ライフサイエンスコーパス: PKC

1 PKC activation triggers down-regulation of Kv1.3 by indu

2 PKC directly phosphorylated PSD-95 and JNK1 in vitro Inh

3 PKC inhibition or the exchange of threonine for alanine

4 PKC inhibitor GF109203X nearly abolished PTP in both con

5 PKC signaling is thus implicated in autocrine regulation

6 ing subunit 85 (MBS85), paxillin and CPI-17 (PKC-potentiated protein phosphatase 1 inhibitor protein

7 In the on state, Ca(2+)-PKC phosphorylation of the MARCKS peptide reverses the P

8 ule in which Ca(2+)-protein kinase C (Ca(2+)-PKC) is hypothesized to phosphorylate myristoylated alan

9 We investigated this hypothesized Ca(2+)-PKC-MARCKS-PIP2-PI3K-PIP3 amplification module and teste

10 These findings 1) show that the Ca(2+)-PKC-MARCKS-PIP2-PI3K-PIP3 system functions as an activat

11 residues Ser-279/Ser-282 (MAPK) and Ser-368 (PKC).

12 Compared with U50,488H, PKC activation promoted much higher S356/T357 phosphoryl

13 hen neurons are treated with calphostin C, a PKC inhibitor that targets the diacylglycerol-binding si

14 tion and p300/beta-catenin interactions in a PKC-dependent manner, likely involving PKCzeta.

15 nduced c-Fos expression through repressing a PKC/MEK/ERK/ELK-1 signaling pathway.

16 c-2 gene disruption abrogated thermotaxis; a PKC-2 transgene, driven by endogenous pkc-2 promoters, r

17 ocytes and stimulated vasoconstriction via a PKC-dependent mechanism that required Rab11A S177.

18 ild-type phenotype, similar to rescue with a PKC construct.

19 s sn-1,3 DAG, which is known not to activate PKC, and insulin signaling was intact.

20 ates diacylglycerol, which in turn activates PKC which induces the actin cytoskeleton reorganization

21 rmore, the antibody is able to detect active PKC in human tissue.

22 PKMzeta is a persistently active PKC isoform proposed to maintain late-LTP and long-term

23 In addition, PKC activation by phorbol ester induced agonist-independ

24 ide gene enhancer in B-cell inhibitor-alpha (PKC-alpha/IkappaB-alpha)-mediated or calcineurin/IkappaB

25 y, and bipolar cell (protein kinase C-alpha [PKC-alpha] and recoverin) immunofluorescence revealed th

26 Although PKC- is dispensable for TCR-independent Treg proliferati

27 Although PKC-mediated phosphorylation of protein kinase D1 (PKD1)

28 EGF stimulation also elicited a Ca(2+)- and PKC-dependent reduction in synaptojanin1 recruitment to

29 diators, and increased TRPC6, PKC-alpha, and PKC-beta expression.

30 ble CD40L and were dependent on PKC-beta and PKC-gamma, respectively.

31 al at 42 degrees C and regulated the CEK and PKC pathways.

32 was prevented, the carbachol-induced DAG and PKC responses were somewhat reduced, but PKCbetaI transl

33 glycerol content and reduced PKC-epsilon and PKC-theta activity in liver and muscle respectively.

34 Inhibitors of dynamin, ERK, and PKC suppressed persistent neuronal excitation.

35 Therefore, agonist-dependent (GRK- and PKC-mediated) and agonist-independent (PKC-promoted) KOP

36 Furthermore, by treating WT, OX40(-/-), and PKC-(-/-) mice with soluble OX40L we established that OX

37 ted with differential activation of PDK1 and PKC-alpha.

38 and varepsilon-dependent phosphorylation and PKC-independent, DAG-mediated membrane recruitment, poss

39 vitro by multiple kinases, including PKA and PKC, and pharmacological activation of these kinases enh

40 protein for Protein Kinases A and C (PKA and PKC, respectively), AKAP facilitates phosphorylation and

41 ently down-regulated novel PKCs PKCdelta and PKC, differences in Ca(2+) sensitivity and diacylglycero

42 glucocorticoid-inducible kinase 1 (SGK1) and PKC-alpha was absent in Rictorfl/fl Ksp-Cre mice, indica

43 Simultaneous inhibition of Syk and PKC revealed additive dilatory effects, whereas combined

44 on calcium-induced de novo transcription and PKC-dependent mRNA stabilization.

45 ild-type mice was performed in wild-type and PKC-theta-deficient (PKC-theta(-/-)) mice.

46 rt is mainly caused by a Cdc42- and atypical PKC-dependent inhibition of dynein-dependent retrograde

47 Atypical PKCs (aPKCs) are implicated as key regulators of epithel

48 ive to WT hDAT, indicating a change in basal PKC activity in H547A.

49 ere we investigated the relationship between PKC and PSD-95.

50 Both PKC and high osmolarity glycerol (HOG) MAPK pathways wer

51 tivity were partially prevented by the broad PKC inhibitor Go6983 and fully prevented by the specific

52 Phosphorylation of Kelch-like 3 by PKC or PKA downstream of AngII or vasopressin signaling,

53 reas modulation of suppressive activities by PKC-theta and Dlgh1 signaling pathways are shared.

54 iol and show that this effect is mediated by PKC.

55 d a Hebbian form of LTP that was mimicked by PKC activation.

56 ites among major classes of brain neurons by PKC-dependent mechanisms.

57 tion, which could be completely prevented by PKC inhibition (1 mum GF109203X).

58 Cellular LTC4S activity is suppressed by PKC-mediated phosphorylation, and recently a downstream

59 signaling in cultured cells and in vitro by PKC and PKA.

60 athway involving sustained protein kinase C (PKC) activation, inhibition of serine/threonine phosphat

61 ine efflux is modulated by protein kinase C (PKC) activation.

62 cked with H89, or when the protein kinase C (PKC) activity was blocked with bisindolylmaleimide II (B

63 phospholipase C (PLC)beta1/protein kinase C (PKC) activity.

64 eptible to reactivation by protein kinase C (PKC) agonists.

65 localized the dynamics of protein kinase C (PKC) and extracellular signal-regulated kinase (ERK) act

66 or, phospholipase C (PLC), protein kinase C (PKC) and phosphoinositide-3-kinase (PI3K), and subsequen

67 nstrate that activation of protein kinase C (PKC) by phorbol myristate acetate, Gq/11-coupled GPCR, o

68 gh various kinases such as protein kinase C (PKC) contribute to the expression of long-term plasticit

69 we demonstrate that human protein kinase C (PKC) family members regulate RNP assembly.

70 The protein kinase C (PKC) family, discovered in the late 1970s, is composed o

71 Protein kinase C (PKC) has been implicated as a link, but the mechanistic

72 a1 (PLCgamma1), Ca(2+), or protein kinase C (PKC) impair clathrin-mediated endocytosis of EGFR, the f

73 endocytosis and activated protein kinase C (PKC) in the cytosol and extracellular signal regulated k

74 ve compounds including the protein kinase C (PKC) inhibitor, staurosporine.

75 lpain-mediated cleavage of protein kinase C (PKC) isoforms, each form of LTF is sensitive to a distin

76 bition of the conventional protein kinase C (PKC) isoforms, particularly PKCalpha, reduced phosphoryl

77 lase (HDAC) inhibitors and protein kinase C (PKC) modulators, provides a promising strategy to reduce

78 nhibitors for PLCgamma1 or protein kinase C (PKC) pathways, while treatment with the PKC stimulator 1

79 (PLC)beta1 activities and protein kinase C (PKC) phosphorylation, although it is unclear how store d

80 Protein kinase C (PKC) plays a regulatory role in key pathways in cancer.

81 Protein kinase C (PKC) promotes synaptic maturation and synaptogenesis via

82 -like phospholipase (PLC)/ protein kinase C (PKC) signaling cascade.

83 a novel axis whereby WNT5a/protein kinase C (PKC) signaling regulates specific beta-catenin/co-activa

84 n model of phospholipase C/protein kinase C (PKC) signaling, which was recently identified as a requi

85 Protein kinase C (PKC) theta, a serine/threonine kinase, is involved in TH

86 synaptic calcium activates protein kinase C (PKC) to increase neurotransmitter release.

87 rmacophores for binding to protein kinase C (PKC) together with a modified bryostatin-like A- and B-r

88 rbol ester binding site of protein kinase C (PKC), induces translocation of PKC to the cell membrane,

89 ated protein 43 (GAP43), a protein kinase C (PKC)-activated phosphoprotein, is often implicated in ax

90 he KCNMA1 gene, permitting protein kinase C (PKC)-dependent channel activation.

91 is associated with rapid, protein kinase C (PKC)-dependent ClC-1 Cl(-) channel inhibition in rodent

92 P results primarily from a protein kinase C (PKC)-dependent increase in release probability (Pr ) and

93 is known to trigger rapid, protein kinase C (PKC)-dependent inhibition of ClC-1 Cl(-) ion channels in

94 of preformed mRNA through protein kinase C (PKC)-induced recruitment of mRNA to polyribosomes.

95 olog 1 (Dlgh1) and exclude protein kinase C (PKC)-theta from immunological synapses formed on support

96 nel modulation via DAG and protein kinase C (PKC).

97 ents current activation by protein kinase C (PKC).

98 tion of kinases, including protein kinase C (PKC).

99 GRK2, GRK3, GRK5, GRK6 and protein kinase C (PKC)].

100 and augmented activity of protein kinase C (PKC)alpha/beta, which was dissociated from PP2A and incr

101 kinase (IRAK)1, MyD88, and protein kinase C (PKC)epsilon to the downstream TLR-signaling complex that

102 mechanistic understanding of phospholipase C/PKC signaling in chemotactic gradient sensing and can gu

103 approaches to determine the role of classic PKC isoforms in PTP.

104 In conclusion, PKC signaling modulates translation efficiency and mRNA

105 oprecipitation and pulldown assays confirmed PKC and beta-catenin as binding partners and revealed th

106 In contrast, PKC activation caused a lower level of agonist-independe

107 did not affect PKCbetaI; thus, conventional PKCs appear generally insensitive to desensitization by

108 hat thermotaxis is controlled by cooperative PKC-2-mediated signaling in both AFD sensory neurons and

109 elease from synaptic vesicles, is a critical PKC-2 effector in AFD.

110 presence of either cTnI RCM mutation or cTnI PKC phosphomimetic.

111 CLR endocytosis and activation of cytosolic PKC and nuclear ERK, which derive from endosomal CLR.

112 ng downstream of the two other essential DAG/PKC substrates, Munc13-1 and Munc18-1.

113 through activation of mTOR via PLCgamma/DAG/PKC signaling, not via Akt/Rheb signaling.

114 gamma pathway activates mTOR through the DAG/PKC signaling branch, independent of the conventional Ak

115 formed in wild-type and PKC-theta-deficient (PKC-theta(-/-)) mice.

116 regulation of beta-catenin levels and define PKC as an important beta-catenin interaction partner and

117 ed downregulation of protein kinase C-delta (PKC-delta), a TLR4-associated signalling mediator requir

118 armacological inhibition of Ca(2+)-dependent PKC isoforms abolished fast alpha1B receptor desensitiza

119 tion, this work elucidates the ADO-dependent PKC-mediated molecular mechanism that triggers immunomod

120 ut (TKO) mice in which all calcium-dependent PKC isoforms have been eliminated (PKCalpha, PKCbeta, an

121 ts onto deprived PV cells through downstream PKC-dependent activation and AMPA receptor exocytosis, t

122 ated PLC activity is responsible for driving PKC-dependent channel gating.

123 Knockdown of either PKC or JNK1 prevented PKC activator-mediated membrane ac

124 and PDAC of Pdx1-Cre;Kras(G12D/+);p53(f/+) (PKC) mice as early as 2 mo, suggesting that GRP78 could

125 ibition and membrane translocation following PKC activation.

126 red using a genetically encoded reporter for PKC activity.

127 Although CD4(+) T-cells from PKC-(-/-) mice were also defective in G-BMDC induced Tre

128 ies of different PKM isoforms generated from PKCs by calpain-mediated cleavage maintain two forms of

129 These results suggest that Gbetagamma/PKC-dependent ERK1/2 activation and heterologous desensi

130 n UNC-18 and on the protein kinase C homolog PKC-1.

131 Thus, influenza virus exploits host PKCs to regulate RNP assembly, a step required for the t

132 providing a mechanistic explanation for how PKC activity influences nuclear size.

133 We identified PKC delta and varepsilon as required and sufficient to a

134 Therefore our findings identify PKC-theta as a critical factor for ILC2 activation that

135 r control conditions it rose dramatically if PKC-dependent ClC-1 inhibition had been prevented with t

136 Neuron ablation in PKC mice also significantly delayed PanIN formation and

137 On the other hand, a significant decrease in PKC activity, and inhibition of nuclear factor kappa B (

138 ingly, the single and combined deficiency in PKC-theta or CARMA-1-the two signal transducers at the N

139 it predominantly localized to the nucleus in PKC knockout cells.

140 Further, beta-catenin overexpression in PKC-deficient podocytes could restore the wild-type phen

141 in-1 phosphorylation is an essential step in PKC-dependent potentiation of synaptic transmission, act

142 We find that PTP is unchanged in PKC triple knock-out (TKO) mice in which all calcium-dep

143 These proposed therapies include PKC and MAPK agonists as well as histone deacetylase inh

144 - and PKC-mediated) and agonist-independent (PKC-promoted) KOPR phosphorylations show distinct phosph

145 ctions stimulate PLCbeta1 activity to induce PKC phosphorylation of TRPC1 and channel gating.

146 K(+) depolarization-induced PKC translocation entirely mirrored DAG spiking, whereas

147 on its relocalisation, but that PMA-induced PKC activity drastically dysregulates the localisation o

148 orylated PSD-95 and JNK1 in vitro Inhibiting PKC, JNK, or calcium/calmodulin-dependent kinase II acti

149 fen analog, 6c, which more potently inhibits PKC than tamoxifen but lacks affinity for the estrogen r

150 , introgression of the Bcl2l1 transgene into PKC-theta null mouse failed to rescue NKT cell developme

151 totagmin-1 (Syt1(T112A)), which prevents its PKC-dependent phosphorylation, abolishes DAG-induced pot

152 ral cell signaling cascades, like NF-kappaB, PKC, ERK, and MAPK, that are involved in autophagy and s

153 tially suppressed by inhibitor of NF-kappaB, PKC, or ERK alone and significantly in combination.

154 vels of the calcium-dependent protein kinase PKC-betaI after a transient up-regulation.

155 s phosphorylation of eNOS by protein kinases PKC and AKT.

156 Mice lacking PKC-theta had reduced ILC2 numbers, TH2 cell numbers and

157 , including WN-8, for which "bryostatin-like PKC modulatory activities" previously was suggested sole

158 ich C kinase substrate by membrane-localized PKC constitutes a positive feedback that is sufficient f

159 Manipulating PKC activity in cultured mammalian cells alters nuclear

160 By mapping PKC phosphorylation sites on LB3 and testing the effects

161 inhibitor of PKC, calphostin C, blocks mbGR/PKC pathway, and rescues GC-mediated inhibition of kerat

162 In AFD neurons, PKC-2 is a Ca(2+) sensor and signal amplifier that opera

163 After U50,488H treatment, GRKs, but not PKC, were involved in agonist-induced KOPR internalizati

164 er U50,488H treatment, GRK-mediated, but not PKC-mediated, KOPR phosphorylation followed by beta-arre

165 Here we demonstrate that a novel PKC-zeta to p47(phox) interaction is required for ROS pr

166 Activation of conventional and novel PKC isoforms is associated with their Ca(2+)- and/or dia

167 iciently recruit both conventional and novel PKCs to the beta cell plasma membrane.

168 though DiC8 efficiently down-regulated novel PKCs PKCdelta and PKC, differences in Ca(2+) sensitivity

169 molecular mechanisms underlying the observed PKC-dependent ClC-1 inhibition are unclear.

170 Increase in membrane accumulation of PKC and phosphorylated PSD-95 (p-PSD-95(S295)) coincided

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

172 Prolonged activation of PKC increased synapse number by 2-fold, increased presyn

173 8 and TRIF pathways and to the activation of PKC, MAP kinase, and NF-kappaB signaling to induce the p

174 l TRPV1 in sensory neurons via activation of PKC.

175 oxidase enzyme via reducing the activity of PKC and the translocation of NF-kB to the nucleus.

176 Vps34 augments the association of PKC-delta with p62 for its phosphorylation at Serine 349

177 viously was suggested solely on the basis of PKC binding.

178 mmatory DC responses and indeed, blocking of PKC-delta degradation by the autophagolysosomal inhibito

179 s study, we tested optimal concentrations of PKC agonist candidates (PEP005/Ingenol-3-angelate, prost

180 desensitization, excluding a contribution of PKC to M1-R-induced IKs modulation.

181 t, possibly explaining the limited effect of PKC inhibitors to durably suppress MAPK in UM.

182 LTD expression by facilitating the effect of PKC on the dissociation of AMPARs from GRIP and thus the

183 kinase II activity prevented the effects of PKC activators on PSD-95 phosphorylation.

184 ce Treg proliferation in vivo independent of PKC- status.

185 Inhibition of PKC reduces AMPH-stimulated dopamine efflux and locomoto

186 Conversely, a selective inhibitor of PKC, calphostin C, blocks mbGR/PKC pathway, and rescues

187 Inhibitors of PKC, p38, ERK, CaMKII, STAT3, and CREB partially blocked

188 Pharmacological interruption of PKC-theta increases and Dlgh1 silencing decreases the ab

189 PKCalpha is a conventional isoform of PKC and a well-known binding partner of beta-catenin, wh

190 Moreover, either knockout of PKC-delta or knockdown of p62 by small interfering RNA i

191 Cell-specific manipulation of PKC-2 activity revealed that thermotaxis is controlled b

192 Finally, we show that modulation of PKC and ERK activities in somules affects motility and r

193 hibits the PDBu-dependent phosphorylation of PKC substrates.

194 f this enzyme family, discusses the roles of PKC enzymes in the development and effector functions of

195 there are concerns about the specificity of PKC activators and inhibitors.

196 lating catalytic activation and stability of PKC family members to allow for flexible and dynamic con

197 ein kinase C (PKC), induces translocation of PKC to the cell membrane, and activates kinase activity.

198 into androgenic control of c-Fos and use of PKC inhibitors in PCa therapy.

199 ent of PKCs and whether different classes of PKCs show characteristic responses.

200 PKMs, the constitutively active isoforms of PKCs generated by calpain cleavage, in the sensory neuro

201 r DAG spiking causes membrane recruitment of PKCs and whether different classes of PKCs show characte

202 tion prevented intermittent translocation of PKCs and reduced insulin secretion but did not affect [C

203 ent with soluble CD40L and were dependent on PKC-beta and PKC-gamma, respectively.

204 lity of active human muscle fibres relies on PKC-dependent ClC-1 inhibition via a gating mechanism.

205 sent in TRPC1(-/-) cells, and store-operated PKC phosphorylation of TRPC1 was inhibited by STIM1 shRN

206 Store-operated PKC phosphorylation of TRPC1 was reduced by knockdown of

207 22 and GF109203X also reduced store-operated PKC-dependent phosphorylation of TRPC1 proteins.

208 The loss of GRK3- or PKC-mediated phosphorylation of Ser-346/7 impaired the r

209 The GABAergic LTP is mimicked with PKA or PKC activation.

210 Second, subthreshold inhibition of PKA or PKC phosphorylation did not prevent TAAR1 suppression of

211 Exposure to PKD or PKC family inhibitors did not prevent PKD1 phosphorylati

212 y activated enzyme that acts much like other PKC isoforms to transduce growth factor-dependent signal

213 tion partner and signaling opponent of other PKC isoforms in podocytes.

214 However, whether other PKC isoforms interact with beta-catenin has not been stu

215 Many AGC-family kinases (AKT, p70S6K, PKC, ROCK1) seem to be regulated similarly.

216 Succinate increases phosphorylation of pan-PKC, especially the atypical PKCzeta level which was blo

217 The only known CNS-permeant PKC inhibitor is the selective estrogen receptor modulat

218 re-directed behaviors elicited by persistent PKC-2 activation or inhibition in AFD (or intestine) dis

219 The pharmacologic PKC-theta inhibitor (Compound 20) administered during al

220 roliferation and survival such as SGK1, PKA, PKC, or ERK1/2.

221 including ATM, CDKs, GSK-3, MAPKs, PKA, PKB, PKC, and SRC.

222 ivation of common (AC/PKA) and distinct (PLC/PKC, intra-/extra-cellular calcium, PI3K/MAPK/mTOR) sign

223 downstream signaling pathways, including PLC/PKC, Rho/Rac, and YAP.

224 Rapid activation of mbGR/PLC/PKC further leads to activation of known biomarkers of n

225 We found that mbGR/PLC/PKC signaling cascade exists in all cell types tested, s

226 RPC1 interactions stimulate Galphaq/PLCbeta1/PKC activity to induce channel gating.

227 Inhibition of PLCgamma/PKC-induced mTOR activation impairs IL-7-mediated B cell

228 ial molecular mediator to integrate positive PKC-theta-dependent TCR signals to induce peak RORgammat

229 r suppression cannot be inferred from potent PKC binding.

230 Knockdown of either PKC or JNK1 prevented PKC activator-mediated membrane accumulation of PSD-95.

231 ine 177 was identified as a high-probability PKC phosphorylation site.

232 ylation of the downstream signaling protein, PKC-alpha, and Ca(2+)/calmodulin-dependent protein kinas

233 luded inositol 1,3,5-triphosphate receptors, PKC, and enhancement of filamentous-actin turnover.

234 ctions in diacylglycerol content and reduced PKC-epsilon and PKC-theta activity in liver and muscle r

235 Taken together, our study shows PKC/NOX-mediated ROS generation and PARP-1 activation as

236 ET-1 stimulates PKC-mediated phosphorylation of Rab11A at serine 177, wh

237 is a potent endogenous modulator, stimulates PKC, thereby causing immunosuppression.

238 r Ser(322), disrupt thermotaxis and suppress PKC-2-dependent cryophilic migration.

239 ction microscopy, fluorescent protein-tagged PKCs, and signaling biosensors, we investigated whether

240 We conclude that PKC isozymes are not the calcium sensors that mediate PT

241 Here we demonstrate that PKC-deficient mice, which develop proteinuria and glomer

242 Taken together, these data demonstrate that PKC-mediated lamin phosphorylation is a conserved mechan

243 ibition in AFD (or intestine) disclosed that PKC-2 regulates initiation and duration of cryophilic dr

244 lear import rates, but provide evidence that PKC activity may contribute to this mechanism.

245 We hypothesized that PKC-theta contributes to ILC2 activation and might be ne

246 Here we report that PKC-mediated phosphorylation of lamin B3 (LB3) contribut

247 Here we report that PKC-theta is expressed in both human and mouse ILC2s.

248 Further analysis revealed that PKC activation caused accelerated internalization and re

249 stimulation of both cell types revealed that PKC positively regulates beta-catenin expression and sta

250 Furthermore, we also show that PKC activity, which correlates with fatty liver and whic

251 We show that PKC-2, a Caenorhabditis elegans cPKC, is essential for a

252 Here we show that PKC-delta-expressing central amygdala neurons are essent

253 The results showed that PKC agonists increased cell activation with different de

254 ailed analysis of this reduction showed that PKC mostly affected the slow gate of ClC-1.

255 We have previously shown that PKC is obligatory for activation of TRPC1 SOCs in VSMCs,

256 Collectively, our data strongly suggest that PKC activation by stolonidiol is responsible for the res

257 by UTP in control epithelia, suggesting that PKC-mediated phosphorylation plays a permissive role in

258 The PKC agonist combinations, or in combination with JQ1, le

259 The PKC inhibitors GF109203x and Go6983 blocked BK activatio

260 The PKC pancreata bearing wild-type Grp78 showed detectable

261 KC inhibitor GF109203 eliminates PTP and the PKC activator PDBu enhances neurotransmitter release and

262 ntibodies, the PLC inhibitor U73122, and the PKC inhibitor GF109203X all inhibited activation of TRPC

263 which may implicate oxidative stress and the PKC pathway in TJ destabilization.

264 Thus ROS and the PKC-zeta to p47(phox) interaction are valid therapeutic

265 In contrast, the PKC pancreata bearing a Grp78(f/+) allele (PKC78(f/+) mi

266 To examine the role of MARCKS in the PKC pathway, we treated MKs with polymethacrylate (PMA),

267 nd find that in wild-type mice 10 mum of the PKC inhibitor GF109203 eliminates PTP and the PKC activa

268 in crd1Delta cells, and up-regulation of the PKC pathway by expression of the PKC1(R398P) gene, which

269 activation, and decreased activation of the PKC pathway leads to defective mitophagy.

270 The overexpression of the PKC phosphorylation-mimicking GAP43(S41D) (constitutive

271 3) the changes of the major molecules of the PKC-alpha/IkappaBalpha- and calcineurin/IkappaB-beta-dep

272 The role of the PKC-dependent ClC-1 inhibition was evaluated from rheoba

273 We show that the PKC activators dicyclopropanated linoleic acid methyl es

274 PTP is sensitive to the PKC inhibitor GF109203X in both control and cKO.

275 he changes in ClC-1 gating that underlie the PKC-dependent ClC-1 inhibition in active muscle using hu

276 e C (PKC) pathways, while treatment with the PKC stimulator 12-O-tetradecanoylphorbol-13-acetate rest

277 ) signaling molecule protein kinase C theta (PKC-theta)-mediated phosphorylation of SRC1 is important

278 Zebrafish studies indicated three PKC-specific phosphorylation sites in beta-catenin that

279 ners and revealed that ablation of the three PKC phosphorylation sites weakens their interaction.

280 stimulates tumor development mainly through PKC-delta- activation of p62.

281 Thus, PKC and ERK are important mediators of host-ligand regul

282 6 and Merle 47 exhibited binding affinity to PKC alpha with Ki values of 7000 +/- 990 and 4940 +/- 47

283 rmore, we found that beta-arrestin2 binds to PKC-phosphorylated AT1R in a distinct active conformatio

284 RPC1-Galphaq-PLCbeta1 complexes that lead to PKC stimulation and channel gating.

285 Group II mGlu receptor activation led to PKC-dependent phosphorylation of the GluN1 subunit.

286 e formation of a signalosome involving TRAF2/PKC- leading to NF-kB activation.

287 inflammatory mediators, and increased TRPC6, PKC-alpha, and PKC-beta expression.

288 The two PKC orthologs Pck1 and Pck2 in the fission yeast Schizos

289 cle, and the molecular mechanisms underlying PKC-dependent ClC-1 inhibition are unclear.

290 in the eye and kidney through reduced VEGFR2/PKC-alpha/CREB signaling.

291 RasGRP3 activation occurs via PKC delta- and varepsilon-dependent phosphorylation and

292 as been linked to dysregulated signaling via PKC in kidney cells such as podocytes.

293 We sought to determine whether PKC or PKD1 is involved in inhibition of AMPK by causing

294 er, many of the detailed mechanisms by which PKC induces synaptogenesis are not fully understood.

295 The mechanism by which PKC-theta drives innate immune cells to instruct TH2 res

296 It is not known which PKC isoforms in the sensory neuron or motor neuron L7 ar

297 lower beta-catenin expression compared with PKC wild-type mice, consistent with an altered phenotype

298 Compared with PKC, the PKC78(f/+) pancreata showed substantial reducti

299 The model reveals how PTPMEG cooperates with PKC to drive LTD expression by facilitating the effect o

300 form-targeted HDAC inhibitors synergize with PKC modulators, namely bryostatin-1 analogues (bryologs)