ライフサイエンスコーパス: protein kinase C

1 lphaq-protein-coupled receptor activation of protein kinase C.

2 lation by Pho85-Pho80, protein kinase A, and protein kinase C.

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

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

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

6 ernalization, possibly through activation of protein kinase C.

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

8 ns require the function of Ca(2+) -dependent protein kinase C.

9 rization that were reversed by inhibitors of protein kinase C, a downstream kinase in the protocadher

10 Moreover, protein kinase C, a downstream target of EGF, was active

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

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

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

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

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

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

17 Compound screening identified a protein kinase c activator that promotes maturation of p

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

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

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

21 cortical actin depolymerization but affected protein kinase C activity and the 14-3-3e substrate.

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

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

24 ts of G protein-coupled serotonin receptors, protein kinase C agonists, and a microbial metabolite no

25 y reversal by histone deactylase inhibitors, protein kinase C agonists, and proteasome inhibitors wit

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

27 erapy identified a crucial role for enhanced protein kinase c alpha (PKCalpha) signaling and downstre

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

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

30 ses electrical and mechanical disruption via protein kinase C alpha/beta (PKCalpha/beta) activation.

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

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

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

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

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

36 Kinase inhibitors aimed at blocking protein kinase C and c-Jun N-terminal kinase had no effe

37 pted such that additional kinases, including protein kinase C and c-Jun N-terminal kinase, contribute

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

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

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

41 ical (vismodegib) and noncanonical (atypical protein kinase C and MRTF inhibitors) HH pathway inhibit

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

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

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

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

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

47 n shown in Xenopus oocytes to be affected by protein kinases C and A, we used different nonselective

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

49 d beta, fibroblast growth factor receptor-1, protein kinase C, and matrix metalloproteinase 2.

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

51 phospholipase C pathways, including calcium, protein kinase C, and phosphoinositide 3-kinase but not

52 regulates MOR recycling via G (betagamma) , protein kinase C, and receptor phosphorylation.

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

54 red for this response together with calcium, protein kinase C, and to some extent, phosphoinositide 3

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

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

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

58 l cell polarity, with expression of atypical protein kinase C (aPKC) at the contact-free domain, nucl

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

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

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

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

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

64 Atypical protein kinase C (aPKC) isozymes are unique in the PKC s

65 Atypical protein kinase C (aPKC) isozymes, PKClambda/iota and PKC

66 noid cultures, we show that the PAR-atypical protein kinase C (aPKC) polarity complex inhibits EMT an

67 the Par complex proteins Par-6 and atypical protein kinase C (aPKC) to specific cortical sites.

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

69 Phosphorylation of Lgl by atypical protein kinase C (aPKC), a component of the partitioning

70 apical Par complex, which contains atypical protein kinase C (aPKC), Bazooka (Par-3), and Par-6, is

71 and Dlg do not directly antagonize atypical protein kinase C (aPKC), but may instead restrict aPKC l

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

73 ogue-sensitive allele of Drosophila atypical Protein Kinase C (aPKC).

74 ivation of Cdc42 and the downstream atypical protein kinase C (aPKC).

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

76 by counteracting the negative influences of protein kinase C beta (PKCbeta) via dephosphorylation an

77 duced phosphorylation of the kinases Lyn and protein kinase C-beta and MAPKs MKK-3/6 and p38MAPK or t

78 VCAM1) on MSCs, leading to the activation of protein kinase C beta1 (PKCbeta1) signaling and repressi

79 We previously demonstrated that beta II protein kinase C (betaIIPKC) activity is elevated in fai

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

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

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

83 We identify protein kinase C, but not protein kinase A, to be respon

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

85 Several protein kinases, including protein kinase C, Ca(2+)/calmodulin-dependent protein ki

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

87 G protein-coupled receptor kinase 6, whereas protein kinase-C can also contribute to agonist-induced

88 Sln1 acts in parallel with the protein kinase C cell-integrity pathway as a regulator o

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

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

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

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

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

94 osphorylation motifs targeted by the kinases protein kinase C, cyclin-dependent kinase, and mitogen-a

95 Purkinje cell-specific inhibition of protein kinase C decreased and phase-shifted the transla

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

97 ence (false discovery rate < .10), including protein kinase C delta (PKCdelta), a CeL microcircuit ce

98 -CUB-domain containing protein 1 (CDCP1) and protein kinase C delta (PKCdelta)-in 56 formalin-fixed,

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

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

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

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

103 ctivation of focal adhesion kinase 1 (FAK1), protein kinase C-delta (PRKCD), and Ephrin (EPH) family

104 Moreover, inhibition of protein kinase C-delta prevented DUSP4 expression declin

105 The differential impact of a protein kinase C-delta TAT peptide inhibitor (PKCdelta-i

106 have previously demonstrated that PKCdelta (protein kinase C-delta) regulates multiple components of

107 tion of neurons, marked by the expression of protein kinase C-delta, in the oval region of the bed nu

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

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

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

111 stabilization of RASSF1A through NOX-1- and protein kinase C- dependent phosphorylation.

112 Thus protein kinase C-dependent cleavage is mediated through

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

114 We demonstrate that OXT, in a protein kinase C-dependent manner, activates eEF2 both i

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

116 s via separate information pathways and that protein kinase C-dependent mechanisms regulate translati

117 s study identifies a G protein-dependent and protein kinase C-dependent signaling pathway that dynami

118 Protein kinase C epsilon (PKCepsilon) AS-ODN also preven

119 oll-like receptor 4 (TLR4) and signaling via protein kinase C epsilon (PKCepsilon) in common, whereas

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

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

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

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

124 quency-dependent activation of PKC(epsilon) (protein kinase C epsilon).

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

126 We reported that protein kinase C-eta (PKCeta) forms a novel (to our know

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

128 (phospholipase C/inositol 1,4,5-triphosphate/protein kinase C/extracellular signal-regulated kinase)

129 ynia induced by inflammatory injuries, while protein kinase C gamma (PKCgamma) neurons at the lamina

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

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

132 Dopamine activated protein kinase C in an ALK-dependent manner and a PKC in

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

134 y dopamine in an ALK-dependent manner, and a protein kinase C inhibitor completely blocked dopamine-i

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

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

137 verexpression of the protein kinase atypical protein kinase C iota (aPKCi), an oncogene, triggers bas

138 During the afterdischarge, protein kinase C is also activated, which in turn elevat

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

140 th the viral capsid (Cap) protein to enhance protein kinase C isoform delta (PKC-delta) activity; thi

141 viral capsid (Cap) protein; simultaneously, protein kinase C isoform delta (PKC-delta) was phosphory

142 protein kinase Mzeta (PKMzeta), an atypical protein kinase C isoform that is thought to sustain memo

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

144 The calcium-dependent protein kinase C isoform, PKCalpha, has been suggested t

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

146 ncreased phosphorylation of stress activated protein kinase/c-Jun N-terminal kinase and that other de

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

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

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

150 bition of G (betagamma,) phospholipase C, or protein kinase C mimicked agonist removal, whereas activ

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

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

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

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

155 e (ZIP), which was originally developed as a protein kinase C/Mzeta (PKCzeta/PKMzeta) inhibitor, is k

156 Neither agent's activity depends on protein kinase C; nor do they inhibit class I/II histone

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 an melanocytes, leading to activation of the protein kinase C pathway.

163 D300f receptor cytoplasmic tail inhibits the protein kinase C phosphorylation of a threonine and is a

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

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

166 gulated by endocytic trafficking, and direct protein kinase C (PKC) activation acutely diminishes DAT

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

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

169 ial link between stress and hERG function is protein kinase C (PKC) activation; however, seemingly co

170 eported that human TRESK is activated by the protein kinase C (PKC) activator PMA (phorbol 12-myrista

171 in the PVN, whether endogenous AT1 receptor-protein kinase C (PKC) activity mediates the augmented N

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

173 Activation of TRPC1-based SOCs requires protein kinase C (PKC) activity, which is proposed to ph

174 Stimulation of TRPC1-based SOCs requires protein kinase C (PKC) activity, with store-operated PKC

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

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

177 on of MOR activates a Galpha(i/o)-Gbetagamma-protein kinase C (PKC) alpha phosphorylation pathway tha

178 DOPr endocytosis and endosomal signaling by protein kinase C (PKC) and extracellular signal-regulate

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

180 CR) signaling is regulated by members of the protein kinase C (PKC) and GPCR kinase (GRK) families, a

181 te our extensive knowledge on the biology of protein kinase C (PKC) and its involvement in disease, l

182 eat protein phosphatase 1 (Phlpp1) regulates protein kinase C (PKC) and other proteins in the control

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

184 Furthermore, we identified that protein kinase C (PKC) beta II is a major mediator of Ca

185 9 regulation include stimulation by Galphas, protein kinase C (PKC) betaII, or calcium-calmodulin kin

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

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

188 We demonstrated that Protein Kinase C (PKC) epsilon is selectively expressed

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

190 functions reveal unexpected features of the protein kinase C (PKC) family of serine/threonine protei

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

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

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

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

195 Spinal protein kinase C (PKC) inhibition with Go6983 or PKCdelt

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

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

198 6-methyl group, exhibit remarkably different protein kinase C (PKC) isoform affinities.

199 ere, we demonstrate that classical and novel protein kinase C (PKC) isoforms distinctly regulate card

200 Although previous work suggests that protein kinase C (PKC) isoforms play a role in cardiac f

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

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

203 Protein kinase C (PKC) isozymes function as tumor suppre

204 Diacylglycerol (DAG)/phorbol ester-regulated protein kinase C (PKC) isozymes have been widely linked

205 We show that protein kinase C (PKC) lambda/iota loss in hepatocytes p

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

207 Protein kinase C (PKC) modulators-including prostratin,

208 2)/inositol 1,4,5-trisphosphate (IP3)/Ca(2+)/protein kinase C (PKC) pathway significantly impaired th

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

210 signaling through the phospholipase C (PLC)/protein kinase C (PKC) pathway.

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

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

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

214 arance of CP-AMPARs and that AKAP79-anchored protein kinase C (PKC) primarily drives the appearance o

215 Protein kinase C (PKC) promotes synaptic maturation and

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 kinase (ROCK) inhibition; however, augmented protein kinase C (PKC) signaling was found to contribute

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

220 Cx43 with serine to alanine mutations at the protein kinase C (PKC) site Cx43(S368A), the casein kina

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

222 and hypothalamus, as being important in the protein kinase C (PKC) supported activity of the GG geno

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

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

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

226 to maintain affinity for bryostatin's target protein kinase C (PKC) while enabling exploration of the

227 act in a linear signaling cascade that, via protein kinase C (PKC), activates in parallel the MAP-ki

228 protein RAC family small GTPase 1 (RAC1) and protein kinase C (PKC), and a later arrestin-scaffolded

229 kinase II (CaMKII), protein kinase A (PKA), protein kinase C (PKC), and AMPA receptor genes that pla

230 rotein kinase M (PKM), the truncated form of protein kinase C (PKC), can maintain long-term changes i

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

232 is regulated through its phosphorylation by protein kinase C (PKC), which plays multiple roles, incl

233 that mutant alpha-syn fails to complex with protein kinase C (PKC), which, in turn, results in impai

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

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

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

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

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

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

240 The angiotensin AT1 receptor expression and protein kinase C (PKC)-mediated NMDA receptor phosphoryl

241 sis and is inhibited in vitro and in vivo by protein kinase C (PKC)-mediated phosphorylation at CaS(T

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

243 -catalyzed PI(4,5)P(2) hydrolysis, activates protein kinase C (PKC).

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

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

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

247 prompts the stimulation of NADPH oxidase and protein kinase C (PKC).

248 ignaling via cAMP/protein kinase A (PKA) and protein kinase C (PKC).

249 of cAMP-dependent protein kinase A (PKA) and protein kinase C (PKC).

250 nhancer factor 2C (MEF2c) expression via the protein kinase C (PKC)/histone deacetylase 5-mediated pa

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

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

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

254 statin-1, a relatively specific activator of protein kinase C (PKC)epsilon, (also of PKCalpha) on imp

255 Here we report that protein kinase C (PKC)lambda/iota is downregulated in de

256 ed proteins from public databases identified protein kinase C (PKC)zeta as a TRIM32-associated protei

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

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

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

260 hat distinct isoforms of persistently active protein kinase Cs (PKMs) maintain distinct forms of long

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

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

263 enzymatic activity of PLCdelta1, leading to protein kinase C/protein kinase D/extracellular signal-r

264 The Ras-binding domain of the protein kinase c-Raf (c-Raf-RBD) is the tightest known b

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

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

267 Inhibition of protein kinase C reduced neuronal aggregation and fascic

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

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

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

271 protein kinase A (Ser-667 and Ser-774), and protein kinase C (Ser-677).

272 malization of KCC2 function was dependent on protein kinase C signaling and phosphorylation of KCC2 a

273 ligin-3 in response to synaptic activity and protein kinase C signaling resulting in reduced synapse

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

275 ring T331, a previously identified potential protein kinase C site.

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

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

278 l-9 on T cells following PMA stimulation via protein kinase C suggests persistent TCR stimulation as

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

280 Protein kinase C-theta (PKCtheta) is an important compon

281 TBKBP1 recruits TBK1 to protein kinase C-theta (PKCtheta) through a scaffold pro

282 nregulated expression of the GIST biomarker, protein kinase C-theta (PRKCQ).

283 ical model demonstrated that neuroendocrine, protein kinase C-theta, and triggering receptor expresse

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

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

286 PKC (protein kinase C) was induced by retinoic acid, and PKC

287 The functions of phospholipase Cbeta and protein kinase C were required for OXTR-induced augmenta

288 oprostanes, NOX2 (NADPH oxidase 2), and PKC (protein kinase C) were measured in obese mice and compar

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

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

291 downstream signaling involves activation of protein kinase C, which phosphorylates and activates wit

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

296 actor-1 receptor, triggers the activation of protein kinase C zeta (PKCzeta).

297 zyme A reductase, phospholipase A2 receptor, protein kinase C zeta type, tubulin beta-4B class IVb, v

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

299 n-induced phosphoinositide 3-kinase (PI3-K), protein kinase C-zeta (PKC-zeta), extracellular signal-r

300 that hypusine biosynthesis was downstream of protein kinase C-zeta and was required for c-Myc-induced