive active protein kinase G, dephosphorylated nuclear factor of act

64 itric oxide, cyclic guanosine monophosphate, protein kinase G, extracellular-signal-regulated kinase,

65 ame tissues, and that downstream blocking of protein kinase G formation with KT5823 (10 microM) inhib

66 yclase/guanosine 3', 5'-cyclic monophosphate/protein kinase G (GC/cGMP/PKG) pathway downstream of NO

67 ynthase -> NO -> guanylyl cyclase -> cGMP -> protein kinase G -> opens vesicular Cl- channel.

68 Inhibition of soluble guanylate cyclase or protein kinase G had no effect on either pathway.

69 nase CK2, cAMP-dependent protein kinase, and protein kinase G, HDAC2 is phosphorylated uniquely by pr

70 lfide bond between the two alpha subunits of protein kinase G I-alpha (PKGI-alpha), which activates t

71 Here we show that protein kinase G Ialpha (PKGIalpha) is oxidant-activated

72 n of myosin light chain (MLC) phosphatase by protein kinase G Ialpha (PKGIalpha).

73 lcium stimulation of NO synthase and NO/cGMP/protein kinase G II-dependent activation of Src, and the

74 thus place p38 MAPK activation downstream of protein kinase G in a SERT-catalytic regulatory pathway,

75 role of cGMP, soluble guanylyl cyclase, and protein kinase G in the potentiating effect of NO on syn

76 Thus, activation of protein kinase G in the ventromedial hypothalamus is nec

77 ed cGMP and separately increased Ca(2+) in a protein kinase G-independent manner leading to microneme

78 clase- and phosphodiesterase 6-dependent but protein kinase G-independent.

79 ailure, promote norepinephrine release via a protein kinase G-induced inhibition of phosphodiesterase

80 Hypertrophy was restored on NOS or protein kinase G inhibition.

81 to a guanylyl cyclase inhibitor (ODQ) and a protein kinase G inhibitor (Rp-8-pCPT-cGMPS).

82 These effects were insensitive to a protein kinase G inhibitor and to HS-142-1, suggesting t

83 cGMP (50 muM), which was not affected by the protein kinase G inhibitor H-8.

84 the vagal bradycardia in the presence of the protein kinase G inhibitor KT5823 (1 microM) but not aft

85 uctive effect of hemin was attenuated by the protein kinase G inhibitor KT5823 and the soluble guanyl

86 that intracerebroventricular infusion of the protein kinase G inhibitor KT5823 inhibits lordosis beha

87 th the PKA inhibitor KT5720 but not with the protein kinase G inhibitor KT5823.

88 DT3, a protein kinase G inhibitor, blocked the antifibrotic eff

89 NO) synthase inhibitor, and Rp 8-Br cGMPs, a protein kinase G inhibitor, had no effect but Rp 8-Br cA

90 t cyclic GMP is a likely candidate since the protein kinase G inhibitor, KT5823, inhibited potentiati

91 ric oxide synthase inhibitor, L-NNA, and the protein kinase G inhibitor, Rp 8-Br cGMPs had no effect

92 lyl cyclase inhibitor, ODQ, and the specific protein kinase G inhibitor, Rp pCPT cGMP, abolished the

93 ed with cGMP elevation and were blocked by a protein kinase G inhibitor.

94 SIL was prevented in cells pretreated with a protein kinase G inhibitor.

95 anosine-3',5'-cyclic monophosphorothioate (a protein kinase G-inhibitor) or glibenclamide (an ATP-sen

96 o[4,3-alpha]quinozalin-1-one (ODQ) or by the protein kinase G inhibitors (8R,9S,11S)-(-)-2-methyl-9-m

97 2,4)-oxadiazolo[4,3-a]-quinoxalin-1-one) and protein kinase G inhibitors (H8, DT-2) block AR stimulat

98 shed at the promoter and protein level using protein kinase G inhibitors (KT5823 and R(p)-8-pCPT-cGMP

99 nt kinase II, myosin light chain kinase, and protein kinase G inhibitors tested.

100 lts suggest that phosphorylation of Smad3 by protein kinase G is a potential molecular mechanism by w

101 Protein kinase G is shown to be a critical downstream ef

102 ight be due to activation of a NO-cyclic GMP-protein kinase G-K(ATP) channel pathway.

103 duction of cGMP and activates cGMP-dependent protein kinase (G kinase), which by an unknown mechanism

104 emonstrated that cyclic GMP (cGMP)-dependent protein kinase (G-kinase) activates the human fos promot

105 soluble guanylate cyclase and cGMP-dependent protein kinase (G-kinase) activity, and CS-54 arterial s

106 normal guanylate cyclase and cGMP-dependent protein kinase (G-kinase) activity.

107 Cyclic GMP-dependent protein kinase (G-kinase) inhibits RhoA activation of SR

108 strated directly for the cGMP/cGMP-dependent protein kinase (G-kinase) signal transduction pathway.

109 tes c-fos gene expression via cGMP-dependent protein kinase (G-kinase), but NO's precise mechanism of

110 cells, which are deficient in cGMP-dependent protein kinase (G-kinase), we show that 8-(4-chloropheny

111 We found that type II cGMP-dependent protein kinase (G-kinase), which is widely expressed in

112 h muscle and glial cells in a cGMP-dependent protein kinase (G-kinase)-dependent fashion.

113 lic guanosine monophosphate (cGMP)-dependent protein kinase (G-kinase).

114 c cells which express type II cGMP-dependent protein kinase (G-kinase); the effect on the fos promote

115 ckade with LY294002, ML-9, and inhibitors of protein kinase G (KT5823) and MEK (PD98059).

116 ith pharmacological antagonists suggest that protein kinase G may be a downstream effector that contr

117 a PI3K/Akt/endothelial nitric-oxide synthase/protein kinase G/mitogen-activated protein kinase cascad

118 Protein kinase G of Mycobacterium tuberculosis has been

119 or was the effect mimicked by the agonist of protein kinase G or 8-BR cGMP.

120 Inhibition of protein kinase C, protein kinase G or calmodulin-activated kinase had no e

121 -cbd was blocked by KT-5823, an inhibitor of protein kinase G, or 1H-[1,2,4]oxadiazolo[4,3-a]quinoxal

122 ORM-2 was not prevented by guanylyl-cyclase, protein kinase G, or thioredoxin inhibitors, and was not

123 ency, suggesting that activation of the cGMP/protein kinase G pathway by LPS involves the TLR4 pathwa

124 vities associated with the nitric oxide/cGMP/protein kinase G pathway had previously been demonstrate

125 ocation through activation of the cyclic GMP/protein kinase G pathway in cardiac fibroblasts.

126 cellular calcium is regulated by the NO/cGMP/protein kinase G pathway in the inner ear.

127 nally projecting PVN neurones through a cGMP-protein kinase G pathway.

128 r inhibitors of the soluble guanylyl cyclase/protein kinase G pathway.

129 Both PKA and cGMP-dependent protein kinase G phosphorylated AQP2 on this COOH-termin

130 Flies with high levels of Protein Kinase G (PKG) (for(R)) do not display deficits

131 nduction requires protein kinase C (PKC) and protein kinase G (PKG) activation, and although PKC phos

132 cyclic guanosine monophosphate content, and protein kinase G (PKG) activity in adjacent cardiomyocyt

133 tal models, both reacted favorably to raised protein kinase G (PKG) activity.

134 compounds induces apoptosis by activation of protein kinase G (PKG) and c-Jun kinase (JNK1).

135 is mediated by nitric oxide (NO) acting via protein kinase G (PKG) and independent of reactive oxyge

136 GMP) in a NO-dependent manner, and activated protein kinase G (PKG) and its downstream effector, the

137 tion of alphaIIbbeta3 by VWF is dependent on protein kinase G (PKG) and mitogen-activated protein (MA

138 rk identifies the integration of the NO/cGMP/protein kinase G (PKG) and NGF/TrkA pathways to induce a

139 We applied cGMP and cAMP analogues and a protein kinase G (PKG) antagonist to the cells.

140 lic guanosine monophosphate (cGMP)-activated protein kinase G (PKG) axis.

141 ncordantly, inhibition of the cGMP-dependent protein kinase G (PKG) blocks egress induced by PKAc1 in

142 The activation of protein kinase G (PKG) by cGMP has become of considerabl

143 anosine 3',5'-monophosphate (cGMP)-dependent protein kinase G (PKG) has become of considerable intere

144 Cyclic GMP-dependent protein kinases protein kinase G (PKG) Ialpha and PKGIbeta are major med

145 nels TRPC3 and TRPC6 and their modulation by protein kinase G (PKG) in controlling cardiac systolic m

146 ining endothelial cell NO synthase (eNOS) or protein kinase G (PKG) increased endothelial cell migrat

147 lo[4,3-a]quinoxalin-1-one (ODQ) (5 muM), the protein kinase G (PKG) inhibitor (RP)-8-Br-PET-cGMP-S (5

148 effects of NECA on 5-HT uptake, whereas the protein kinase G (PKG) inhibitor N-[2-(methylamino)ethy]

149 e guanylate cyclase inhibitor ODQ and by the protein kinase G (PKG) inhibitor Rp-8-CPT-cGMP.

150 Protein kinase G (PKG) is a major receptor of cGMP and c

151 Protein kinase G (PKG) mediates classic nitric oxide-dep

152 ized that cGMP-dependent pathways activating protein kinase G (PKG) modulate motoneuronal inspiratory

153 and D1R agonists, signaling through the cGMP/protein kinase G (PKG) pathway, suppressed cell viabilit

154 that requires a nitric oxide (NO)-cyclic GMP-protein kinase G (PKG) pathway.

155 /guanosine 3',5'-cyclic monophosphate (cGMP)/protein kinase G (PKG) pathway.

156 ctance by activating the cGMP-cGMP-dependent protein kinase G (PKG) pathway.

157 Protein kinase G (PKG) plays an important role in the re

158 This site is predicted to be a protein kinase G (PKG) recognition site and is a strictl

159 nylyl cyclase or of the cGMP effector kinase protein kinase G (PKG) reduced both ERK activation and p

160 rol mechanisms, we examined clock-controlled protein kinase G (PKG) regulation in the mammalian SCN.

161 eptor, glycoprotein Ib-IX (GPIb-IX), via the protein kinase G (PKG) signaling pathway.

162 ale mice resulted in increased activation of protein kinase G (PKG) signaling, which was further enha

163 have questioned the role of myocyte PDE5 and protein kinase G (PKG) to this process, proposing altern

164 Protein kinase G (PKG) was manipulated genetically and p

165 vity and expression levels of cGMP-dependent protein kinase G (PKG) were significantly increased in C

166 he infusion of specific inhibitors of sGC or protein kinase G (PKG), a target of cGMP, prevents subla

167 3',5'-cyclic guanosine monophosphate (cGMP), protein kinase G (PKG), and the BK(Ca) channel were used

168 ial nitric-oxide synthase, guanylyl cyclase, protein kinase G (PKG), and the mitochondrial K(ATP) cha

169 Previously, the protein kinase G (PKG), EGL-4/PKG-1, was shown necessary

170 Cardiac cGMP, which activates protein kinase G (PKG), is regulated by nitric oxide (NO

171 Experiments with inhibitors of protein kinase G (PKG), protein kinase A (PKA), phosphod

172 actin filament organization and activity of protein kinase G (PKG), protein kinase A (PKA), Rho guan

173 ntracellular levels of cGMP, thus activating protein kinase G (PKG), which then activates pathways th

174 Depletion of protein kinase G (PKG)-1 from VSMCs did not change KCC3

175 e residues in its target proteins, including protein kinase G (PKG)-Ialpha, thereby modulating their

176 unit (MBS), with the N-terminal LZ domain of protein kinase G (PKG)-Ialpha.

177 Pharmacological increase of [cGMP](i) caused protein kinase G (PKG)-mediated depolarization, switchin

178 nitric oxide synthase, guanylyl cyclase, and protein kinase G (PKG).

179 h cGMP-gated channels and phosphorylation by protein kinase G (PKG).

180 Rp-8-Br-cGMP, an inhibitor of cGMP-dependent protein kinase G (PKG).

181 MP through activation of adenylyl cyclase by protein kinase G (PKG).

182 , cyclic guanosine monophosphate (cGMP), and protein kinase G (PKG).

183 e (nNOS), cGMP, and the cGMP effector kinase protein kinase G (PKG).

184 city for 5-HT uptake stimulation after acute protein kinase G (PKG)/p38 mitogen-activated protein kin

185 ndothelial nitric oxide (NO) synthase (eNOS)/protein kinase G (PKG)/vasodilator-stimulated phosphopro

186 NOS3) to enhance cGMP synthesis and activate protein kinase G (PKG-1).

187 apsaicin and after infusion of inhibitors of protein kinase G (PKG; KT5823) or protein kinase A (PKA;

188 tivity of the cGMP-dependent protein kinase (protein kinase G, PKG) in CNG channel deficiency.

189 ation" of the cGMP-dependent protein kinase (protein kinase G, PKG).

190 part through cGMP-dependent protein kinase (protein kinase G; PKG) to raise levels of cytosolic Ca(2

191 Protein kinase G (PknG), a thioredoxin-fold-containing e

192 0(S6k), whereas only selective inhibitors of protein kinase G prevented the activation of the kinases

193 s of cGMP: the cGMP-gated (CNG) channels and protein kinase G (PRKG), and how each may contribute to

194 vel, signalling through the EGF receptor and protein kinase G promotes quiescent states in both worms

195 addition of inhibitors of protein kinase A, protein kinase G, protein tyrosine kinase, or phosphatid

196 Six vertebrate protein kinases (G-protein-coupled receptor kinases; GRK

197 ied 77 significantly mutated genes including protein kinases, G-protein-coupled receptors such as GRM

198 members of the cAMP-dependent protein kinase/protein kinase G/protein kinase C extended family and bl

199 tail of AGC (c-AMP-dependent protein kinase/protein kinase G/protein kinase C) kinases, controls the

200 nhibitors or activators of protein kinase A, protein kinase G, rhodopsin kinase, CaM kinase II, casei

201 ors of soluble guanylyl cyclase (LY83583) or protein kinase G (Rp-8-bromo-cyclic GMP or KT5823), the

202 ar mechanism by which activation of ANP/cGMP/protein kinase G signaling disrupts TGF-beta1-induced nu

203 ion of atrial natriuretic peptide (ANP)/cGMP/protein kinase G signaling inhibits transforming growth

204 h Ca2+-dependent guanylyl cyclase-cyclic GMP-protein kinase G signaling pathway.

205 is inhibited by NO which acts via a cGMP and protein kinase G signaling pathway.

206 tion may contribute to a decline in cGMP and protein kinase G signaling, exacerbating dysfunction.

207 ndent of both cAMP/protein kinase A and cGMP/protein kinase G signaling.

208 llagen synthesis and increases MMPs via cGMP-protein kinase G signaling.

209 The potential role of differential cGMP and protein kinase G stimulation by these 2 modulators was a

210 Therefore, to identify novel protein kinase G substrates in vascular cells, a lambda

211 ctivation of the guanylyl cyclase-cyclic GMP-protein-kinase-G system with nitroprusside or membrane-p

212 Aplysia PKG (cGMP-dependent protein kinase; protein kinase G) that is homologous to vertebrate type-

213 SERT is phosphorylated by cGMP-dependent protein kinase G through interactions with anchoring pro

214 m CB1 or CB2, which signals through cGMP and protein kinase G to increase channel availability or the

215 n of 8-bromocyclic GMP was shown to activate protein kinase G, to block Ca2+ mobilization, as well as

216 sensitive pathways, Rho kinase activity, and protein kinase G type-1 (PKG-1) signaling.

217 Finally, protein kinase G was sufficient to directly phosphorylat