Name | protein kinase C (protein family or complex) |
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Synonyms | Protein kinase C; PKC |
Name | 4-aminopyridine |
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CAS | 4-pyridinamine |
PubMed | Abstract | RScore(About this table) | |
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19073169 | Hung KL, Wang CC, Huang CY, Wang SJ: vitamin B12, depresses release through inhibition of voltage-dependent Ca2+ influx in rat cerebrocortical nerve terminals (synaptosomes). Eur J Pharmacol. 2009 Jan 14;602(2-3):230-7. Epub 2008 Dec 6. Furthermore, 4-aminopyridine-induced phosphorylation of protein kinase C was significantly reduced by |
113(1,2,2,3) | Details |
16026936 | Wang SJ: Activation of neuropeptide Y Y1 receptors inhibits release through reduction of voltage-dependent Ca2+ entry in the rat cerebral cortex nerve terminals: suppression of this inhibitory effect by the protein kinase C-dependent facilitatory pathway. Neuroscience. 2005;134(3):987-1000. Moreover, NPY-mediated inhibition of 4-aminopyridine-evoked release was insensitive to KT 5720 and Ro32-0432 but was suppressed when protein kinase C was stimulated with phorbol ester. |
83(1,1,1,3) | Details |
12880946 | Barbar E, Rola-Pleszczynski M, Payet MD, Dupuis G: Protein kinase C inhibits the transplasma membrane influx of Ca2+ triggered by 4-aminopyridine in Jurkat T lymphocytes. Biochim Biophys Acta. 2003 Jul 23;1622(2):89-98. |
82(1,1,1,2) | Details |
17804632 | Miura M, Saino-Saito S, Masuda M, Kobayashi K, Aosaki T: Compartment-specific modulation of GABAergic synaptic transmission by mu-opioid receptor in the mouse striatum with green fluorescent protein-expressing islands. J Neurosci. 2007 Sep 5;27(36):9721-8. These effects of MOR were mediated principally by 4-aminopyridine-sensitive K+ conductance via a cAMP-dependent pathway, which was further augmented by previous blockade of the protein kinase C cascade. |
81(1,1,1,1) | Details |
12500029 | Goirand F, Bardou M, Guerard P, Dumas JP, Rochette L, Dumas M: ETA, mixed ETA/ETB receptor antagonists, and protein kinase C inhibitor prevent acute hypoxic pulmonary vasoconstriction: influence of channels. J Cardiovasc Pharmacol. 2003 Jan;41(1):117-25. The aims of this study were to investigate the effects of a selective ETA (BQ-123), a selective ETB (BQ-788), and a specific mixed ETA/ETB receptor antagonist (bosentan) on the pulmonary vasoconstriction induced by hypoxia in the isolated perfused rat lung, and the role of -sensitive (KATP), large conductance Ca+-activated (BKCa) and 4-aminopyridine-sensitive voltage-gated K channels (K+) in the relaxant effects of the selective ETA receptor antagonist BQ-123 and a protein kinase C inhibitor, bisindolylmaleimide I. |
34(0,1,1,4) | Details |
12694813 | Berg T: The vascular response to the K+ channel inhibitor 4-aminopyridine in hypertensive rats. Eur J Pharmacol. 2003 Apr 18;466(3):301-10. These results indicated an increased catecholamine, angiotensin AT (1) and endothelin ET (A) activation of the phospholipase C-protein kinase C pathway in SHR, inhibiting the 4-aminopyridine-sensitive K+ channels. |
32(0,1,1,2) | Details |
10822151 | Ramakers GM, Pasinelli P, van Beest M, van der Slot A, Gispen WH, De Graan PN: Activation of pre- and postsynaptic protein kinase C during tetraethylammonium-induced long-term potentiation in the CA1 field of the hippocampus. Neurosci Lett. 2000 May 26;286(1):53-6. |
2(0,0,0,2) | Details |
17372967 | Wang SJ: cerebral cortex nerve terminals (synaptosomes) through activation protein kinase C pathway: an interaction with presynaptic adenosine A1 receptors. Synapse. 2007 Jun;61(6):401-11. The present study used nerve terminals (synaptosomes) isolated from rat cerebral cortex to investigate the relationship between and 4-aminopyridine (4AP)-evoked endogenous excitatory neurotransmitter release. |
facilitation of release from rat 2(0,0,0,2) | Details |
17146969 | Choi S, Parajuli SP, Lim GH, Kim JH, Yeum CH, Yoon PJ, Jun JY: inhibits A-type delayed rectifier and ATP-sensitive K+ currents independent of G-protein and protein kinase C in murine proximal colonic myocytes. Arch Pharm Res. 2006 Nov;29(11):998-1005. Early peak currents were inhibited by the application of 4-aminopyridine, whereas sustained currents were inhibited by the application of TEA. |
2(0,0,0,2) | Details |
17663453 | Chou CW, Huang WJ, Tien LT, Wang SJ: (-)-activation of protein kinase C in rat cerebral cortex. Synapse. 2007 Nov;61(11):889-902. Results showed that the release of evoked by 4-aminopyridine (4AP) was facilitated by in a concentration-dependent manner, and this effect resulted from an enhancement of vesicular exocytosis and not from an increase in Ca2+-independent efflux via transporter. |
the most active polyphenolic in green tea, presynaptically facilitates Ca2+-dependent release via 2(0,0,0,2) | Details |
11553034 | Tanaka H, Habuchi Y, Suto F, Morikawa J: Effects of myocytes. Clin Exp Pharmacol Physiol. 2001 Sep;28(9):743-7. In the present study, we investigated the effects of peroxide (H2O2) on the 4-aminopyridine-sensitive transient outward current (I (TO)) in rabbit atrial myocytes using the amphotericin B-perforated patch voltage-clamp method. 2. Bisindolylmaleimide (100 nmol/L), an inhibitor of protein kinase C, significantly attenuated the H2O2-induced effects on I (TO). 4. |
peroxide on the transient outward current in rabbit atrial 2(0,0,0,2) | Details |
19657079 | Deng P, Pang ZP, Lei Z, Xu ZC: Excitatory roles of protein kinase C in striatal cholinergic interneurons. J Neurophysiol. 2009 Oct;102(4):2453-61. Epub 2009 Aug 5. These excitatory effects of PKC could be partially mimicked and occluded by blockade of I (A) with potassium channel blocker 4-aminopyridine. |
2(0,0,0,2) | Details |
17071736 | Brueggemann LI, Moran CJ, Barakat JA, Yeh JZ, Cribbs LL, Byron KL: protein kinase C-dependent inhibition of KCNQ5 in A7r5 rat aortic smooth muscle cells. Am J Physiol Heart Circ Physiol. 2007 Mar;292(3):H1352-63. Epub 2006 Oct 27. The AVP-sensitive I (Kv) was resistant to 4-aminopyridine, iberiotoxin, and glibenclamide but was fully inhibited by the selective KCNQ channel blockers linopirdine (10 microM) and XE-991 (10 microM) and enhanced by the KCNQ channel activator flupirtine (10 microM). |
stimulates action potential firing by 2(0,0,0,2) | Details |
17016851 | Wang SJ, Wang KY, Wang WC, Sihra TS: Unexpected inhibitory regulation of release from rat cerebrocortical nerve terminals by presynaptic 5-hydroxytryptamine-2A receptors. J Neurosci Res. 2006 Nov 15;84(7):1528-42. DOI potently inhibited 4-aminopyridine (4AP)-evoked release. Mechanistically, DOI modulation of 4AP-evoked release appeared to involve a phospholipase C/protein kinase C signaling cascade, insofar as pretreatment of synaptosomes with the phospholipase C inhibitor U73122 or protein kinase C inhibitors Ro320432 or GF109203X all effectively occluded the inhibitory effect of the agonist. |
2(0,0,0,2) | Details |
16330128 | Wang SJ: Facilitatory effect of nerve terminals: involvement of protein kinase C pathway. Neurochem Int. 2006 Feb;48(3):181-90. Epub 2005 Dec 2. The Ca (2+)-dependent release of evoked by 4-aminopyridine (4AP) was facilitated by in a concentration-dependent manner, but the 4AP-evoked Ca (2+)-independent release was not modified. |
on release from rat hippocampal 2(0,0,0,2) | Details |
19428798 | Lin TY, Lu CW, Wang SJ: Inhibitory effect of release from rat cerebrocortical synaptosomes by dextromethorphan and its metabolite 3-hydroxymorphinan. Neurochem Int. 2009 Jul;54(8):526-34. Epub 2009 Mar 4. DM or 3-HM inhibited the Ca (2+)-dependent release of that was evoked by exposing synaptosomes to the K (+) channel blocker 4-aminopyridine (4-AP), and this presynaptic inhibition was concentration-dependent. DM or 3-HM modulation of 4-AP-evoked release appeared to involve a protein kinase C (PKC) signaling cascade, insofar as pretreatment of synaptosomes with the PKC inhibitors GF109203X or Ro318220 all effectively occluded the inhibitory effect of DM or 3-HM. |
1(0,0,0,1) | Details |
18037536 | Yang TT, Wang SJ: Facilitatory effect of nerve terminals by a major component. Neurochem Int. 2008 May;52(6):979-89. Epub 2007 Oct 18. Results showed that facilitated the Ca2+-dependent but not the Ca2+-independent release evoked by 4-aminopyridine (4AP). In addition, modulation of release appeared to involve a protein kinase C (PKC) signalling cascade, insofar as pretreatment of synaptosomes with the PKC inhibitor GF109203X effectively suppressed the facilitatory effect of on 4AP- or ionomycin-evoked release. |
exocytosis from rat cerebrocortical 1(0,0,0,1) | Details |
18156198 | Walsh KB, Zhang J: Neonatal rat cardiac fibroblasts express three types of voltage-gated K+ channels: regulation of a transient outward current by protein kinase C. Am J Physiol Heart Circ Physiol. 2008 Feb;294(2):H1010-7. Epub 2007 Dec 21. I (to) was inhibited by the antiarrhythmic agent flecainide (100 microM) and BaCl (2) (1 mM) but was unaffected by 4-aminopyridine (4-AP; 0.5 and 1 mM). |
1(0,0,0,1) | Details |
12826968 | Moe MC, Berg-Johnsen J, Larsen GA, Kampenhaug EB, Vinje ML: The effect of isoflurane and sevoflurane on cerebrocortical presynaptic Ca2+ and protein kinase C activity. J Neurosurg Anesthesiol. 2003 Jul;15(3):209-14. After 8 minutes of anesthetic exposure, 1 mM 4-aminopyridine was added to induce membrane depolarization. |
2(0,0,0,2) | Details |
10713079 | O'Kelly I, Lewis A, Peers C, Kemp PJ: O (2) sensing by airway chemoreceptor-derived cells. J Biol Chem. 2000 Mar 17;275(11):7684-92. Protein kinase c activation reveals functional evidence for involvement of oxidase.. |
2(0,0,0,2) | Details |
11744003 | Moe MC, Berg-Johnsen J, Roste GK, Vinje ML: Stimulated increase in free cytosolic Ca (2+) and protein kinase C activity in human cerebrocortical synaptosomes. Brain Res. 2002 Jan 4;924(1):116-9. Membrane depolarisation by 4-aminopyridine (4-AP) 1 mM increased the [Ca (2+)](i) fluorescence by 14.4+/-2.2% and the PKC activity fluorescence by 16.7+/-1.6%. |
2(0,0,0,2) | Details |
19072841 | Yang TT, Wang SJ: Facilitation of nerve terminals (synaptosomes) by and Synapse. 2009 Mar;63(3):215-23. Data showed that both PS and PC potently facilitate 4-aminopyridine (4-AP)-evoked Ca (2+)-dependent and Ca (2+)-independent release. Furthermore, PS- or PC-mediated facilitation of 4-AP-evoked release was superseded or suppressed by protein kinase C (PKC) activator and inhibitor, respectively. |
release from rat cerebrocortical glutamatergic 1(0,0,0,1) | Details |
16543267 | Ma X, Bielefeldt K, Tan ZY, Whiteis CA, Snitsarev V, Abboud FM, Chapleau MW: Dual mechanisms of angiotensin-induced activation of mouse sympathetic neurones. J Physiol. 2006 May 15;573(Pt 1):45-63. Epub 2006 Mar 16. The IA channel blocker 4-aminopyridine triggered AP generation in TNs and prevented the Ang II-induced APs but not the depolarization. |
0(0,0,0,0) | Details |
18643787 | Qu L, Leung LS: Mechanisms of hyperthermia-induced depression of GABAergic synaptic transmission in the immature rat hippocampus. J Neurochem. 2008 Sep;106(5):2158-69. Epub 2008 Jul 15. Furthermore, hyperthermia-induced depression of evIPSCs was attenuated by 4-aminopyridine, but not by BaCl (2). |
0(0,0,0,0) | Details |
19887885 | Park SY, Park SU, Sohn UD: Regulators involved in the electrically stimulated response of feline esophageal smooth muscle. Pharmacology. 2009;84(6):346-55. Epub 2009 Nov 3. Furthermore, 4-aminopyridine (4-AP), voltage-dependent K (+) (K (v)) channel blocker, did not significantly enhance off-contraction. |
0(0,0,0,0) | Details |
12065624 | Donald AN, Wallace DJ, McKenzie S, Marley PD: Phospholipase C-mediated signalling is not required for -induced catecholamine secretion from bovine chromaffin cells. J Neurochem. 2002 Jun;81(5):1116-29. Blocking various K (+) channels with apamin, charybdotoxin, Ba (2+), tetraethylammonium, 4-aminopyridine, tertiapin or glibenclamide failed to reduce the ability of to evoke secretion. |
0(0,0,0,0) | Details |
10836990 | Lang R, Lee G, Liu W, Tian S, Rafi H, Orias M, Segal AS, Desir GV: KCNA10: a novel ion channel functionally related to both voltage-gated and CNG cation channels. Am J Physiol Renal Physiol. 2000 Jun;278(6):F1013-21. The phorbol ester phorbol 12- 13- an activator of protein kinase C, inhibited whole cell current by 42%. The channel displays an unusual inhibitor profile because, in addition to being blocked by classical K channel blockers (barium tetraethylammonium and 4-aminopyridine), it is also sensitive to inhibitors of cyclic nucleotide-gated (CNG) cation channels and pimozide). |
1(0,0,0,1) | Details |
12933338 | Gupte SA, Arshad M, Viola S, Kaminski PM, Ungvari Z, Rabbani G, Koller A, Wolin MS: Pentose phosphate pathway coordinates multiple redox-controlled relaxing mechanisms in bovine coronary arteries. Am J Physiol Heart Circ Physiol. 2003 Dec;285(6):H2316-26. Epub 2003 Aug 21. High doses of K+ channel blockers [e.g., TEA (10 mM) and 4-aminopyridine (10 mM)] only partially inhibited the relaxation to 6-AN. |
0(0,0,0,0) | Details |
15694920 | Kubo T, Hagiwara Y: Protein kinase C activation-induced increases of neural activity are enhanced in the hypothalamus of spontaneously hypertensive rats. Brain Res. 2005 Feb 8;1033(2):157-63. Pressure application of 4-aminopyridine, a blocker of the transient current, onto angiotensin II-sensitive neurons increased their firing rate and the increase of unit firing rate was almost the same in WKY and SHR. |
1(0,0,0,1) | Details |
16325966 | Cannizzaro C, D'Amico M, Preziosi P, Martire M: Presynaptic effects of nerve endings isolated from rat hippocampus. Neurochem Int. 2006 Feb;48(3):159-65. Epub 2005 Dec 2. Release was evoked with three different stimuli: (1) KCl-induced membrane depolarization, which activates voltage-dependent Ca (2+) channels and causes limited neurotransmitter exocytosis, presumably from ready-releasable vesicles docked in the active zone; (2) exposure to the Ca (2+) ionophore-A23187, which causes more extensive transmitter release, presumably from intracellular reserve vesicles; and (3) K (+) channel blockade by 4-aminopyridine (4-AP), which generates repetitive depolarization that stimulates release from both ready-releasable and reserve vesicles. AEA's enhancement of the [(3) H] d-ASP release induced by the Ca (2+) ionophore was mimicked by 4-beta-PMA, which is known to activate protein kinase C (PKC), and the increases produced by both compounds were completely reversed by synaptosome treatment with staurosporine (1 microM), a potent PKC blocker. |
and WIN55,212-2 on glutamatergic 1(0,0,0,1) | Details |
19628631 | Yang TT, Wang SJ: inhibits depolarization-evoked release in nerve terminals from rat cerebral cortex: a possible neuroprotective mechanism?. J Pharmacol Exp Ther. 2009 Oct;331(1):244-54. Epub 2009 Jul 23. Furthermore, the effect on 4-AP-evoked release was abolished by the protein kinase C (PKC) inhibitors bisindolylmaleimide I (GF109203X) or bisindolylmaleimide IX (Ro318220), and significantly decreased the 4-AP-induced phosphorylation of PKC, PKCalpha, and myristoylated alanine-rich C kinase substrate. inhibited the release of that was evoked by exposing synaptosomes to the K (+) channel blocker 4-aminopyridine (4-AP), and this phenomenon was concentration-dependent. |
1(0,0,0,1) | Details |
18792989 | Sy HN, Wu SL, Wang WF, Wang SJ: Mechanisms underlying the honokiol inhibition of evoked release from glutamatergic nerve terminals of the rat cerebral cortex. Synapse. 2008 Dec;62(12):890-901. Honokiol potently inhibited 4-aminopyridine (4-AP)-evoked release in a concentration-dependent manner, and this effect resulted from a reduction of vesicular exocytosis and not from an inhibition of Ca (2+)-independent efflux via transporter. In addition, honokiol modulation of 4-AP-evoked release appeared to involve a protein kinase C (PKC) signaling cascade, in so far as pretreatment of synaptosomes with the PKC inhibitors Ro318220 or GF109203X all effectively occluded the inhibitory effect of honokiol. |
1(0,0,0,1) | Details |
11152736 | Zhang YH, Kenyon JL, Nicol GD: Phorbol ester-induced inhibition of currents in rat sensory neurons requires voltage-dependent entry of J Neurophysiol. 2001 Jan;85(1):362-73. The whole cell patch-clamp technique was used to examine the effects of protein kinase C (PKC) activation (via the phorbol ester, phorbol 12,13 dibutyrate, PDBu) on the modulation of currents (I (K)) in cultured -sensitive neurons isolated from dorsal root ganglia from embryonic rat pups and grown in culture. The potassium channel blockers tetraethylammonium (TEA, 10 mM) and 4-aminopyridine (4-AP, 3 mM and 30 microM) reduced I (K), but only TEA attenuated the ability of PDBu to further inhibit the current, suggesting that the I (K) modified by PDBu was sensitive to TEA. |
1(0,0,0,1) | Details |
19489007 | Lu CW, Lin TY, Chiang HS, Wang SJ: Facilitation of cerebral cortex nerve terminal by subanesthetic concentration propofol. Synapse. 2009 Sep;63(9):773-81. Results showed that subanesthetic concentration propofol facilitated 4-aminopyridine (4-AP), but not KCl- or ionomycin-evoked release from nerve terminals. Furthermore, protein kinase C (PKC) inhibition suppressed propofol-mediated facilitation of release. |
release from rat 1(0,0,0,1) | Details |
11934810 | Heredia MP, Fernandez-Velasco M, Benito G, Delgado C: Neuropeptide Y increases 4-aminopyridine-sensitive transient outward current in rat ventricular myocytes. Br J Pharmacol. 2002 Apr;135(7):1701-6. The effect of NPY on 4-AP I (to) density was prevented by pretreatment with 500 ng ml (-1) pertussis toxin (PTX) and by the specific protein kinase C (PKC) inhibitor, calphostin C (100 nM). 5. |
1(0,0,0,1) | Details |
14982967 | Wang SJ, Sihra TS: Noncompetitive metabotropic glutamate5 receptor antagonist (E)-2-methyl-6-styryl- (SIB1893) depresses release through inhibition of voltage-dependent Ca2+ entry in rat cerebrocortical nerve terminals (synaptosomes). J Pharmacol Exp Ther. 2004 Jun;309(3):951-8. Epub 2004 Feb 24. SIB1893 caused a potent inhibition of the Ca (2+)-dependent release of evoked by 4-aminopyridine (4AP). That the implied mGlu (5) R-mediated modulation was contingent on diacylglycerol stimulation of protein kinase C (PKC) was indicated by PKC activator phorbol dibutyrate and PKC inhibitor Ro 32-0432 (bisindolylmaleimide XI), respectively, superceding or suppressing the inhibitory effect of SIB1893. |
1(0,0,0,1) | Details |
12950453 | Craig TJ, Evans GJ, Morgan A: Physiological regulation of Munc18/nSec1 phosphorylation on serine-313. J Neurochem. 2003 Sep;86(6):1450-7. Munc18-1/nSec1 is essential for exocytosis in neurones, and is known to be phosphorylated by protein kinase C (PKC) in vitro at Ser-313. Furthermore, Ser-313 is rapidly and transiently phosphorylated in intact synaptosomes in response to depolarization by KCl treatment or by 4-aminopyridine, and by the metabotropic glutamate receptor agonist dihydroxyphenylglycine. |
1(0,0,0,1) | Details |
16093396 | Shen W, Hamilton SE, Nathanson NM, Surmeier DJ: Cholinergic suppression of KCNQ channel currents enhances excitability of striatal medium spiny neurons. J Neurosci. 2005 Aug 10;25(32):7449-58. Finally, acceleration of cholinergic interneuron spiking with 4-aminopyridine mimicked the effects of exogenous agonist application. Inhibition of protein kinase C reduced the efficacy of the muscarinic modulation. |
1(0,0,0,1) | Details |
19038273 | Chen GP, Ye Y, Li L, Yang Y, Qian AB, Hu SJ: Endothelium-independent vasorelaxant effect of on rat thoracic aorta. Life Sci. 2009 Jan 16;84(3-4):81-8. Epub 2008 Nov 14. The vasorelaxant effect of SF was unaffected by various K (+) channel blockers such as tetraethylammonium, glibenclamide, 4-aminopyridine, and barium In addition, SF concentration-dependently reduced the contraction induced by phorbol-12- -13- an activator of protein kinase C (PKC), in the absence of extracellular Ca (2+), with the pD (2) of 2.9+/-0.03. |
1(0,0,0,1) | Details |
18551429 | Liu YR, Ye WL, Zeng XM, Ren WH, Zhang YQ, Mei YA: K+ channels and the cAMP-PKA pathway modulate TGF-beta1-induced migration of rat vascular myofibroblasts. J Cell Physiol. 2008 Sep;216(3):835-43. Our previous studies have indicated that TGF-beta1 exerts its effect on the expression of A-type channels (I (A)) in rat vascular myofibroblasts by activation of protein kinase C during the phenotypic transformation of vascular fibroblasts to myofibroblasts. Blocking I (A) channel expression by 4-aminopyridine (4-AP) significantly inhibits TGF-beta1- and PMA-induced myofibroblast migration. |
1(0,0,0,1) | Details |
17362934 | Sculptoreanu A, de Groat WC: Neurokinins enhance excitability in neurons. . Exp Neurol. 2007 May;205(1):92-100. Epub 2007 Feb 14. The effects of SP were similar to the effect of heteropodatoxin II (0.05 microM) or low concentrations of 4-aminopyridine (50 microM) that block A-type K (+) currents. The effects of SP in C-R phasic neurons were fully reversed by an NK (2) receptor antagonist (MEN10376, 0.5 microM) but only partially by a protein kinase C (PKC) inhibitor (bisindolylmaleimide, 0.5 microM). |
-responsive DRG 1(0,0,0,1) | Details |
15769451 | Cogolludo A, Moreno L, Lodi F, Tamargo J, Perez-Vizcaino F: Postnatal maturational shift from PKCzeta and voltage-gated K+ channels to RhoA/Rho kinase in pulmonary vasoconstriction. Cardiovasc Res. 2005 Apr 1;66(1):84-93. Epub 2005 Jan 27. We therefore investigated the role of L-type Ca (2+) channels, protein kinase C (PKC) zeta, voltage-gated K (+) channels (K (V)), and RhoA/Rho kinase in TXA (2)-induced pulmonary vasoconstriction during postnatal maturation. This was consistent with a greater contraction to the K (V) inhibitor, 4-aminopyridine, and with a leftward shift in the increase in intracellular Ca (2+) by U46619 in newborn versus older animals. |
1(0,0,0,1) | Details |
11389202 | Ishikawa T, Takahashi T: Mechanisms underlying presynaptic facilitatory effect of cyclothiazide at the calyx of Held of juvenile rats. J Physiol. 2001 Jun 1;533(Pt 2):423-31. The magnitude of inhibition of presynaptic K (+) currents by CTZ (100 microM) was comparable to that by 5 microM 4-aminopyridine (4-AP). |
0(0,0,0,0) | Details |
15219818 | Jun JY, Choi S, Yeum CH, Chang IY, You HJ, Park CK, Kim MY, Kong ID, Kim MJ, Lee KP, So I, Kim KW: Substance P induces inward current and regulates pacemaker currents through tachykinin NK1 receptor in cultured interstitial cells of Cajal of murine small intestine. Eur J Pharmacol. 2004 Jul 8;495(1):35-42. Tetrodotoxin, nifedipine, tetraethylammonium, 4-aminopyridine, or glibenclamide did not change the frequency and amplitude of pacemaker currents. Substance P continued to produce tonic inward currents in external Ca2+-free solution or in the presence of chelerythrine, a protein kinase C inhibitor. |
1(0,0,0,1) | Details |
12687635 | Wang SJ, Su CF, Kuo YH: Fluoxetine depresses exocytosis in the rat cerebrocortical nerve terminals (synaptosomes) via inhibition of P/Q-type Ca2+ channels. Synapse. 2003 Jun 15;48(4):170-7. In the present study we investigated the effects of fluoxetine on 4-aminopyridine (4AP)-evoked release in cerebrocortical nerve terminals (synaptosomes). Furthermore, the inhibitory action of fluoxetine was completely abolished in synaptosomes pretreated with P/Q type Ca (2+) channel blocker omega-agatoxin IVA (omega-AgTX IVA) or protein kinase C (PKC) stimulator 4beta-phorbol 12, 13-dibutyrate (PDBu). |
1(0,0,0,1) | Details |
10884519 | Ko WH, Yao XQ, Lau CW, Law WI, Chen ZY, Kwok W, Ho K, Huang Y: Vasorelaxant and antiproliferative effects of Pretreatment with putative K (+) channel blockers, such as tetrapentylammonium ions (1-3x10 (-6) M), 4-aminopyridine (10 (-3) M), or Ba (2+) (3x10 (-4) M), significantly attenuated the -induced relaxation in endothelium-denuded arteries. |
. Eur J Pharmacol. 2000 Jul 7;399(2-3):187-96.0(0,0,0,0) | Details |
14623765 | White AM, Kylanpaa RA, Christie LA, McIntosh SJ, Irving AJ, Platt B: Presynaptic group I metabotropic glutamate receptors modulate synaptic transmission in the rat superior colliculus via 4-AP sensitive K (+) channels. Br J Pharmacol. 2003 Dec;140(8):1421-33. Epub 2003 Nov 17. The K+ channel antagonist 4-aminopyridine (4-AP, 50-100 microm) converted the inhibitory effect of into facilitation. |
0(0,0,0,0) | Details |
17822718 | Wang Y, Shi JG, Wang MZ, Che CT, Yeung JH: Mechanisms of the vasorelaxant effect of 1-coronary artery. Life Sci. 2007 Sep 1;81(12):1016-23. Epub 2007 Aug 17. In endothelium-denuded coronary artery rings, the vasorelaxant effect of HM-1 was unaffected by potassium channel blockers such as tetraethylammonium (10 mM), iberiotoxin (100 nM), barium (100 microM) and 4-aminopyridine (1 mM). |
-2, 3, 5-trimethoxy-xanthone, isolated from a Tibetan herb, Halenia elliptica, on rat 0(0,0,0,0) | Details |
18045622 | Wang Y, Shi JG, Wang MZ, Che CT, Yeung JH: Mechanisms of the vasorelaxant effect of 1, 5-dihydroxy-2, 3-dimethoxy-xanthone, an active metabolite of 1- -2, 3, 5-trimethoxy-xanthone isolated from a Tibetan herb, Halenia elliptica, on rat coronary artery. Life Sci. 2008 Jan 2;82(1-2):91-8. Epub 2007 Nov 1. The same concentration of HM-5 inhibited (by 62.3%) the contractile response to 10 microM phorbol 12, 13- (PDA), a protein kinase C activator, in Ca2+-free solutions. In endothelium-denuded coronary artery rings, the vasorelaxant effect of HM-5 was inhibited by a potassium channel blocker, TEA (10 mM), and 4-aminopyridine (4-AP, a K (v) blocker; 1 mM) but not by other K+ channel blockers such as iberiotoxin (100 nM), barium (100 microM) and glibenclamide (10 microM). |
1(0,0,0,1) | Details |
20221277 | Park SY, Shim JH, Kim M, Sun YH, Kwak HS, Yan X, Choi BC, Im C, Sim SS, Jeong JH, Kim IK, Min YS, Sohn UD: MLCK and PKC Involvements via Gi and Rho A Protein in Contraction by the Electrical Field Stimulation in Feline Esophageal Smooth Muscle. Korean J Physiol Pharmacol. 2010 Feb;14(1):29-35. Epub 2010 Feb 28. In this study, we investigated whether protein kinase C (PKC) may require the on-contraction in response to EFS using feline esophageal smooth muscle. The on-contraction was abolished in Ca (2+)-free buffer but reappeared in normal Ca (2+)-containing buffer indicating that the contraction was Ca (2+) dependent. 4-aminopyridine (4-AP), voltage-dependent K (+) channel blocker, significantly enhanced on-contraction. |
1(0,0,0,1) | Details |
15201307 | Yang K, Fujita T, Kumamoto E: inhibits GABAergic and glycinergic transmission in adult rat substantia gelatinosa neurons. J Neurophysiol. 2004 Nov;92(5):2867-77. Epub 2004 Jun 16. This reduction in frequency disappeared in the presence of a K+ -channel blocker (4-aminopyridine) but not in the absence of Ca2+. |
0(0,0,0,0) | Details |
11219402 | Blandizzi C, Colucci R, Tognetti M, De Paolis B, Del Tacca M: H3 receptor-mediated inhibition of intestinal release: pharmacological characterization of signal transduction pathways. Naunyn Schmiedebergs Arch Pharmacol. 2001 Feb;363(2):193-202. Tetraethylammonium or 4-aminopyridine, acting as inhibitors of voltage-dependent K+ channels, enhanced the evoked tritium outflow when tested alone, and apparently counteracted the inhibitory effect of |
0(0,0,0,0) | Details |
15910800 | Wang SJ, Chen HH: Ginkgolide B, a constituent of Ginkgo biloba, facilitates exocytosis from rat hippocampal nerve terminals. Eur J Pharmacol. 2005 May 9;514(2-3):141-9. Ginkgolide B facilitated the Ca2+-dependent release of evoked by 4-aminopyridine in a concentration-dependent manner. |
0(0,0,0,0) | Details |
10987837 | Sistiaga A, Sanchez-Prieto J: Protein phosphatase 1 and 2A inhibitors prolong the switch in the control of release by group I metabotropic glutamate receptors: characterization of the inhibitory pathway. J Neurochem. 2000 Oct;75(4):1566-74. This inhibitory action was suppressed by addition of the protein kinase C activator 4beta-phorbol 12,13-dibutyrate. |
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11597902 | Shimoda LA, Sylvester JT, Booth GM, Shimoda TH, Meeker S, Undem BJ, Sham JS: Inhibition of voltage-gated K (+) currents by endothelin-1 in human pulmonary arterial myocytes. Am J Physiol Lung Cell Mol Physiol. 2001 Nov;281(5):L1115-22. K (V) currents were isolated by addition of 100 nM charybdotoxin and were identified by current characteristics and inhibition by 4-aminopyridine (10 mM). Staurosporine (1 nM), a protein kinase C (PKC) inhibitor, abolished the effect of ET-1. |
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19605735 | Straub SV, Girouard H, Doetsch PE, Hannah RM, Wilkerson MK, Nelson MT: Regulation of intracerebral arteriolar tone by K (v) channels: effects of glucose and PKC. Am J Physiol Cell Physiol. 2009 Sep;297(3):C788-96. Epub 2009 Jul 15. Arteriolar constriction was prevented by inhibition of protein kinase C (PKC), consistent with previous studies showing enhanced PKC activity in the presence of elevated Isolated, pressurized parenchymal arterioles and arterioles in cortical brain slices exhibited robust constriction in the presence of the K (v) channel inhibitor 4-aminopyridine (4-AP). 4-AP also decreased the amplitude of K (v) currents recorded from SMCs. |
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