ライフサイエンスコーパス: protein kinase C

1 dulin-dependent protein kinase kinase 2, and protein kinase C.

2 sed in host cells gamma134.5 targets p32 and protein kinase C.

3 osphorylation by protein kinase A but not by protein kinase C.

4 ing the UL31/UL34 complex, cellular p32, and protein kinase C.

5 alpha) via its serine 248 phosphorylation by Protein Kinase C.

6 ) stores, but was dependent on activation of protein kinase C.

7 by parallel signaling via either calcium or protein kinase C.

8 regulation by other proteins, including the protein kinases C.

9 ly in part by spatially restricting atypical protein kinase C, a negative regulator of non-muscle myo

10 s and actin-based protrusions, bind atypical protein kinase C, activate RAC1, and activate STAT3 at c

11 Hence, by inhibiting production of the protein kinase C-activating lipid, diacylglycerol, cAMP/

12 Protein kinase C activation also led to fewer Insulin+ c

13 ations of diabetes and is caused by abnormal protein kinase C activation as a result of increased dia

14 rotein--tagged Rab proteins, pharmacological protein kinase C activation mimicked alpha1B-AR traffic

15 couple to Gq proteins, calcium signaling and protein kinase C activation; subsequently, the receptors

16 mbrane complexes and observed that different protein kinase C activators differentially position the

17 am-V or phorbol 12-myristate 13-acetate, two protein kinase C activators, leads to altered morphology

18 red actin rearrangement, tyrosine kinase and protein kinase C activities, and both clathrin and lipid

19 cible mitochondrial function is dependent on protein kinase C activity, and is required to fine-tune

20 latter interaction was abrogated by blocking protein kinase C activity, resulting in receptor retenti

21 We showed that protein kinase C agonists in combination with bromodomai

22 nd extraterminal bromodomain inhibitors, and protein kinase C agonists, also scored positive in this

23 Protein kinase C alpha (PKCalpha) can activate both pro-

24 Here we show that protein kinase C alpha (PKCalpha) interacts with TRM61,

25 Here we present data linking protein kinase C alpha (PKCalpha) to the regulated expre

26 We found out that in bystander AL cells, protein kinase C alpha (PKCalpha) translocated from cyto

27 traspanin membrane scaffold, CD82, regulates protein kinase c alpha (PKCalpha)-mediated signaling cri

28 n a manner that is codependent upon EGFR and protein kinase C alpha (PKCalpha).

29 thase, syntrophins, protein interacting with protein kinase C alpha 1, syntenin-1, and sorting nexin

30 d cell-to-cell contact and fusion, decreased protein kinase C alpha expression, and ultimately reduce

31 in basic protein upon phosphorylation by the protein kinase C-alpha (PKC-alpha) in the presence of ad

32 Ca2+ transporting, plasma membrane 4(ATP2B4)-protein kinase C-alpha (PRKCA) fusion transcript.

33 ssion electron microscopy, and bipolar cell (protein kinase C-alpha [PKC-alpha] and recoverin) immuno

34 protein expression, by means of blunting the protein kinase C-alpha pathway.

35 xpression, respectively, blocks and augments protein kinase C-alpha/nuclear factor of kappa light pol

36 We modified this structure by modulation of protein kinase C, an enzyme regulating neurite growth an

37 es for the design of simpler, more effective protein kinase C analogs and could also prove relevant t

38 relative contributions of signaling kinases protein kinase C and Ca(2+)/Calmodulin-dependent protein

39 We previously reported that the protein kinase C and casein kinase II substrate in neuro

40 tor stimulation activate feedforward calcium-protein kinase C and cyclic AMP-protein kinase A signali

41 We find that protein kinase C and cyclin-dependent kinase phosphoryla

42 n E2, PGE2-G, mobilizes Ca(2+) and activates protein kinase C and ERK, suggesting the involvement of

43 endent, whereas IL-17 requires activation of protein kinase C and intracellular calcium signaling.

44 ell stage is directed by Phospholipase C and Protein kinase C and occurs in two phases: polarisation

45 inate receptors and activation of G protein, protein kinase C and phospholipase C.

46 occurs at least partly through inhibition of protein kinase C and receptor tyrosine kinase activity.

47 Elevated glucose activated the protein kinase C and Rho/Rho-kinase signaling pathways a

48 The roles of protein kinase C and the small GTPase, Rab9, in alpha1B-

49 holipase C pathway, leading to activation of protein kinase C and, in turn, sphingosine kinase (SphK)

50 RPA1 by mechanisms that required Gbetagamma, protein kinase C, and Ca(2+).

51 s dependent on C5aR1, intracellular calcium, protein kinase C, and calmodulin, and downstream signali

52 echanism dependent on intracellular calcium, protein kinase C, and phosphatidylinositol 3-kinases-bas

53 otif phosphatase for the protein kinase AKT, protein kinase C, and S6 kinase.

54 lear egress cooperatively with cellular p32, protein kinase C, and the nuclear egress complex.

55 Partitioning defective 6) and PKC-3/atypical protein kinase C, and the WAVE actin nucleation complex

56 A431 epithelial cells transduced Gbetagamma-protein kinase C- and Gbetagamma-metalloproteinase/EGFR-

57 f KV 1.5, but not KV 2.1, channels through a protein kinase C- and lysosome-dependent mechanism, redu

58 Also, BLT2 activation inhibited protein kinase C- and protein kinase A-mediated sensitiz

59 of the PI3K signaling intermediate atypical protein kinase C (aPKC) constrains food intake, weight g

60 Atypical protein kinase C (aPKC) enzymes signal on protein scaffo

61 proteins PAR-3, PAR-6, CDC-42, and atypical protein kinase C (aPKC) form a core unit of the PAR prot

62 amined insulin signaling to Akt and atypical protein kinase C (aPKC) in liver and muscle and hepatic

63 Atypical protein kinase C (aPKC) is a key apical-basal polarity d

64 Activity of the atypical protein kinase C (aPKC) is a key output of the Par compl

65 m diverse systems suggests that the atypical Protein Kinase C (aPKC) is a key regulator of cell fate

66 Individual loss of either atypical protein kinase C (aPKC) isoform, PKCzeta or PKClambda/io

67 Atypical protein kinase C (aPKC) isoforms are overexpressed and a

68 Atypical protein kinase C (aPKC) isozymes modulate insulin signal

69 In this paper, we report that atypical protein kinase C (aPKC) phosphorylates Yrt to prevent it

70 lg) links the Par complex component atypical Protein Kinase C (aPKC) to the essential spindle orienta

71 ated brain protein kinases, Akt and atypical protein kinase C (aPKC), were maximally increased.

72 The current study identifies the protein kinase C-associated kinase (PKK), which is also

73 We have identified protein kinase C beta (PKCbeta) as a critical mediator o

74 we identify the calcium-regulated classical protein kinase C beta (PKCbeta) as a repressor of myogen

75 Protein kinase C beta (PKCbeta) regulated MIF-induced IL

76 Protein kinase C-beta (PKC-beta) is immediately downstre

77 d that combined small-molecule inhibition of protein kinase C-beta (PKCbeta) and glycogen synthase ki

78 ling, but GC cells signaled less through the protein kinase C-beta-NF-kappaB pathway and produced str

79 siRNA-mediated silencing of protein kinase C-beta1 abolished tumor necrosis factor-a

80 pharmacological inhibitor demonstrated that protein kinase C-beta1 mediates phosphorylation of Nox1

81 thermal titration calorimetry indicated that protein kinase C-beta1 phosphorylates Nox1 at threonine

82 We conclude that protein kinase C-beta1 phosphorylation of threonine 429

83 This effect required protein kinase C-betaII and was influenced by miR-33, a

84 Bisindolylmaleimide (BIM; a protein kinase C blocker), a protein kinase C inhibitory

85 ependent AKT phosphorylation are mediated by protein kinase C but not by protein phosphatase 2A.

86 CBF reduction required protein kinase C but was not associated with changes in

87 Finally, selective kinase inhibition of protein kinase C by targeted allelic replacement with an

88 f extracellular signal-regulated kinase 1/2, protein kinase C, c-Jun N-terminal kinase, or GRK5 did n

89 utative amplification module in which Ca(2+)-protein kinase C (Ca(2+)-PKC) is hypothesized to phospho

90 ecules crucial to PMA-induced NETs including protein kinase C, calcium, reactive oxygen species, the

91 It binds to protein kinase C competitively with diacylglycerol, the

92 Protein kinase C constitutes a family of serine-threonin

93 ecreased expression of the calcium-dependent protein kinase C conventional subclass alpha/beta leadin

94 We previously reported that conventional protein kinase C (cPKC) contributes to nuclear size redu

95 Ca(2+)- and diacylglycerol (DAG)-activated protein kinase C (cPKC) promotes learning and behavioral

96 equired for the activation of a conventional protein kinase C (cPKC).

97 gy allows the development of potential novel protein kinase C delta (PKCdelta) analogues for better t

98 Protein kinase C delta (PKCdelta) and p38delta are key p

99 ation of central amygdala neurons expressing protein kinase C delta (PKCdelta) as key elements of the

100 pendent or -independent for co-dependency on protein kinase C delta (PKCdelta).

101 d ErbB3-binding protein 1 phosphorylation by protein kinase C delta are both required for optimal PCN

102 rtantly, chemical inhibition or knockdown of protein kinase C delta was sufficient to rescue the phen

103 -induced Mvarphi polarization, and PKCdelta (protein kinase C delta) as a downstream target.

104 w here that ES-62-mediated downregulation of protein kinase C-delta (PKC-delta), a TLR4-associated si

105 The diverse roles of protein kinase C-delta (PKCdelta) in cellular growth, su

106 Protein kinase C-delta (PKCdelta) is an allosterically a

107 rated that phosphorylation of GAPDH by delta protein kinase C (deltaPKC) inhibits this GAPDH-dependen

108 nal approach to identify inhibitors of delta protein kinase C (deltaPKC), each inhibiting the phospho

109 tivation of focal adhesion kinase (FAK) in a protein kinase C dependent manner.

110 cribe a mechanism by which Ang II stimulates protein kinase C-dependent KV 1.5 channel degradation, r

111 e AT1 R stimulates actin polymerization by a protein kinase C-dependent mechanism, but independently

112 ma line, HVCN1S responded more profoundly to protein kinase C-dependent phosphorylation.

113 Protein kinase D (PKD) isoforms are protein kinase C effectors in signaling pathways regulat

114 e a target deletion of PKC1, the single copy protein kinase C-encoding gene, proved unsuccessful.

115 ApoE3 also induced expression of protein kinase C epsilon (PKCepsilon) and PKCepsilon ret

116 Protein kinase C epsilon (PKCepsilon) is emerging as a p

117 Previous results using protein kinase C epsilon (PKCepsilon) knockout mice, RNA

118 duced by agonists at receptors that activate protein kinase C epsilon (PKCepsilon), occurs in male bu

119 d to determine whether SIRT5 is activated by protein kinase C epsilon (PKCepsilon)-mediated increases

120 nes (SKH-1 hairless mice, wild-type FVB, and protein kinase C epsilon (PKCvarepsilon)-overexpressing

121 ycerol-mediated (DAG-mediated) activation of protein kinase C-epsilon (PKCepsilon) and the consequent

122 for ROS production, NADPH assembly capacity, protein kinase C expression, and calcium release in resp

123 3 (Cav-3), altered Ca(2+) cycling, increased protein kinase C expression, and hyperactivation of calc

124 g defined, one common theme is activation of protein kinase C family members in the interphase nucleu

125 protein kinase G and phospholipid-dependent protein kinase C family), is a substrate of TOR.

126 interneurons, that a small number coexpress protein kinase C gamma (PKCgamma), but that none coexpre

127 se activity, the phosphorylation of Pah1p by protein kinase C had a small stimulatory effect on the e

128 Protein kinase C has been implicated in the phosphorylat

129 ase M zeta (PKMzeta), an atypical isoform of protein kinase C, has been suggested to be necessary and

130 WC(ON) release relies upon UNC-18 and on the protein kinase C homolog PKC-1.

131 mon intermediate were found to interact with protein kinase C in a manner that correlates well with t

132 ivation is facilitated through initiation of protein kinase C-induced ADAM activity.

133 desensitization (but not ME) was reduced by protein kinase C inhibition in wild-type MOPr and abolis

134 for WC1 endocytosis in Jurkat cells, the pan-protein kinase C inhibitor Go6983 blocked endocytosis of

135 The protein kinase C inhibitor sotrastaurin markedly potenti

136 of which were suppressed by chelerythrine, a protein kinase C inhibitor, DPI, a NADPH-dependent oxida

137 leimide (BIM; a protein kinase C blocker), a protein kinase C inhibitory peptide or bafilomycin A (a

138 n and colocalization of MT1-MMP and atypical protein kinase C iota (aPKCiota) in hormone receptor-neg

139 Activation of atypical protein kinase C iota/lambda (aPKCiota/lambda) mediates

140 ng a novel complex with two other oncogenes, protein kinase C, iota and epithelial cell transforming

141 n considered together, these results suggest protein kinase C is essential for growth and development

142 endent lines of evidence which indicate that protein kinase C is essential for viability of Magnaport

143 catalase, and activation of the pro-oxidant protein kinase C isoform beta-II (PKCbetaII)-dependent p

144 e Mzeta (PKMzeta), a brain-specific atypical protein kinase C isoform, is important for maintaining l

145 rimary intracellular target of calcium to be protein kinase C isoforms alpha and beta (PKCalpha and P

146 Sotrastaurin, a small molecule targeting protein kinase C isoforms, failed to provide adequate im

147 epends on Galphaq-signaling and conventional protein kinase C isoforms.

148 associated with decrease in stress-activated protein kinase/c-Jun N-terminal kinase activity.

149 ) all-atom molecular dynamics simulations of protein kinase C-ligand-membrane complexes and observed

150 Protein kinase C-mediated HSPB1 phosphorylation confers

151 n/LLGL1 interaction is inhibited by atypical protein kinase C-mediated phosphorylation of LLGL1, rest

152 we found that KCC2 recycling is enhanced by protein kinase C-mediated phosphorylation of the GluK2 C

153 Data suggest that protein kinase C modulates alpha1B-adrenergic receptor t

154 histone deacetylase inhibitors (HDACis) and protein kinase C modulators (PKCms).

155 ng the activity of integrin-linked kinase or protein kinase C mu either by small interfering RNA-medi

156 e mechanistic insights revealed CXCR2-driven protein kinase C mu-dependent integrin-linked kinase to

157 kemic cells, partly via Toll-like receptor-2/protein kinase C/nuclear factor-kappaB signaling, and po

158 how bryostatin interacts with membrane-bound protein kinase C, offering insights for the design of br

159 KF neurons was not enhanced by activation of protein kinase C or in slices from morphine-treated rats

160 synthase (eNOS) at Thr497 (eNOS(pThr497)) by protein kinase C or RhoA-activated kinase is a major reg

161 Of these, the ternary Par3-atypical protein kinase C-Par6 polarity complex mediates asymmetr

162 n neutrophil migration and inhibition of the protein kinase C pathway.

163 drenergic receptors that had been mutated at protein kinase C phosphorylation sites (S396A, S402A) we

164 , well-known Cx43 Akt, protein kinase A, and protein kinase C phosphorylation sites located in the vi

165 Protein kinase C (PKC) activation irreversibly diminishe

166 Protein kinase C (PKC) activation reduced Ih amplitude a

167 Protein kinase C (PKC) activation was necessary and suff

168 mplex signalling pathway involving sustained protein kinase C (PKC) activation, inhibition of serine/

169 H-stimulated dopamine efflux is modulated by protein kinase C (PKC) activation.

170 ) activity was blocked with H89, or when the protein kinase C (PKC) activity was blocked with bisindo

171 subunit (Galphaq)/phospholipase C (PLC)beta1/protein kinase C (PKC) activity.

172 roduced by massed 5-HT depends on persistent protein kinase C (PKC) activity.

173 orrelation between CDCP1 expression, SFK and protein kinase C (PKC) activity.

174 syntaxin-1, but required calcium influx and protein kinase C (PKC) activity.

175 ation but are susceptible to reactivation by protein kinase C (PKC) agonists.

176 d and functionally localized the dynamics of protein kinase C (PKC) and extracellular signal-regulate

177 opamine transporter function is regulated by protein kinase C (PKC) and other signaling pathways thro

178 actor (FGF) receptor, phospholipase C (PLC), protein kinase C (PKC) and phosphoinositide-3-kinase (PI

179 ogenous NLGN4X is robustly phosphorylated by protein kinase C (PKC) at T707, and R704C completely eli

180 TRIF pathways, the Tat protein activated the protein kinase C (PKC) betaII isoform, the mitogen-activ

181 Here we demonstrate that activation of protein kinase C (PKC) by phorbol myristate acetate, Gq/

182 Activation of protein kinase C (PKC) by the diacylglycerol mimic phorb

183 Rs) triggers a Gi-Gbetagamma-phospholipase C-protein kinase C (PKC) cascade that promotes ADAM17-depe

184 Although various kinases such as protein kinase C (PKC) contribute to the expression of l

185 Here we demonstrate that human protein kinase C (PKC) family members regulate RNP assem

186 The protein kinase C (PKC) family, discovered in the late 19

187 Here, we identify protein kinase C (PKC) gamma, a serine/threonine kinase

188 Protein kinase C (PKC) has been implicated as a link, bu

189 hospholipase Cgamma1 (PLCgamma1), Ca(2+), or protein kinase C (PKC) impair clathrin-mediated endocyto

190 annels and that Kv7 activity is regulated by protein kinase C (PKC) in response to vasoconstrictors i

191 RP) stimulated CLR endocytosis and activated protein kinase C (PKC) in the cytosol and extracellular

192 hile this rescue effect was prevented by the protein kinase C (PKC) inhibitor GF 109203X.

193 dolylmaleimide I, a specific ATP-competitive protein kinase C (PKC) inhibitor, rules out that this in

194 biologically active compounds including the protein kinase C (PKC) inhibitor, staurosporine.

195 Protein kinase C (PKC) is a family of serine/threonine k

196 aimed to investigate the role of nociceptor protein kinase C (PKC) isoforms in PIPN.

197 ium that in turn activates calcium-dependent protein kinase C (PKC) isoforms to phosphorylate targets

198 are formed from calpain-mediated cleavage of protein kinase C (PKC) isoforms, each form of LTF is sen

199 effect, while inhibition of the conventional protein kinase C (PKC) isoforms, particularly PKCalpha,

200 Protein kinase C (PKC) isozymes have remained elusive ca

201 To address a potential role of protein kinase C (PKC) isozymes in the resistance to TKI

202 Since their discovery in the late 1970s, protein kinase C (PKC) isozymes represent one of the mos

203 Previous findings have suggested that protein kinase C (PKC) may be involved in the regulation

204 Here we show that although protein kinase C (PKC) mediates PTP at the calyx of Held

205 Protein kinase C (PKC) modulators are currently of great

206 as histone deacetylase (HDAC) inhibitors and protein kinase C (PKC) modulators, provides a promising

207 Within the family of protein kinase C (PKC) molecules, the novel isoform PRKC

208 aptic activation of the diacylglycerol (DAG)/protein kinase C (PKC) pathway is a central event in sho

209 a new and unexpected role in regulating the protein kinase C (PKC) pathway.

210 gly repressed by inhibitors for PLCgamma1 or protein kinase C (PKC) pathways, while treatment with th

211 q)/phospholipase C (PLC)beta1 activities and protein kinase C (PKC) phosphorylation, although it is u

212 presumably by rendering DP inaccessible for protein kinase C (PKC) phosphorylation.

213 Protein kinase C (PKC) plays a regulatory role in key pa

214 Protein kinase C (PKC) promotes synaptic maturation and

215 (DAG) content leading to activation of novel protein kinase C (PKC) resulting in decreased insulin si

216 y activating a Wnt-like phospholipase (PLC)/ protein kinase C (PKC) signaling cascade.

217 m, and identified a novel axis whereby WNT5a/protein kinase C (PKC) signaling regulates specific beta

218 reaction-diffusion model of phospholipase C/protein kinase C (PKC) signaling, which was recently ide

219 MARCKS is a protein kinase C (PKC) substrate that binds PIP2.

220 Protein kinase C (PKC) theta, a serine/threonine kinase,

221 ing mechanism, presynaptic calcium activates protein kinase C (PKC) to increase neurotransmitter rele

222 This burst engages protein kinase C (PKC) to trigger the insertion of a cov

223 the requisite pharmacophores for binding to protein kinase C (PKC) together with a modified bryostat

224 Protein kinase C (PKC), a validated therapeutic target f

225 ed AGC kinase superfamily, including AKT and protein kinase C (PKC), and is implicated in important c

226 9/150 interacts with protein kinase A (PKA), protein kinase C (PKC), and protein phosphatase 2B (calc

227 of the nuclear lamina by recruiting cellular protein kinase C (PKC), as occurs with certain other her

228 ght/temperature regimens displayed modulated protein kinase C (PKC), extracellular signal-regulated k

229 l binds to the phorbol ester binding site of protein kinase C (PKC), induces translocation of PKC to

230 ctivation of phospholipase Cgamma (PLCgamma)-protein kinase C (PKC), which, in turn, activates mTOR.

231 Growth-associated protein 43 (GAP43), a protein kinase C (PKC)-activated phosphoprotein, is ofte

232 means or by treatment with an orally active protein kinase C (PKC)-activator, prostratin, represses

233 exon (STREX) in the KCNMA1 gene, permitting protein kinase C (PKC)-dependent channel activation.

234 at muscle activity is associated with rapid, protein kinase C (PKC)-dependent ClC-1 Cl(-) channel inh

235 position 8 were also partial agonists of the protein kinase C (PKC)-dependent ERK pathway via atypica

236 es suggest that PTP results primarily from a protein kinase C (PKC)-dependent increase in release pro

237 potentials (APs) is known to trigger rapid, protein kinase C (PKC)-dependent inhibition of ClC-1 Cl(

238 s) causes GlyR endocytosis in a calcium- and protein kinase C (PKC)-dependent manner, leading to redu

239 y oxLDL/CD36 required Src-family kinases and protein kinase C (PKC)-dependent phosphorylation and act

240 depends on the modulation of inactivation by protein kinase C (PKC)-dependent phosphorylation of the

241 TBP-mediated Purkinje cell degeneration via protein kinase C (PKC)-dependent signaling.

242 ted by translation of preformed mRNA through protein kinase C (PKC)-induced recruitment of mRNA to po

243 Since a RhoA/protein kinase C (PKC)-mediated pathway is known to inhi

244 uit Disc large homolog 1 (Dlgh1) and exclude protein kinase C (PKC)-theta from immunological synapses

245 reduction and augments current activation by protein kinase C (PKC).

246 ressing PA-LTF, which required activation of protein kinase C (PKC).

247 ROS are known to activate protein kinase C (PKC).

248 the timely activation of kinases, including protein kinase C (PKC).

249 e release, or channel modulation via DAG and protein kinase C (PKC).

250 protein kinases [GRK2, GRK3, GRK5, GRK6 and protein kinase C (PKC)].

251 sphatase 2A (PP2A) and augmented activity of protein kinase C (PKC)alpha/beta, which was dissociated

252 and adenoviral transduced dominant negative protein kinase C (PKC)beta2 in HAECs.

253 Protein kinase C (PKC)delta has been shown to be increas

254 IL-1R-associated kinase (IRAK)1, MyD88, and protein kinase C (PKC)epsilon to the downstream TLR-sign

255 e transcriptional start site in the atypical protein kinase C (PKC)zeta isoform, which removes N-term

256 eptors mediated resistance in part through a protein-kinase-C (PKC)-dependent mechanism.

257 Protein kinase C (Pkc1) relays signals in the pathway by

258 n the conserved Rho1 GTPase and its effector protein kinase C (Pkc1) with septin ring stability in ye

259 dependent signals control phosphorylation of protein kinase C (Pkc1), which plays an essential role i

260 In addition, we find that the protein kinase C (Pkc1)/MAPK cascade, a well-established

261 Activation of the delta isoform of protein kinase C (PKCdelta) was increased in postmortem

262 Da regulatory light chains (LC20) but not of protein kinase C-potentiated inhibitory protein for myos

263 The brain-specific gamma isoform of protein kinase C (Prkcc) is one of the affected signalin

264 Conversely, activation of protein kinase C promoted aggregation of neurons into cl

265 however, we found striking reductions in the protein kinase C, Pyk 2 and Src kinase activity that in

266 ule for diacylglycerol and phorbol esters in protein kinase C, Ras guanine nucleotide releasing prote

267 osphorylation of Pah1 by protein kinase A or protein kinase C reduced its subsequent phosphorylation

268 Inhibition of protein kinase C reduced neuronal aggregation and fascic

269 METHODS AND ET-1, through activation of PKC (protein kinase C), reduced surface beta1 abundance and t

270 titively with diacylglycerol, the endogenous protein kinase C regulator, and plant-derived phorbol es

271 ation end products, L-type calcium channels, protein kinase C, Rho-kinase, actin polymerization, and

272 omycin and was not affected by inhibition of protein kinase C, Rho-kinase, or extracellular signal-re

273 We found that protein kinase C selectively controlled firing rate adap

274 reversal agent properties appear to activate protein kinase C signaling.

275 Targeting protein kinase C signalling may therefore prove an effec

276 d GPCR-kinase interacting protein-1-mediated protein kinase C-stimulated phosphorylation of MaxiKbeta

277 Mutations in protein kinase C substrate 80K-H (PRKCSH), which encodes

278 e HIF-alpha network, we identified the major protein kinase C substrate MARCKS (myristoylated alanine

279 roteins, :MARCKS (Myristoylated Alanine-Rich protein Kinase C substrate) and Grin1 (G protein regulat

280 Inhibition of ERK and protein kinase C sustains a transgene-independent rewire

281 greater number of phosphorylation sites for protein kinase C than other cereal species, which may be

282 RNA knockdown experiments demonstrated that protein kinase C, the small GTPase Cdc42 and palladin we

283 ly, T cell receptor (TCR) signaling molecule protein kinase C theta (PKC-theta)-mediated phosphorylat

284 osphoinhibition of GIV-GEF by the fatty acid/protein kinase C-theta pathway triggers IR.

285 lation of ZAP70, phospholipase C-gamma1, and protein kinase C-theta, and impaired nuclear translocati

286 an sulfate of syndecan-4 recruit cytoplasmic protein kinase C to target serine714 of TRPC7 with subse

287 In infected cells, wild-type virus recruits protein kinase C to the nuclear membrane and triggers it

288 amma receptors, signaling via Syk, PI3K, and protein kinase C to trigger the production of toxic reac

289 Here, we report a protein kinase C-varepsilon (PKCvarepsilon)- and ATF2-me

290 of p38 mitogen-activated protein kinase and protein kinase C, which drives IL-17A expression.

291 This process is mediated by protein kinase C, which is activated by BA/A.

292 These data indicate that Ang II activates protein kinase C, which stimulates KV 1.5 channel degrad

293 e A with H89, or by blocking the activity of protein kinase C with bisindolylmaleimide II.

294 eded due to difficulties in co-crystallizing protein kinase C with relevant ligands.

295 Atypical Protein Kinase C zeta (PKCzeta) forms Partitioning-defec

296 itro and insulin resistance in vivo activate protein kinase C zeta (PKCzeta) in pancreatic islets and

297 tes a direct interaction between Galphaq and protein kinase C zeta (PKCzeta), leading to the stimulat

298 neural progenitors was dependent on atypical protein kinase C zeta, a mediator of stem cell polarity,

299 MGB1, whose release of HMGB1 induced a rapid protein kinase C zeta-mediated internalization of surfac

300 lled CPC differentiation via integrin-beta1, protein kinase C-zeta, and v-akt murine thymoma viral on