ライフサイエンスコーパス: PKC-alpha

1 equent activation of protein kinase C alpha (PKC alpha).

2 he hydrophobic motif, but not turn motif, of PKC alpha.

3 gulation of actin organization by mTORC2 via PKC alpha.

4 termine the interaction sites between 4V and PKC alpha.

5 und to a peptide containing the C2 domain of PKC alpha.

6 regulate mTORC2-mediated effects on SGK1 or PKC alpha.

7 erfering RNA (siRNA) specific for ADAM-10 or PKC-alpha.

8 to occur through a pathway involving AKT and PKC-alpha.

9 on in control cells hyperphosphorylated with PKC-alpha.

10 part, to increased activity and signaling of PKC-alpha.

11 , and cytoplasm-to-membrane translocation of PKC-alpha.

12 for activation of the cyclin D1 promoter by PKC-alpha.

13 C overexpressing a dominant negative form of PKC-alpha.

14 as by knockdown of PKC-delta but not that of PKC-alpha.

15 of phosphatidylinositol 3-kinase (PI3K) and PKC-alpha.

16 T inhibits O(2)(-) release via inhibition of PKC-alpha.

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

18 is through activation of ET-A receptors and PKC-alpha.

19 We concluded that active PKC-alpha 1) prevents injury-induced decreases in levels

20 In contrast, knockdown of PKC-alpha (a classical PKC isoform) or PKC-epsilon (a no

21 PKC alpha, a G(q) effector, transduced Nix transcription

22 ists that differ in their ability to sustain PKC alpha activation and growth arrest in IEC-18 cells,

23 analysis of the signaling events linking PKC/PKC alpha activation to changes in the cell cycle regula

24 uired for critical downstream effects of PKC/PKC alpha activation, including cyclin D1 down-regulatio

25 The results show that the blocking of PKC-alpha activation by classical inhibitors, pseudosubs

26 inhibition was the result of the absence of PKC-alpha activation in HBMECs treated with the antibodi

27 PKC-alpha activation may play an important role in the p

28 Protein kinase Calpha (PKC-alpha) activation was found to be the downstream tar

29 PKC/PKC alpha activity promoted GTP loading of Ras, activati

30 the magnitude/duration of input signal (i.e. PKC alpha activity) and of activation of the ERK cascade

31 Syndecan 4V peptide directly potentiates PKC alpha activity, leading to "superactivation" of the

32 Mechanistically, modulation of PKC-alpha activity affects dephosphorylation of the sarc

33 caveolar endocytosis required src kinase and PKC-alpha activity as shown by i) use of pharmacological

34 We find that PKC-alpha activity is regulated by Rack1-keratin interac

35 ion of the keratin pair K5/14, inhibition of PKC-alpha activity, or blocking of endocytosis reconstit

36 Protein kinase C alpha (PKC alpha) activity was shown to be elevated in rictor-o

37 gether they regulate protein kinase C alpha (PKC alpha) activity.

38 t that N-cadherin cleavage is regulated by a PKC-alpha-ADAM-10 cascade in GBM cells and may be involv

39 mGluR activation but requires activation of PKC alpha after G protein coupling to phospholipase C.

40 Short hairpin RNA-mediated knockdown of PKC alpha also significantly attenuated stretch-induced

41 in the C terminus of the catalytic domain of PKC alpha (amino acid sequence 513-672).

42 GnRH stimulation caused translocation of PKC alpha and -epsilon to the cell membrane and enhanced

43 hese findings identify a direct link between PKC alpha and beta 1 integrin that is critical for direc

44 lated PLD activity and translocation of ARF, PKC alpha and beta, and RhoA when recombined with cell m

45 n kinase C (PKC) results in translocation of PKC alpha and betaII to the pericentrion, a dynamic subs

46 nd to protein kinase C (PKC) and translocate PKC alpha and delta isoforms to plasma and internal memb

47 ly prolonging the translocated state of both PKC alpha and delta.

48 nce between the lowering effects of Abeta on PKC alpha and epsilon versus the lowering effects of PKC

49 This reduction, particularly of PKC alpha and epsilon, occurs in association with elevat

50 -1, restores normal or supranormal levels of PKC alpha and epsilon, reduces the level of soluble Abet

51 a support a mechanism where syndecan-4 binds PKC alpha and localizes it to focal adhesions, whose ass

52 ane and enhanced the association of Src with PKC alpha and PKC epsilon, Pyk2, and the EGF receptor.

53 To distinguish between PKC alpha and PKC ss, we used tubules expressing dominan

54 Together, these data indicate that PKC alpha and RAF1 are important in the translational re

55 that Ras is necessary for the activation of PKC alpha and Smad signaling.

56 involves both the activation of the classic PKC alpha and the novel PKC delta isozymes.

57 Taken together, the data point to PKC alpha and the Ras/Raf/MEK/ERK cascade as key regulat

58 mRNA is also augmented after the addition of PKC alpha and theta antisense oligonucleotides, indicati

59 arate inhibition, of phorbol ester-dependent PKC alpha and theta isoforms is crucial for the inductio

60 a cell cycle checkpoint pathway regulated by PKC alpha and theta isoforms.

61 regulated in response to the suppression of PKC alpha and theta.

62 Thus, inhibition of PKC-alpha and -beta can ameliorate the proinflammatory s

63 PKC-alpha and -beta isozymes are among the growth-associ

64 as well as small interfering RNA (siRNA) to PKC-alpha and -beta resulted in significantly decreased

65 ice, diabetes increased the translocation of PKC-alpha and -beta1 to the membrane, whereas only PKC-a

66 KC-delta and -epsilon and the Ca2+-dependent PKC-alpha and -betaI were translocated to the nucleus up

67 inase C (PKC) activity, and translocation of PKC-alpha and -betaII and p47phox were increased in THP-

68 ecretion; upstream regulators of PKD include PKC-alpha and -delta and Rho/ROK.

69 ated PKD activity, whereas overexpression of PKC-alpha and -delta enhanced PKD activity.

70 inase-dead mutants supported a role for only PKC-alpha and -delta in CEP4 phosphorylation.

71 Our results suggest that activation of PKC-alpha and -delta mediates a novel positive feedback

72 PKC-alpha and -delta siRNA attenuated PKD activity, wher

73 Phosphoprotein profiles generated by PKC-alpha and -delta were similar and differed markedly

74 blot analysis also revealed up-regulation of PKC-alpha and -delta, decreased PKCepsilon, but no chang

75 PDBu) binding to PKD similarly as it does to PKC-alpha and -delta, implying that the PH domain in PKD

76 l-length PKD and compared them with those of PKC-alpha and -delta.

77 ing to PKD was intermediate between those of PKC-alpha and -delta.

78 Thus, our study shows that PKC-alpha and beta are necessary for sustaining the home

79 , we show that the concurrent suppression of PKC-alpha and beta induces cells ectopically expressing

80 sion of PKC-delta, without co-suppression of PKC-alpha and beta, is not apoptotic to the cells, sugge

81 Inhibition of cisplatin-induced PKC-alpha and ERK1/2 activation using Go6976 and PD98059

82 These changes were preceded by PKC-alpha and ERK1/2 activation.

83 ha translocation to mitochondria, suggesting PKC-alpha and JNK interplay in a feed-forward mechanism

84 odonium chloride [DPI]), and an inhibitor to PKC-alpha and other isoforms (2,2',3,3',4,4'-hexahydroxy

85 PKC-alpha and other PKC(s) regulate death (JNK) and surv

86 gy of combining small molecule inhibitors of PKC-alpha and PI3K could provide a new treatment paradig

87 with the increased expression/activation of PKC-alpha and PKC-beta and enhanced oxidative and nitros

88 These results support our hypothesis that PKC-alpha and PKC-beta contribute to the pathogenesis of

89 Treatment with CGP41252, which inhibits PKC-alpha and PKC-beta, is able to prevent the developme

90 reased IP(3) and Ca(2+) levels and activated PKC-alpha and PKC-beta-II.

91 uclear compartment where it colocalized with PKC-alpha and PKC-delta together with the endocytic recy

92 h glucose induces TLR2 and -4 expression via PKC-alpha and PKC-delta, respectively, by stimulating NA

93 The constitutively active mutants of PKC-alpha and PKC-epsilon also activated c-fos, c-jun, a

94 UDCA stimulated the translocation of PKC-alpha and PKC-epsilon to the plasma membrane.

95 ed that the constitutively active mutants of PKC-alpha and PKC-epsilon were the most potent activator

96 for activation of the cyclin D1 promoter by PKC-alpha and PKC-epsilon.

97 We found that Pin1 interacted with both PKC-alpha and protein phosphatase 2A, which together con

98 Conversely, in glio-pial tissue, PKC-alpha and RACK1 were upregulated, whereas PKC-gamma,

99 inducers activate a signaling pathway using PKC-alpha and the PKC-regulated protein phosphatase 1 in

100 dentify conventional protein kinase C-alpha (PKC-alpha) and PKC-beta as important negative regulators

101 fic ET receptors and protein kinase C-alpha (PKC-alpha), and analyzed ET-1-related gene/protein expre

102 AG)-dependent isoforms of PKC (PKC-betaI and PKC-alpha), and MARCKS-GFP, but only in Ca2+-containing

103 al 1.8 +/- 0.1 for PKC beta, 1.3 +/- 0.1 for PKC alpha, and 1.4 +/- 0.1 for PKC gamma).

104 microM for PKC gamma, 1.4 +/- 0.1 microM for PKC alpha, and 5.0 +/- 0.2 microM for PKC beta), and coo

105 ; HG-induced O(2)(-) release is triggered by PKC-alpha, and AT inhibits O(2)(-) release via inhibitio

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

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

108 Go6976, bisindolylmaleimide, and Rottlerin), PKC-alpha, and PKC-delta small interfering (si)RNAs but

109 H induced the activation of ERK1, ERK2, JNK, PKC-alpha, and PKC-gamma, inhibitors of these kinases an

110 may be due to the selective upregulation of PKC-alpha, and ultimately lead to the impairment of neur

111 l mediator of tumour promotion, acting via a PKC alpha- and AP-1-dependent pathway.

112 dependent of p53 and most likely mediated by PKC-alpha-, and -epsilon-dependent signaling pathways.

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

114 In tubules expressing dominant-negative PKC alpha, Ang II failed to stimulate O2.

115 The interaction of syndecan-4 with PKC alpha appears unique since PKC delta and epsilon did

116 a, and epsilon revealed a necessary role for PKC alpha as a mediator of agonist-induced cardiomyocyte

117 Here we identify PKC-alpha as a fundamental regulator of cardiac contract

118 gest that by phosphorylating the MARCKS PSD, PKC alpha attenuates DGK zeta activity.

119 ary gland and the pro-(BAX:Bcl(2)) and anti-[PKC alpha*(Bcl(2)/BAX)] apoptotic ratios were evaluated.

120 y significant decreases in protein levels of PKC alpha, beta I, beta II, and gamma isozymes were also

121 f wild-type and dominant negative mutants of PKC alpha, beta II, delta, and epsilon (only wild-type z

122 In contrast, expression of dominant negative PKC alpha, beta II, delta, and epsilon revealed a necess

123 Overexpression of wild-type PKC alpha, beta II, delta, and epsilon revealed distinct

124 RNA levels of various PKC isozymes, such as PKC alpha, beta, and gamma, were determined in the prefr

125 proliferation, indicating the involvement of PKC alpha, beta, or gamma.

126 Overexpression of PKC-alpha, -beta, and -delta (but not PKC-) induced an S

127 ecific inhibitor treatment demonstrated that PKC-alpha/beta are the primary kinases responsible for R

128 PKC-alpha/beta double-knockdown cells exhibited markedly

129 ptozotocin (STZ)-induced diabetic homozygous PKC-alpha/beta double-knockout mice (PKC-alpha/beta(-/-)

130 to the cells, suggesting that PKC-delta and PKC-alpha/beta function oppositely to facilitate cells h

131 Coimmunoprecipitation showed that PKC-alpha/beta interact with RIG-I under normal conditio

132 lar matrix production were diminished in the PKC-alpha/beta(-/-) mice compared with wild-type control

133 it was not completely abolished in diabetic PKC-alpha/beta(-/-) mice.

134 ozygous PKC-alpha/beta double-knockout mice (PKC-alpha/beta(-/-)).

135 Thus, these findings demonstrate that PKC-alpha/beta-induced RIG-I phosphorylation is a critic

136 omeostasis caused by different PKC isoforms (PKC-alpha, -beta1/2, and PKC-delta) are linked to the de

137 MP-9, not MMP-2, expression and activity; 2) PKC-alpha/beta1 act upstream of JNKs, not ERK1/2; 3) PKC

138 Inhibition of ERK1/2, JNKs, and PKC-alpha/beta1 had no effect on NF-kappaB activation, w

139 Selective inhibition of PKC-alpha/beta1 using Go6976 inhibited JNKs activation a

140 Furthermore, the PKC-alpha/beta2 inhibitor decreased p38MAPK and the resu

141 e BAV group, classic and novel PKC isoforms (PKC-alpha, betaI, gamma, epsilon, theta) were increased,

142 Six PKC isozymes-PKC-alpha, -betaI, -betaII, -delta, - epsilon, and - mic

143 min, and IgG were decreased, but pleckstrin, PKC-alpha, -betaI, -betaII, -eta, -epsilon, -delta, and

144 Membrane-associated PKC alpha, betaII, delta, and zeta were increased in dec

145 accompanied by changes in the expression of PKC-alpha, betaII, gamma, delta, and epsilon Second, tho

146 he membrane-associated state; membrane-bound PKC alpha binds two Ca(2+) ions, and a third binds weakl

147 expression of a dominant negative mutant of PKC-alpha blunts Ang II-induced leucine incorporation in

148 higher than that needed to inhibit purified PKC alpha but in a range comparable with that required f

149 ycystin-1 stimulated protein kinase C-alpha (PKC-alpha), but not the extracellular signal-regulated k

150 Indeed, overexpression of wild-type PKC alpha, but not betaI I, delta, epsilon, or zeta indu

151 PMA and PKC alpha, but not PKC epsilon or dominant negative PKC

152 Overexpression of PKC alpha, but not PKC epsilon, PKC delta or PKC zeta is

153 Furthermore, activation of PKC alpha by phorbol 12-myristate 13-acetate inhibited t

154 map out the membrane docking surface of the PKC alpha C2 domain.

155 lasmon resonance analysis indicates that the PKC-alpha C2 domain strongly prefers the cytoplasmic pla

156 r the docking of the protein kinase C alpha (PKC alpha) C2 domain to membranes.

157 One pathway involves PKC-alpha catalyzed phosphorylation of CREB and the othe

158 Mitochondrial PKC-alpha co-immunoprecipitated with alpha-, beta-, and

159 Also, PKC-alpha colocalizes with virus particles and is requir

160 rin dissociates the EGFR/GM3/caveolin-1/CD82/PKC-alpha complex and prevents the inhibitory effect of

161 caffolding a DP-PKP2-protein kinase C alpha (PKC alpha) complex, which is disrupted by PKP2 knockdown

162 cted with 4V by yeast two-hybrid assays, but PKC alpha constructs that lack the pseudosubstrate regio

163 Thus, PKC-alpha could provide a new pharmacological target for

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

165 Deletion of PKC-alpha decreased levels of alpha-, beta-, and gamma-s

166 tion and protein levels, whereas deletion of PKC-alpha decreased protein levels of alpha-, beta-, and

167 d zeta and troponin T (cTnT) associated with PKC alpha, delta, and epsilon.

168 PK) analysis showed that IL-1alpha increased PKC alpha, delta, and zeta activity 4.5-, 3.1-, and 2.6-

169 beta 2 isoform but not by the expression of PKC alpha, delta, and zeta isoforms.

170 involved protein kinase C (PKC), especially PKC-alpha, -delta, and -iota, and addition of PKC inhibi

171 tested, only CEP4 was phosphorylated by pure PKC-alpha, -delta, and -zeta isoforms in vitro, and by e

172 to silencing of each of the three isoforms (PKC-alpha, -delta, and -zeta), whereas testing of kinase

173 that in TALs, Ang II stimulates O. via ATand PKC alpha-dependent NADPH oxidase activation.In rat TALs

174 production via activation of ATreceptors and PKC alpha-dependent NADPH oxidase.

175 upstream from the initiation site abolished PKC-alpha-dependent activation of cyclin D1 expression.

176 PKC-alpha directly phosphorylates protein phosphatase in

177 Herein, the role of PKC-alpha during the early stages of RSV infection in no

178 was blocked by selective inhibition of CN or PKC alpha/epsilon or elimination of fibroblasts.

179 Immunoblotting revealed that PKC-alpha expression and activation was unaltered in ear

180 Notably, in the gray matter, PKC-alpha expression significantly decreased, while pT51

181 in cross-linking protein and a substrate for PKC-alpha, from the membrane to cytosol.

182 Thus, PKC-alpha functions as a nodal integrator of cardiac con

183 Overexpression of PKC epsilon, but not PKC alpha, -gamma, -delta, or -zeta was found to dramati

184 rm may be critical in OPG regulation because PKC-alpha gene expression is enhanced by PMA and reduced

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

186 nels plays an essential role in AIAD via the PKC-alpha/IkappaB-alpha- and calcineurin/IkappaB-beta-de

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

188 ic agent HK654, which selectively stimulates PKC alpha in LNCaP cells, also induced the dephosphoryla

189 ent evidence to support a requisite role for PKC alpha in mediating these effects.

190 Our results implicate PKC alpha in the potentiation of Ca v 2.3 currents by MC

191 Cardiac-specific activation of PKC alpha in transgenic mice led to impaired beta-agonis

192 rexpression of a dominant negative mutant of PKC-alpha in HBMEC abolished the E. coli invasion withou

193 verexpression of a dominant negative form of PKC-alpha in HBMECs blocked the E. coli-induced increase

194 ment of beta 4, and argue for a key role for PKC-alpha in regulating these structures.

195 I3A bound to PKC-alpha in the presence of phosphatidylserine with hig

196 erexpression of dominant-negative mutants of PKC-alpha in these cells leads to significantly decrease

197 tifying substrates of protein kinase Calpha (PKC-alpha) in nontransformed human breast MCF-10A cells.

198 osphorylation by the protein kinase C-alpha (PKC-alpha) in the presence of adenosine 5'-[gamma-thio]

199 iated role of PKC isozymes, and specifically PKC alpha, in senescence, our data introduce the paradig

200 in vivo phosphorylated on serine residues by PKC-alpha, in human, rat, and avian CNS cells and cell l

201 ha, but not PKC epsilon or dominant negative PKC alpha, increased Nix transcription.

202 ce (4V(YF): LGKKPIFKK) did not interact with PKC alpha, indicating that tyrosine 192 in the syndecan-

203 The in vitro kinase activity of PKC-alpha induced by I3A was lower than that induced by

204 rmore, our studies showed that activation of PKC-alpha induces the translocation of myristoylated ala

205 anslocation was significantly reduced by the PKC-alpha inhibitor Go6976 [12-(2-cyanoethyl)-6,7,12,13-

206 Pretreatment with the PKC-alpha inhibitor safingol reversed ET-1-induced respo

207 bsence or presence of BAPTA/AM and Go6976 (a PKC-alpha inhibitor).

208 ist, an endothelin-B (ET-B) antagonist, or a PKC-alpha inhibitor.

209 This study tested whether mitochondrial PKC-alpha interacts with and phosphorylates F0F1-ATPase.

210 e transfer of dominant-negative or wild-type PKC-alpha into cardiac myocytes enhances or reduces cont

211 Our results indicate that PKC-alpha is a necessary regulator of EEA1-dependent Akt

212 mia-induced renal matrix production, whereby PKC-alpha is involved in the development of albuminuria.

213 We also found that PKC-alpha is required for organizing Ang II-induced, EEA

214 Protein kinase C-alpha (PKC-alpha) is the kinase responsible for phosphorylating

215 The PKC-alpha isoform may be critical in OPG regulation beca

216 is revealed a crucial role for the classical PKC alpha isozyme as mediator of the G2/M arrest and sen

217 PKC signal transduction pathway and that the PKC alpha isozyme is specifically involved in the pathwa

218 aches, we determined a specific role for the PKC-alpha isozyme.

219 ns caused comparably increased levels of the PKC alpha-isozyme substrate calexcitin in identified typ

220 onse in the presence of a known inhibitor of PKC-alpha kinase.

221 d phosphorylation of myelin basic protein by PKC-alpha kinase.

222 more tightly with IF is mimicked by PKP2 and PKC alpha knockdown and PKC pharmacological inhibition,

223 Furthermore, PKC-alpha knockdown decreased TLR2 by 61% (P < 0.05), wh

224 PKC-alpha knockdown impaired the juxtanuclear localizati

225 t not expression of the YF mutant, increased PKC alpha localization to focal adhesions.

226 We showed previously that active PKC-alpha maintains F0F1-ATPase activity, whereas inacti

227 There is evidence that PKC-alpha may be of particular importance.

228 inocytes lacking all keratins show elevated, PKC-alpha-mediated desmoplakin phosphorylation and subse

229 PKC-alpha-mediated NG2 phosphorylation at Thr(2256) is t

230 phosphorylation of Smad1/5, suggesting that PKC alpha mediates the activation of Smad signaling and

231 mber A, Rho-associated protein kinase 2, and PKC-alpha/-mu pathways.

232 tains F0F1-ATPase activity, whereas inactive PKC-alpha mutant (dnPKC-alpha) blocks recovery of F0F1-A

233 omplex and prevents the inhibitory effect of PKC-alpha on EGFR phosphorylation, suggesting that caveo

234 (PP-1), which may account for the effects of PKC-alpha on PLB phosphorylation.

235 we used tubules expressing dominant-negative PKC alpha or -ss.

236 of beta-adducin through activation of either PKC alpha or beta.

237 PKC beta(I) and PKC beta(II), but not PKC alpha or PKC gamma, were co-immunoprecipitated from

238 sera to PKC beta(I) and PKC beta(II) but not PKC alpha or PKCg amma were able to co-immunoprecipitate

239 negative (dn) PKC-epsilon or -zeta, but not PKC-alpha or -delta, blocked S1P-induced migration.

240 t affected by wild-type or dominant negative PKC-alpha or -delta.

241 lex containing either cTnT phosphorylated by PKC-alpha or a mutant cTnT.

242 These results demonstrate that MMP-9 and PKC-alpha or PKC-delta may provide putative therapeutic

243 express the constitutively active mutants of PKC-alpha or PKC-epsilon displayed increased expression

244 ults provide evidence that the activation of PKC-alpha or PKC-epsilon in mouse fibroblasts can play a

245 Its exclusive phosphorylation by PKC-alpha or replacement by Glu (mimicking phosphorylati

246 and RhoA translocation, but not ARF1, ARF6, PKC alpha, or PKC beta translocation.

247 sitol 4,5-bisphosphate (PIP(2)) and activate PKC alpha, participates in mediating the effects of fibr

248 d activates BMP/Smad signaling via a Ras and PKC alpha pathway in breast epithelial cells.

249 ptosis-inducing factor, phospho-Bad, phospho-PKC-alpha, phospho-PKC-beta1, and cleaved poly(adenosine

250 ucing factor, Bcl-2 family proteins, phospho-PKC-alpha, phospho-PKC-beta1, and poly(adenosine diphosp

251 e tested full-length DGK zeta and found that PKC alpha phosphorylated DGK zeta on serines within the

252 w that activation of protein kinase C-alpha (PKC-alpha) phosphorylated and down-regulated LRP express

253 Taken together, these results indicate that PKC alpha phosphorylates DGK zeta in cells, and this pho

254 PKC-alpha phosphorylation increased further in cells tre

255 ected in PLC-z/HBMEC upon infection, whereas PKC-alpha phosphorylation is completely abolished, indic

256 EEA1 expression enables PKC-alpha phosphorylation, which in turn regulates Akt u

257 results strongly suggest the involvement of PKC-alpha/PI3K signaling pathways in the regulation of L

258 ors for a variety of representative Ser/Thr (PKC alpha, PKC betaIota, PKC delta, Pim2, Akt1, MK2, and

259 Additional studies revealed that PKC-alpha, PKC-delta, and p47Phox knockdown significantl

260 Myocyte PKC-alpha protein level was not altered by H-R, but its

261 by EC(50)) before and after incubation with PKC-alpha, protein phosphatase type 1 (PP1), or PP2a.

262 Here, we examined PKC-alpha quantity, activity, and signaling to myofilame

263 llular matrix production, but independent of PKC-alpha, Raf-1, and p44/42 activities.

264 down or pharmacological inhibition of PAR-2, PKC-alpha, Raf-1, or p44/42.

265 Tryptase stimulated HLF growth in a PAR-2/PKC-alpha/Raf-1/p44/42-dependent manner and potentiated

266 ring carbachol perfusion of glands, in situ, PKC-alpha redistributed across glandular membrane compar

267 cules, the ability of CD82 to associate with PKC-alpha requires the presence of caveolin-1, whereas t

268 that the activating conformational change in PKC alpha results from the dissociation of intra-molecul

269 5H-indolo[2,3-a]pyrrolo[3 ,4-c]carbazole] or PKC-alpha short hairpin RNA.

270 by Go 6976, an inhibitor of cPKC isozymes or PKC alpha siRNA.

271 ttenuated by PKC inhibitors, MMP-9 antibody, PKC-alpha siRNA, or PKC-delta siRNA.

272 phosphoinositide 3-kinase (PI3K) inhibitor, PKC-alpha small interfering RNA (siRNA), and short hairp

273 scription factor Sp-1, and basal and PMA- or PKC alpha-stimulated Nix promoter activity was suppresse

274 DGK zeta also coimmunoprecipitated with PKC alpha, suggesting that they reside in a regulated si

275 C activity; overexpressing dominant negative PKC-alpha suppressed taxane-mediated stimulation of both

276 The molecular interactions upstream to PKC-alpha that influence its suppression of EGFR, howeve

277 ng Ras activity blocked the translocation of PKC alpha to the plasma membrane and the phosphorylation

278 ctor 1, RhoA, protein kinase C (PKC)-beta or PKC-alpha to the plasma membrane in G-CSF or cytochalasi

279 e A(2) (cPLA(2)) and protein kinase C-alpha (PKC-alpha) to vesicles that model cell membranes they ar

280 nduced inhibition of EGFR signaling requires PKC-alpha translocation and serine/threonine phosphoryla

281 APAP treatment resulted in PKC-alpha translocation to mitochondria and phosphorylat

282 d 2 silencing in vivo decreased APAP-induced PKC-alpha translocation to mitochondria, suggesting PKC-

283 PKC-alpha treatment induced a 30% decline in F(max) and

284 side GM3 enable the association of EGFR with PKC-alpha, ultimately leading to inhibition of EGFR sign

285 Knockdown of PKC-alpha using antisense (ASO) in mice also protected a

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

287 Moreover, when PKC-alpha was downregulated, the Ras-GAP activity of CSR

288 pha and -beta1 to the membrane, whereas only PKC-alpha was elevated in PKC-beta(-/-) mice.

289 antly, inhibition of classical PKC isoforms (PKC-alpha) was able to effectively suppress PA-induced a

290 A-induced signalling in basal keratinocytes, PKC alpha, was also differentially regulated in wild-typ

291 Full-length PKC alpha weakly interacted with 4V by yeast two-hybrid

292 e oocytes to MCh led to the translocation of PKC alpha whereas PMA activated PKC betaII and epsilon i

293 eletal and signaling proteins tested, except PKC-alpha, which has enhanced expression in the patient'

294 a member of the conventional family of PKC, PKC-alpha, which requires calcium for activation.

295 6 and Merle 47 exhibited binding affinity to PKC alpha with Ki values of 7000 +/- 990 and 4940 +/- 47

296 -1, whereas the interaction of caveolin-1 or PKC-alpha with EGFR requires the presence of CD82 and ga

297 phosphorylation and increases association of PKC-alpha with PKC scaffold receptor for activated C-kin

298 The association of PKC-alpha with these subunits decreased in injured RPTC

299 CD82, and ganglioside interact with EGFR and PKC-alpha within intact cholesterol-enriched membrane mi

300 Wild-type PKC-alpha (wtPKC-alpha) and dnPKC-alpha were overexpress