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1 itive to 30 muM H-89 or 100 nM myristoylated protein kinase A inhibitor).
2 these effects were blocked by co-addition of protein kinase A inhibitor.
3 was blocked 80% to 85% by 70 microM H-89, a protein kinase A inhibitor.
4 n stimulation and significantly inhibited by protein kinase A inhibitor.
5 icantly reduced in cells treated with H89, a protein kinase A inhibitor.
6 ts as a protein phosphatase 1 inhibitor or a protein kinase A inhibitor.
7 tion was also down-regulated by p38 MAPK and protein kinase A inhibitors.
8 mimicked by an EP2 agonist and attenuated by protein kinase A inhibitors.
9 ir glucose modifying effects were reduced by protein kinase A inhibitors.
10 ster, 10 micromol/L), and inhibited by H-89 (protein kinase A inhibitor, 10 micromol/L), PD98059 (MEK
11 ffects of ACTH, whereas inhibition of PKA by protein kinase A inhibitor 14-22 amide blocked the modul
12 suppressed by forskolin and enhanced by the protein kinase A inhibitor 14-22 amide or H-89, suggesti
13 adenylyl cyclase activator forskolin or the protein kinase A inhibitor 14-22 amide or H-89, whereas
14 y by ATP in excised, inside-out patches in a protein kinase A inhibitor 5-24 dependent manner, sugges
15 y by ATP in excised, inside-out patches in a protein kinase A inhibitor 5-24 dependent manner, sugges
16 duction by YC-1 was prevented by ODQ and the protein kinase A inhibitor (9S,10S, 12R)-2,3,9,10,11,12-
17 eatments with either a VPAC1 antagonist or a protein kinase A inhibitor abolish IL-10 stimulation and
18 PACAP-evoked exocytosis was blocked by the protein kinase A inhibitor adenosine 3'5'-cyclic monopho
20 tivation of adenylyl cyclase, and blocked by protein kinase A inhibitor and an adenosine A1 receptor
21 GLT-1 protein expression was abolished by a protein kinase A inhibitor and an NF-kappaB inhibitor.
22 ation of I(h) persisted in the presence of a protein kinase A inhibitor and is therefore potentially
23 uppression of VIP induction of Th17 cells by protein kinase A inhibitors and enhancement by pharmacol
24 rease in 36Cl- permeability is diminished by protein kinase A inhibitors and is not mediated by an in
25 -beta-S [guanosine 5'-O-(2-thiodiphosphate], protein kinase A inhibitors, and an A-kinase anchoring p
26 eatment with pertussis toxin, but not with a protein kinase A inhibitor, antagonized morphine's inhib
27 on protein N-cadherin and PKI (an endogenous protein kinase A inhibitor) are localized to the right s
28 nhibitor, had no effect but Rp 8-Br cAMPs, a protein kinase A inhibitor, attenuated hypotensive dilat
30 cin (protein synthesis inhibitor) or KT5720 (protein kinase A inhibitor) blocked LTF, accumulation of
32 onamide that is commonly used as a selective protein kinase A inhibitor, blocked both ER export and h
33 on was prevented by a beta-antagonist and by protein kinase A inhibitors but not by an NF kappa B inh
34 imulation by growth factors and prevented by protein kinase A inhibitors but not by inhibitors of the
36 the inhibitory action of EGF, whereas H-89 (protein kinase A inhibitor) failed to alter the effect o
38 NE-stimulated apoptosis was abolished by the protein kinase A inhibitor H-89 (20 micromol/L) or the v
41 rtially, but significantly, inhibited by the protein kinase A inhibitor H-89 but not by tyrosine kina
42 osphodiesterase inhibitor W-7 but not by the protein kinase A inhibitor H-89 nor the protein kinase C
44 classes of kinase inhibitors, including the protein kinase A inhibitor H-89, the mitogen activated p
46 the other hand, pretreatment of muscles with protein kinase A inhibitors H-7 and KT5720 completely su
48 pre-incubation in suramin and by a selective protein kinase A inhibitor (H-89), and is mimicked (and
50 se A in As4.1 cells since treatment with the protein kinase A inhibitor, H-89, caused a significant r
54 d cAMP levels in spinal neurons and that the protein kinase A inhibitor H89 attenuated CGRP-induced C
55 he protein kinase C inhibitor H7 but not the protein kinase A inhibitor H89 blocked the response to A
56 ) on flagellar and channel function, and the protein kinase A inhibitor H89 blocks these actions.
57 ylation; this increase was unaffected by the protein kinase A inhibitor H89 but was reduced by the mi
58 r no effect on HEF1 phosphorylation, and the protein kinase A inhibitor H89 failed to detectably inhi
59 cAMP caused decreased G6PD activity, and the protein kinase A inhibitor H89 led to a increase in G6PD
64 of forskolin were completely reversed by the protein kinase A inhibitor H89, whereas H89 alone increa
66 lase inhibitor (2',5'-dideoxyadenosine) or a protein kinase A inhibitor (H89) also significantly atte
69 In contrast, neither forskolin nor H89, a protein kinase A inhibitor, had a significant effect on
70 icromol/L isoproterenol in the presence of a protein kinase A inhibitor increased the whole-cell sodi
71 added to the internal pipette solution, the protein kinase A inhibitor KT 5720 (0.6 microM), but not
76 ibitor staurosporine but not by the specific protein kinase A inhibitor N-(2-(methylamino)ethyl)-5-is
77 s dose-dependently inhibited by the specific protein kinase A inhibitor N-[2-(4-bromocinnamylamino)et
80 or clustering was prevented by addition of a protein kinase A inhibitor or by coexposure to a low con
81 production, could not be reversed by either protein kinase A inhibitors or an exchange protein direc
82 sfection of expression plasmids encoding the protein kinase A inhibitor, or an inactive protein kinas
83 hibitor peptide or exposure to myristoylated protein kinase A inhibitor peptide (M-PKI; 100 nM) reduc
85 tors blunted both KV1-C peptide-mediated and protein kinase A inhibitor peptide-mediated vasoconstric
89 by substituting well-defined snurportin-1 or protein kinase A inhibitor (PKIA) CRM1-binding NESs into
90 ide conjugates composed of the NES of either protein kinase A inhibitor protein (PKI) or the HIV-1 Re
91 activation as intracellular perfusion with a protein kinase A inhibitor rendered the same degree of a
92 t of CGS-21680 and, furthermore, Rp-cAMPS, a protein kinase A inhibitor, reversed the inhibitory effe
93 pial arteriole dilation was decreased by the protein kinase A inhibitor Rp 8-Br cAMPs (16+/-1 and 30+
94 igration and calpain activation; and (c) the protein kinase A inhibitor Rp-8-Br-cAMPS abrogated IP-10
95 as on peak IBa was entirely abolished by the protein kinase A inhibitor Rp-8-Br-cAMPS, or the adenyly
97 e subsequently tested in the presence of the protein kinase A inhibitor Rp-cAMP or protein kinase C i
99 annels to Gbetagamma was not affected by the protein kinase A inhibitors Rp-8-Br-cAMPS and KT 5720, o
101 ression caused by fasting was inhibited by a protein kinase A inhibitor, Rp-8-Br-cAMPS, when the comp
103 ibitor, dideoxyadenosine (10 microM) and the protein kinase A inhibitor, Rp-cAMP (10 microM), blocked
104 hanical hyperalgesia by adenylate cyclase or protein kinase A inhibitors spinally follows a similar p
105 ocinnamylamino)ethyl]-5-isoquinoline (H89; a protein kinase A inhibitor) stimulated cAMP accumulation
106 a DYRK3 C-terminal region and was blocked by protein kinase A inhibitors, suggesting functional inter
108 epletes intracellular Ca2+ stores), and H89 (protein kinase A inhibitor), that PDGF-stimulated secret
109 the peptide substrate, ATP and H-89, a known protein kinase A inhibitor, were performed and the kinet
110 with a prostacyclin receptor antagonist and protein kinase A inhibitor, whereas genes expressed at h
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