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1 ological inhibitors of PKC (calphostin C and chelerythrine).
2 e classical protein kinase C (PKC) inhibitor chelerythrine.
3 abrogated by the protein kinase C inhibitor chelerythrine.
4 s blocked by PKC inhibitors calphostin C and chelerythrine.
5 ertussis toxin, Gi3 antibodies, D609, and by chelerythrine.
6 ristoylated zeta inhibitory peptide (ZIP) or chelerythrine.
7 3) for 10 s UV), which could be inhibited by chelerythrine.
8 D609, and by the protein kinase C inhibitor chelerythrine.
9 rfusion are abolished by PKC inhibition with chelerythrine.
10 is effect was prevented by the coinfusion of chelerythrine.
11 confirm the reported inhibitory activity of chelerythrine.
12 /C5 channel activity, which was prevented by chelerythrine.
13 nd blocked by the protein kinase C inhibitor chelerythrine.
14 was blocked by a protein kinase C inhibitor, chelerythrine.
15 on of PKC by IPC was blocked by verapamil or chelerythrine.
16 ttenuated by the treatment with verapamil or chelerythrine.
17 e or the specific protein kinase C inhibitor chelerythrine.
18 D occludes the synaptic depression caused by chelerythrine.
19 nted by the protein kinase C (PKC) inhibitor chelerythrine.
20 ted with the protein kinase inhibitors H7 or chelerythrine.
21 is abolished by the PKC-selective inhibitor chelerythrine.
22 s increased by CPA and PDBu but decreased by chelerythrine.
23 ed O(2)(.-) generation that was inhibited by chelerythrine.
24 apocynin and the protein kinase C inhibitor chelerythrine.
25 nel opening (NP(o)) and this was reversed by chelerythrine.
26 ne on Isus were blocked by the PKC inhibitor chelerythrine.
27 ion of TRPC6 proteins which was inhibited by chelerythrine, 0 [Ca(2+)](o) and the anti-TRPC1 antibody
28 pplication of the protein kinase C inhibitor chelerythrine (1-10 microM) had no effect on either OAG-
32 roM, 4 min), a phospholipase C inhibitor, or chelerythrine (10 microM, 4 min), a protein kinase C (PK
33 ), and the protein kinase C (PKC) inhibitors chelerythrine (10 micrometer) or PKC 19-36 peptide (1 mi
35 solution, and was blocked by PKC inhibitors chelerythrine (10 mumol/L) and staurosporine (100 nmol/L
36 and partially restored by the PKC inhibitor chelerythrine (10(-7) M) or the O(-)(2) free radical sca
37 hibitors staurosporine (10(-9) to 10(-7) M), chelerythrine (10(-9) to 5 x 10(-8) M), or calphostin C
38 l]-3-(1H-indol-3-yl) maleimide, 1 microm; or chelerythrine, 10 microm) did not prevent the generation
39 iferase activity was completely inhibited by chelerythrine, 2-aminopurine, genistein, and W-7 and onl
41 ytosolic Ca2+, exposure to the PKC inhibitor chelerythrine (25 microM) and downregulation of PKC by p
44 300 U/mL), PEG-SOD+PEG-catalase (1000 U/mL), chelerythrine (3 micromol/L), or tetrahydrobiopterin (20
45 itoK(ATP) channel blocker (56.5+/-2.7%), and chelerythrine (5 mg/kg IV), an effective PKC inhibitor (
48 C) inhibitors, calphostin C (0.5 microM) and chelerythrine (5 microM), or a nitric oxide synthase (NO
49 nhibition with staurosporine (2 x 10-6M) and chelerythrine (5 x 10-5M) on endothelin-1-induced pulmon
50 Of the protein kinase inhibitors tested, chelerythrine, 6-dimethylaminopurine, H-89, K252a, ML-9,
57 , a reactive oxygen species (ROS) scavenger, chelerythrine, a protein kinase C (PKC) inhibitor, and l
58 by diazoxide was not blocked by 5 micromol/L chelerythrine, a protein kinase C antagonist, given eith
59 inine, a nitric oxide synthase inhibitor, or chelerythrine, a protein kinase C inhibitor (both given
60 cell death, all of which were suppressed by chelerythrine, a protein kinase C inhibitor, DPI, a NADP
62 sphorylation was substantially attenuated by chelerythrine, a protein kinase C-selective inhibitor.
66 were blocked almost completely by 25 microM chelerythrine, a specific, noncompetitive PKC inhibitor.
68 athways by administration of the PKC blocker chelerythrine abrogated the ischemic protection afforded
69 tly inhibited by the PKC catalytic inhibitor chelerythrine added before and concomitant with EPO.
71 n IL-1 receptor antagonist, a PKC inhibitor (chelerythrine), an IP3 receptor inhibitor (2-aminoethoxy
75 Repeated administration of PKC inhibitors chelerythrine and 1-(5-isoquinolinesulfonyl)-2-methylpip
77 eversible by the protein kinase C inhibitors chelerythrine and 2-[1-(3-dimethylaminopropyl)-1H-indol-
78 ited by the protein kinase C (PKC) inhibitor chelerythrine and activated by the phorbol ester phorbol
80 rotein kinase C-specific inhibitors, such as chelerythrine and bisindolylmaleimide I, did not reduce
83 ited by the protein kinase C (PKC) inhibitor chelerythrine and by anti-TRPC1 antibodies indicating th
90 ts overcome the effects of blocking PKC with chelerythrine and resulted in a rescue of the wing morph
92 in, or the protein kinase C (PKC) inhibitors chelerythrine and staurosporine or by the angiotensin-co
94 have been reported in studies conducted with chelerythrine, and alteration of PKC activity has been c
96 ant (TAM67) were exposed to calphostin C and chelerythrine, and c-jun expression was monitored at bot
97 ced Hsp70i message levels, whereas SB203580, chelerythrine, and curcumin reversed the subcellular red
98 nates, which was attenuated by PKC inhibitor chelerythrine, and enhanced evoked potentials during cos
99 ed TRPC5 channel activity was potentiated by chelerythrine, and inhibited by PDBu, PIP(2), and PIP(3)
100 nt pharmacological manipulations (L-NA, MPG, chelerythrine, and lavendustin A) produced similar inhib
101 opionyl glycine, protein kinase C antagonist chelerythrine, and mitochondrial K(ATP) channel closer 5
102 ls treated with calphostin C, staurosporine, chelerythrine, and PKCalpha antisense, respectively.
103 C), PKC (including pseudosubstrate peptides, chelerythrine, and the alpha/beta isoform-specific inhib
104 tor wortmannin, the protein kinase C blocker chelerythrine, and the mitogen activated protein kinase
105 We found that the protein kinase C inhibitor chelerythrine antagonized BMP7-induced protection agains
106 r dialysis accelerated this current, whereas chelerythrine antagonized it, suggesting the involvement
107 ver in cell-attached patches pretreated with chelerythrine, application of 100 nM Ang II activated Ic
109 nt to downregulate PKC and the PKC inhibitor chelerythrine, arguing that PKCepsilon plays a critical
110 tudies use zeta inhibitory peptide (ZIP) and chelerythrine as inhibitors of PKMzeta to block long ter
111 d by the administration of the PKC inhibitor chelerythrine at a dose of 5 mg/kg (group VI) (particula
113 study tested whether inhibition of PKC with chelerythrine before daily stress would protect prefront
114 ol esters and is inhibited by staurosporine, chelerythrine, bisindolylmaleimide I, calphostin C, and
116 of 1 microm bisendolylmaleimide or 1 microm chelerythrine, both protein kinase C inhibitors, potenti
117 dependence, was blocked by pretreatment with chelerythrine but not by NMLA, ddA, TMB-8, or Quin-2.
118 ase C inhibitors (GF109203x, calphostin C or chelerythrine) but not by tyrosine kinase inhibitors (ty
119 ited by the protein kinase C (PKC) inhibitor chelerythrine, but not by the protein kinase A (PKA) inh
120 This effect of PKC epsilon was prevented by chelerythrine, by the specific PKC epsilon peptide antag
121 ptide 5-24) and protein kinase C inhibitors (chelerythrine, calphostin C, and peptide 19--63) did not
122 o different PKC inhibitors, calphostin C and chelerythrine; calphostin C also blocked the fenoldopam-
124 Inhibition of protein kinase C (PKC) with chelerythrine (CHE, 2 micromol/L) completely abrogated b
125 re-ischaemic blockade of PKC was achieved by chelerythrine (Chel) in male (M + C) and female (F + C)
127 inhibitors [staurosporine (5 micromol/L) and chelerythrine chloride (10 micromol/L)], and a replicati
128 rs bisindolylmaleimide I (BIM; 30 microM) or chelerythrine chloride (100 microM) through a microdialy
129 gated by prior inhibition of either PKC with chelerythrine chloride (5 mg/kg) or of TKs with lavendus
130 0mg/kg, s.c.), midazolam (2mg/kg, i.p.), and chelerythrine chloride (a non-specific PKC inhibitor, 10
132 tors bisindolylmaleimide I (BIS; 100 nM) and chelerythrine chloride (CHE; 25 microM) and was not mimi
133 the protein kinase C group A and B isoforms, chelerythrine chloride (chelerythrine), to enhance the k
137 the effects of protein kinase C inhibitors (chelerythrine chloride and sphingosine) or of chronic tr
140 y selective protein kinase C (PKC) inhibitor chelerythrine chloride leads to profound cell cycle arre
141 ally inhibited by the specific PKC inhibitor chelerythrine chloride or by downregulation of PKC with
142 e specific protein kinase C (PKC) inhibitors chelerythrine chloride or calphostin C completely blocke
143 I(Na) were antagonized by the PKC inhibitors chelerythrine chloride or staurosporine or by down-regul
144 nt of cells with PKC translocation inhibitor chelerythrine chloride suppressed the induced extracellu
145 n the side ipsilateral to the injection when chelerythrine chloride was administered intrathecally be
146 se (U0126) and broad spectrum PKC inhibitor (chelerythrine chloride) and decreased cell proliferation
147 ) inhibitor (10.0 mum Ro 31-8220 or 30.0 mum chelerythrine chloride) attenuated cocaine seeking.
148 e, a specific MitoKATP channel inhibitor, or chelerythrine chloride, a PKC inhibitor, during diazoxid
149 Finally, treatment of Jurkat cells with chelerythrine chloride, a protein kinase C inhibitor, pr
153 tin C, a blocker of the PMA binding site, or chelerythrine chloride, an inhibitor of the active site,
154 orylation in monocytes, and pertussis toxin, chelerythrine chloride, and staurosporine significantly
155 hemistry to examine whether a PKC inhibitor, chelerythrine chloride, blocks the enhanced phosphorylat
156 taurosporine and the PKC-selective inhibitor chelerythrine chloride, but was activated by the phospha
157 o selective inhibitors of PKC, GF109203X and chelerythrine chloride, effectively block the phosphoryl
158 was inhibited by pertussis toxin, U73122, or chelerythrine chloride, inhibitors of Gi-protein, phosph
162 ent with a protein kinase C (PKC) inhibitor, chelerythrine chloride; the FP receptor antagonist, AL-8
165 DAMGO-tolerant paws was acutely reversed by chelerythrine, ddA, TMB-8, or Quin-2 but not by NMLA.
169 t), but the protein kinase C (PKC) inhibitor chelerythrine did not inhibit either the OAG- or ET-1-in
171 ions of thiolic antioxidants fully prevented chelerythrine-driven caspase activation and necrotic-lik
172 er, reducing PKC activity by inhibition with chelerythrine during chronic exposure to ethanol or down
173 ate IPC, but blockade of PKC activation with chelerythrine during IPC blocked its neuroprotection.
175 eta inhibitory peptide) or the PKC inhibitor chelerythrine erased the memory for long-term sensitizat
176 apses on cells loaded with the PKC inhibitor chelerythrine exhibited PTP followed by a significant de
178 whereas pretreatment with the PKC inhibitor chelerythrine (given at doses that have previously been
180 , as a related benzophenanthridine alkaloid, chelerythrine, has been reported to mediate a variety of
181 ults uncover a novel biochemical property of chelerythrine, i.e. activation of MEKK1- and MKK4-depend
183 or disruption of caveolae but was blocked by chelerythrine, implicating protein kinase C, but not pho
186 kinase C (PKC) activity by calphostin C and chelerythrine increased the activity of the exchanger in
188 rsed by the protein kinase C (PKC) inhibitor chelerythrine indicating a G-protein pathway inhibits ch
198 of thiolic antioxidants partially prevented chelerythrine-mediated cytotoxicity and allowed cells to
200 , several lines of evidence demonstrate that chelerythrine-mediated G2 phase arrest results from sele
202 7, as well as selective inhibition of PKC by chelerythrine, mimics and occludes the maintenance phase
203 from a variety of mammalian species, neither chelerythrine nor angoline inhibited activity with high
204 the effects of herbimycin A, wortmannin, and chelerythrine on iC5b67-induced PMN chemotaxis, iC5b67 s
205 observe any significant inhibitory effect of chelerythrine on the activities of PKC isozymes present
206 o PKC antagonists (D-erythro-sphingosine and chelerythrine) on input-output (I-O) relations in the Sc
207 of protein kinase C such as calphostin C and chelerythrine or (b) chronic pre-exposure to the non-tum
208 he presence of protein kinase C antagonists, chelerythrine or bis-indolylmaleimide hydrochloride (GF
212 om LY294002, and was unaffected by 10 microm chelerythrine or incubating cells in pertussis toxin (PT
216 ocynin, the protein kinase C (PKC) inhibitor chelerythrine or staurosporin or the removal of extracel
220 rabbit hearts inhibition of PKCepsilon with chelerythrine, p38 MAP kinase, with SB203580 and JUN kin
221 e particulate fraction and pretreatment with chelerythrine (PKC inhibitor) blocked the protective eff
224 alone or in combination with midazolam, and chelerythrine prevented the development of morphine tole
226 incubation with the protein kinase inhibitor chelerythrine prevented the PMA effects; and (3) a hydro
227 eatment of cells with the pan-PKC inhibitor, chelerythrine, prevented the activation of endothelial a
229 or), uric acid (scavenger of peroxynitrite), chelerythrine (protein kinase C inhibitor), N(G)-nitro-L
230 eated with 100 nmol/L GF109203X or 5 mumol/L chelerythrine (protein kinase C inhibitors), neither 5 U
231 of PKC with staurosporine, calphostin C, and chelerythrine reduced cell proliferation to 7%, 31%, and
234 tivator phorbol 12, 13-dibutyrate (PDBu) and chelerythrine, respectively, decreased and increased NP(
235 s or the newly identified Bcl-X(L) inhibitor chelerythrine restores cellular sensitivity to injury an
236 T5823, and protein kinase C (PKC) inhibitors chelerythrine, Ro318220, and PKC-epsilon peptide antagon
237 GF109203X, Ro 31-8220, calphostin C, and chelerythrine (selective protein kinase C inhibitors) ha
239 Inhibition of protein kinase C (PKC) using chelerythrine, staurosporine, or calphostin C inhibited
240 protein kinase inhibitors staurosporine and chelerythrine stimulated a normally silent component of
242 not by the protein kinase C (PKC) inhibitor chelerythrine, the adenylyl cyclase inhibitor 2',5'-dide
243 kinase C (PKC) inhibitors staurosporine and chelerythrine, the phospholipase C (PLC) inhibitors D609
244 up A and B isoforms, chelerythrine chloride (chelerythrine), to enhance the killing effects of ionizi
248 When the protein kinase C (PKC) inhibitor chelerythrine was coadministered with adenosine, the PAE
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