ライフサイエンスコーパス: protein kinase G

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

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

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

4 by okadaic acid or KT-5823, an inhibitor of 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 NO) signalling with downstream activation of protein kinase G.

8 the cyclic guanosine monophosphate-dependent protein kinase G.

9 cyclase/3',5'-cyclic guanosine monophosphate/protein kinase G.

10 ling, stimulating phosphorylation changes by protein kinase G.

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

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

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

14 concomitantly driving adipogenesis via NPR-B/protein kinase-G.

15 hile it reacts more readily with its target, protein kinase G 1a.

16 that then relaxes arteries via oxidation of protein kinase G 1a.

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

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

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

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

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

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

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

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

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

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

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

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

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

30 BH4 did not enhance net protein kinase G activity.

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

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

33 molecular remodeling, increasing myocardial protein kinase G activity.

34 ial cGMP-PKG (cyclic guanosine monophosphate-protein kinase G) activity has been associated with incr

35 ind relevant interactions for ligands toward protein kinase G, an essential protein of Mycobacterium

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

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

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

39 ion of both monomeric and dimerized forms of protein kinase G and of the cGMP hydrolyzing phosphodies

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

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

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

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

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

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

46 nd is controlled by phosphorylation via PKG (protein kinase G) and CDPK1 (calcium-dependent protein k

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

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

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

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

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

52 Protein kinase A and protein kinase G are regulated by oxidants in this way,

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

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

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

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

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

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

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

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

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

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

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

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

65 lular signaling pathway engaging cyclic GMP, protein kinase G, Ca(2+), and the phosphatidyl inositol

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

67 y) cells, S-nitrosoglutathione led to a PKG (protein kinase G)-dependent increase in plasmalemmal den

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

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

70 a calcium/calmodulin-dependent kinase II and protein kinase G-dependent manner.

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

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

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

74 We also demonstrated that protein kinase G-dependent phosphorylation of PDE3A at S

75 f these two mutants by nitric oxide-mediated/protein kinase G-dependent phosphorylation.

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

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

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

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

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

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

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

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

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

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

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

87 nitric oxide-cyclic guanosine monophosphate-protein kinase G (i.e. NO/cGMP/PKG) signalling pathway.

88 nitric oxide-cyclic guanosine monophosphate-protein kinase G (i.e. NO/cGMP/PKG) signalling, these fi

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

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

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

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

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

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

95 guanosine monophosphate (cGMP) by activating protein kinase G increase 26S proteasome activities, pro

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

116 2,4)-oxadiazolo[4,3-a]-quinoxalin-1-one) and protein kinase G inhibitors (H8, DT-2) block AR stimulat

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

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

119 m potentiation through the nitric oxide/cGMP/protein kinase G intracellular cascade consistent with a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

138 Protein kinase G of Mycobacterium tuberculosis has been

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

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

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

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

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

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

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

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

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

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

149 d are mediated through the nitric oxide/cGMP/protein kinase G pathway.

150 asmodium falciparum encodes a cGMP-dependent protein kinase G (PfPKG) that is critical for its life c

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

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

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

154 ne monophosphate (cGMP) leading to increased protein kinase G (PKG) activity and vascular smooth musc

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

156 l NO synthase (eNOS), cyclic GMP (cGMP), and protein kinase G (PKG) activity independently of diet, w

157 mutation have a three-fold increase in basal protein kinase G (PKG) activity, and develop age-depende

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

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

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

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

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

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

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

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

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

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

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

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

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

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

172 NOS inhibition in Syrian golden hamsters and protein kinase G (PKG) inhibition in WT mice also abroga

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

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

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

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

177 Phosphorylation of RGS2 D40Y and R44H by protein kinase G (PKG) may explain their maintained func

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

179 ve suggested that phosphorylation of RyR2 by protein kinase G (PKG) might contribute to the cardiopro

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

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

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

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

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

185 edly post-translationally enhanced by direct protein kinase G (PKG) phosphorylation at S20 (mouse, S1

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

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

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

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

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

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

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

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

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

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

196 3',5'-cyclic guanosine monophosphate (cGMP), protein kinase G (PKG), and the BK(Ca) channel were used

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

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

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

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

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

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

203 ctivity against other AGC kinases, including protein kinase G (PKG), whose inhibition could potential

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

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

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

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

208 Mechanistically, PRL induced the protein kinase G (PKG)-mediated phosphorylation of the V

209 synthesis of cGMP and subsequently activates protein kinase G (PKG).

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

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

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

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

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

215 vels of ubiquitinated proteins by activating protein kinase G (PKG).

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

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

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

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

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

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

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

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

224 Protein kinase G (PknG), a Serine/Threonine kinase, is e

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

226 0(S6k), whereas only selective inhibitors of protein kinase G prevented the activation of the kinases

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

243 and inhibiting fibroblast activation through protein kinase G signaling.

244 signaling, calcium signaling, and cGMP-PKG (protein kinase G) signaling are among the pathways that

245 t partially stemmed from restoration of PKG (protein kinase G) signaling in HF patient-derived CF, wh

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

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

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

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

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

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

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

253 of AR stimulated plasma membrane-associated protein kinase G type 2 (PKG2), leading to the activatio

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

255 Finally, protein kinase G was sufficient to directly phosphorylat

256 NO activates protein kinase G with the subsequent production of cGMP,