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1 erentiated cells (PKB alpha, Stat3, Src, and PKC epsilon).
2 CK1 inhibitory peptide, but it does not bind PKC epsilon.
3 ble with that required for the inhibition of PKC epsilon.
4 delta and only slightly activated by that of PKC epsilon.
5 diacylglycerol to stimulate actin binding to PKC epsilon.
6 in vitro test here by a peptide inhibitor of PKC epsilon.
7 n of the cyclin D1 promoter by PKC-alpha and PKC-epsilon.
8 ovel protein kinase C isozymes PKC-delta and PKC-epsilon.
9 itor, also had no effect, likely implicating PKC-epsilon.
10 alcium-independent novel PKCs, in particular PKC-epsilon.
11 by dominant negative mutants of PKC-alpha or PKC-epsilon.
12 ssing PKC-delta and those that overexpressed PKC-epsilon.
13 f ESO is mediated by the calcium-independent PKC-epsilon.
14 ated form of PKC-alpha and an 86-kDa form of PKC-epsilon.
15 hondrial membrane by a pathway that includes PKC-epsilon.
16 s was significantly less than that of intact PKC-epsilon.
18 pmol/mg/min, four experiments, p < 0.05) and PKC epsilon (42.8 +/- 3.1 versus 19.1 +/- 3.9 pmol/mg/mi
19 wn of PKC-alpha (a classical PKC isoform) or PKC-epsilon (a novel isoform) does not inhibit these TPA
21 tified and determined the mechanism by which PKC-epsilon, a novel PKC isoform, modulates drug resista
24 NKs, not ERK1/2; 3) PKC-zeta and -theta, not PKC-epsilon, act upstream of JNKs, ERK1/2, and NF-kappaB
25 nstitutively active mutants of PKC-alpha and PKC-epsilon activated the transactivation domain of c-Ju
26 nstitutively active mutants of PKC-alpha and PKC-epsilon activated the transactivation domain of Elk-
27 ipase C, which resulted in PI hydrolysis and PKC epsilon activation in part by stimulation of the loc
28 ponse to PMA stimulation, demonstrating that PKC epsilon activity is required for MAPK activation by
31 vealed an increase in myofilament-associated PKC-epsilon after PHE or ET exposure of WT preparations.
34 nstitutively active mutants of PKC-alpha and PKC-epsilon also activated c-fos, c-jun, and cyclin E pr
36 localization, kinetics, and reversibility of PKC-epsilon anchoring in permeabilized rat cardiac myocy
37 , n = 5) prevented the translocation of both PKC epsilon and eta induced by ischemic PC, whereas the
38 that an isoform specific interaction between PKC epsilon and filamentous actin may serve as a necessa
39 creased with a conditional overexpression of PKC epsilon and increased with its knock-out by small in
40 croscopy demonstrated the co-localization of PKC epsilon and integrin beta 1 on the vesicular membran
44 oreactive amounts of cytosolic PKC alpha and PKC epsilon and of membrane PKC zeta were significantly
45 rotocols caused significant translocation of PKC epsilon and PKC eta isoforms from the cytosolic to t
47 owed an isoform-specific interaction between PKC epsilon and sterols, suggesting that sterols may dir
48 was enhanced by overexpression of wild-type PKC-epsilon and abolished by a dominant negative PKC-eps
51 l PKC-delta isozyme, together with the novel PKC-epsilon and conventional PKCs, contributed to the ba
52 r, hepatic insulin resistance, activation of PKC-epsilon and JNK1, and defects in insulin signaling.
53 y stimulating gluconeogenesis and activating PKC-epsilon and JNK1, which may interfere with tyrosine
55 ctions in diacylglycerol content and reduced PKC-epsilon and PKC-theta activity in liver and muscle r
56 signals through S1P(1) and G(i) to activate PKC-epsilon and, subsequently, a PLD2-PKC-zeta-Rac1 casc
57 pathway involving phospholipase C (PKC alpha/PKC epsilon) and intracellular calcium (PKC alpha) may c
58 ated activation of protein kinase C epsilon (PKC epsilon) and that the major PKC epsilon target is th
59 ion of protein kinase B and translocation of PKC epsilon, and it increased NO production, and these e
60 vely active mutants of PKC-alpha, PKC-delta, PKC-epsilon, and PKC-zeta to determine the roles of indi
61 expression of PKC-alpha and -delta, but not PKC-epsilon, and prevented the Ca2+-spiking responses to
62 geal cells, contraction was inhibited by the PKC-epsilon antiserum but not by antisera against other
63 erentiation (beating), while upregulation of PKC epsilon appeared to amplify differentiation (beating
67 s proposed to account for a new function for PKC epsilon as part of a sterol-sensitive signal transdu
68 of phospholipase C-gamma1 and activation of PKC-epsilon as evidenced by its translocation from solub
69 activation and establish a new function for PKC-epsilon as part of a mechano-sensitive signal transd
70 ciation of phosphorylated Bad with PKC-mu or PKC-epsilon, as shown by immunoprecipitation, indicated
71 ith phorbol esters completely down-regulated PKC-epsilon, as shown by Western blots, and abolished th
72 xtent of phagocytosis, their accumulation of PKC-epsilon at the phagosome, and their sensitivity to U
73 d norepinephrine-induced phosphorylations of PKC epsilon (at the C-terminal hydrophobic motif) and PK
77 epsilon and abolished by a dominant negative PKC-epsilon, but it was not affected by wild-type or dom
79 lot analysis demonstrates that expression of PKC-epsilon, but not other PKC isoforms, is associated w
83 porter plasmid, indicated that PKC-alpha and PKC-epsilon, but not PKC-delta or PKC-zeta, mediate SRE
88 , these findings indicate that PKC-alpha and PKC-epsilon can enhance the activities of at least three
89 ression of PKC epsilon in MCF-7 cells (MCF-7/PKC epsilon ) caused a decrease in p53 and an increase i
91 on of the novel PKC isoform, PKC epsilon, in PKC epsilon(-/-) cells is shown here to stimulate direct
92 ming phagosome in Ca-replete cells, but only PKC epsilon colocalized with phagosomes in Ca2+-depleted
93 re treated with phorbol ester only wild-type PKC-epsilon colocalized with actin in zones of cell adhe
94 tivity in immunoprecipitated c-N-Ras.c-Raf-1.PKC epsilon complexes is stimulated by PMA and is inhibi
95 fections of a dominant-negative or wild-type PKC epsilon construct did not affect either mucin secret
97 gth enzyme, indicating that other domains in PKC-epsilon contribute to anchoring by prolonging the bo
99 nstitutively active mutants of PKC-alpha and PKC-epsilon could also induce a mutant c-fos promoter wh
100 both the regulatory and catalytic domains of PKC-epsilon could independently induce NIH3T3 transforma
101 cks the redistribution of PKC alpha, but not PKC epsilon; D609 and BAPTA do not influence the partiti
103 epsilon delta, cells that overexpressed the PKC-epsilon delta chimera, induced a dramatically increa
104 KC-delta and -epsilon (PKC-delta epsilon and PKC-epsilon delta) were constructed by exchanging regula
106 alphaCT1 increases Cx43-pS368 in vitro in a PKC-epsilon-dependent manner and in the IBZ in vivo acut
109 he functional cooperation between GATA-1 and PKC-epsilon displayed dependence on cellular milieu, as
110 onstitutively active mutants of PKC-alpha or PKC-epsilon displayed increased expression of endogenous
111 orders, whereas the novel PKCs, PKC-delta or PKC-epsilon, displayed little or no redistribution in mu
113 n, pulldown and binding assays, we show that PKC epsilon does not bind to CFTR, but does bind to a re
115 protein kinase C-delta (PKC-delta), but not PKC-epsilon, enables the mouse myeloid cell line 32D to
117 N-terminal 144-amino-acid variable region of PKC-epsilon (epsilonV1-GFP), but not an analogous N-term
118 uggest that one potential mechanism by which PKC epsilon exerts its oncogenic activity is through der
120 that half-maximally repressed PKC alpha and PKC epsilon expression was approximately 0.5 nmol/L.
124 induces the redistribution of PKC alpha and PKC epsilon from the soluble to the particulate compartm
125 tituted in vitro system, the dissociation of PKC epsilon from these vesicles is shown to be dependent
135 stitutively associated with both c-Raf-1 and PKC epsilon in a biochemically silent, but latent, signa
136 own IPC signaling components such as PKG and PKC epsilon in addition to the mitochondrial ATP-sensiti
138 In this study, we investigated the role of PKC epsilon in breast cancer development and progression
143 lectively, these results identify a role for PKC epsilon in nPKC activation loop phosphorylations and
145 hormone specifically represses PKC alpha and PKC epsilon in the neonatal heart and PKC epsilon in the
146 Immunoblot analysis revealed the presence of PKC epsilon in the reconstitutively active fraction.
147 rotein interaction is sufficient to maintain PKC-epsilon in a catalytically active conformation.
149 evidence that the activation of PKC-alpha or PKC-epsilon in mouse fibroblasts can play an important r
151 ession of either PKC-theta in MCF-7 cells or PKC-epsilon in R6 and NIH 3T3 fibroblasts had no detecta
152 , our findings suggest an important role for PKC-epsilon in regulating survival of lung cancer cells.
153 er reveals that the failure of expression of PKC-epsilon in the chemo-sensitive phenotype of small ce
154 een, lung) We suggest that overexpression of PKC-epsilon in the epidermis may lead to the induction o
161 specific inhibitor peptides for PKC-delta or PKC-epsilon inhibited the DA-mediated increase in Na,K-A
164 ation loop but not the hydrophobic motif; DN-PKC epsilon is phosphorylated at the hydrophobic motif b
165 mma), representing 51% of this subgroup, and PKC epsilon is the most abundant among the nPKCs (delta,
167 med to represent activation of PKC alpha and PKC epsilon) is detectable by 1 h, sustained for up to 2
170 ate that up-regulation of c-myc requires the PKC-epsilon isoform and that this pathway is required fo
172 of PKC epsilon function either by expressing PKC epsilon(KR) or by small interfering RNA (siRNA)-medi
174 ase-inactive, dominant-negative PKC epsilon, PKC epsilon(KR), led to a significant inhibition of prol
176 essive breast cancer cell line with elevated PKC epsilon levels, resulted in a cell phenotype that wa
177 ERK/MAPK signaling occurred independently of PKC-epsilon levels and correlated more closely with mega
180 epsilonV1 domain is important in determining PKC-epsilon localization and translocation kinetics in c
181 s DAG that binds to epsilonC1B, facilitating PKC-epsilon localization to phagosomes for efficient IgG
184 ta induced by AOM, as well as to up-regulate PKC-epsilon, may underlie its ability to prevent adenoma
185 n vivo tumor growth of small interfering RNA-PKC epsilon MDA-MB231 clones was retarded by a striking
189 he trigger of this process by activating the PKC epsilon-MEK-1/2-p44/42 mitogen-activated protein kin
190 ern blot analysis revealed a 70% increase in PKC epsilon mRNA, indicating that the regulatory effects
191 WT) and dominant negative (DN) PKC delta and PKC epsilon mutants were introduced into cardiomyocyte c
192 of PKD induced by thrombin, whereas neither PKC epsilon nor PKC zeta affects thrombin-induced PKD ac
194 no-sensitive ERK1/2 activation, as antisense PKC-epsilon oligonucleotides did not inhibit ERK1/2 acti
197 onV1.2, a peptide translocation inhibitor of PKC epsilon or PKC epsilon siRNA inhibited PMA action.
199 Overexpression of dominant negative (dn) PKC-epsilon or -zeta, but not PKC-alpha or -delta, block
200 es, but this mechanism cannot be employed by PKC-epsilon or other PKC isoforms lacking a Ca2+-binding
201 When NIH 3T3 cells overexpressing either PKC-epsilon or the deletion mutant of this isozyme were
203 e knockdown of Bad, Bid, Akt1, Akt2, PKC-mu, PKC-epsilon, or PKC-theta was achieved by transient tran
204 utively active mutants of both PKC alpha and PKC epsilon overcame the inhibitory effects of dominant
205 und that PKC-theta but neither PKC-alpha nor PKC-epsilon participates in JNK activation, whereas all
207 acetate, hydrogen peroxide, and the specific PKC epsilon peptide agonist, psi epsilonRACK, each activ
208 prevented by chelerythrine, by the specific PKC epsilon peptide antagonist, epsilonV(1-2), and by th
210 lly inhibited by transfection with antisense PKC-epsilon phosphorothioate oligonucleotides (1,000 nM
214 y using a kinase-inactive, dominant-negative PKC epsilon, PKC epsilon(KR), led to a significant inhib
215 ediated cytosol-to-membrane translocation of PKC-epsilon, PKC-delta, and PKA-alpha, -gamma, and -IIal
217 Taken together, these results revealed that PKC epsilon plays a critical and causative role in promo
220 Antisense treatment decreased endogenous PKC epsilon protein levels and completely blocked induct
222 selective 60% increase in the expression of PKC epsilon protein that corresponded to an increase in
223 nsity tissue microarray analysis showed that PKC epsilon protein was detected in 73.6% (106 of 144) o
224 mouse lines that overexpress (8- or 18-fold) PKC-epsilon protein in basal epidermal cells and cells o
226 erexpress in epidermis approximately 18-fold PKC-epsilon protein more than their wild-type littermate
227 224) that expresses approximately eightfold PKC-epsilon protein more than their wild-type littermate
232 B7-2 deficiency significantly diminished the PKC-epsilon response in APCs upon CD28-Ig stimulation.
233 lls that expressed PKC-deltaepsilon retained PKC-epsilon's full potency of tumorgenicity when injecte
234 ion studies, the isolated variable domain of PKC-epsilon selectively blocked exogenous activation of
235 mationally hidden actin binding motif in the PKC-epsilon sequence becomes exposed upon activation of
237 , these results reveal an important role for PKC epsilon signaling in lung cancer and suggest that on
238 tivating ETA receptor-phospholipase C-beta 1-PKC-epsilon signaling complexes preferentially localized
239 nduced translocation/activation of PKC alpha/PKC epsilon, since the response is slower in onset, slow
246 aximally stimulated PKC enzyme activity with PKC epsilon substrate peptide (epsilon pep) but not with
247 e C epsilon (PKC epsilon) and that the major PKC epsilon target is the myristoylated, alanine-rich C-
248 n in immunoreactivity for both PKC alpha and PKC epsilon that was associated with significant reducti
249 rminus and the other to the COOH terminus of PKC-epsilon, that epsilon is present in both ferret port
252 assays demonstrate dose-dependent binding of PKC epsilon to RACK1 which is inhibited by an 8-amino ac
253 te but not an inactive congener translocated PKC epsilon to the particulate fraction and produced a d
257 of the epsilon isoform of protein kinase C (PKC-epsilon) to the membrane of a small fraction of fres
259 2 to 96 hours after cytokine withdrawal, the PKC epsilon transfectants remain distributed in all phas
262 the resultant accumulation of putrescine in PKC epsilon transgenic mice are linked to growth and mai
264 escine levels approximately 3-4-fold more in PKC epsilon transgenic mice than their wild-type litterm
266 thracene (100 nmol)-TPA (5 nmol) protocol in PKC epsilon transgenic mice was completely prevented by
269 ether there was an imbalance of cytokines in PKC-epsilon transgenic mice (line 215), resulting in abe
273 Complete pathological analysis of the second PKC-epsilon transgenic mouse (line 224) that expresses a
275 d PKC-betaII, -gamma, and -epsilon, and only PKC-epsilon translocated to the membrane fraction in res
277 ch-mediated inositol phosphate accumulation, PKC epsilon translocation is not prevented by AT1 recept
282 topoietic cells of protein kinase C-epsilon (PKC-epsilon) up-regulation and of extracellular signal-r
283 immunohistochemistry that overexpression of PKC epsilon was detected in the vast majority (>90%) of
287 LDL receptor gene transcription, endogenous PKC epsilon was specifically inhibited by transfection w
294 nstitutively active mutants of PKC-alpha and PKC-epsilon were the most potent activators of this repo
295 azoxide-pretreated hearts, and PKC-alpha and PKC-epsilon were translocated to sarcolemma and intercal
296 oxia-induced redistribution of PKC alpha and PKC epsilon, whereas chelation of intracellular calcium
297 n in K562 cells of protein kinase C-epsilon (PKC-epsilon), which has recently been implicated in regu
300 C-alpha, PKC-beta, PKC-gamma, PKC-delta, and PKC-epsilon) within major cerebellar cell types as well
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