| Name | ATPase |
|---|---|
| Synonyms | ATP7A; MK; ATPase; Cation transporting ATPase; ATP7A protein; ATPase Cu(2+) transporting alpha polypeptide; Copper pump 1; Copper transporting ATPase 1… |
| Name | 4-aminopyridine |
|---|---|
| CAS | 4-pyridinamine |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 11719847 | Chiba T, Marcus DC: Basolateral K+ conductance establishes driving force for cation absorption by outer sulcus epithelial cells. J Membr Biol. 2001 Nov 15;184(2):101-12. On the other hand, TEA (20 mm), charybdotoxin (100 nm), apamin (100 nm), glibenclamide (10 microm), 4-aminopyridine (1 mm) and gadolinium (1 mm) had no significant effect. These data suggest that the large K+ conductance, in concert with the Na+,K+-ATPase, of the basolateral membrane of outer sulcus cells provides the driving force for cation entry across the apical membrane, thereby energizing vectorial cation absorption by this epithelium and contributing to the homeostasis of endolymph. |
1(0,0,0,1) | Details |
| 14532716 | Chang SJ, Cho ET, Heo GS, Park CG, Kim MW, Chang IY, Shin MK, Cha KH, Yeum CH, Jun JY: [Characterization of pacemaking currents in cultured interstitial cells of Cajal from mice small intestine]. Korean J Gastroenterol. 2003 Aug;42(2):121-7. Thapsigargin and cyclopiazoic acid, inhibitors of Ca2+-ATPase in endoplasmic reticulum, abolished pacemaker currents. In addition, tetraethylammonium, 4-aminopyridine and glibenclamide did not affect on the pacemaker currents. |
1(0,0,0,1) | Details |
| 11022968 | Storr M, Franck H, Saur D, Schusdziarra V, Allescher HD: Mechanisms of alpha,beta-methylene atp-induced inhibition in rat ileal smooth muscle: involvement of intracellular Ca2+ stores in purinergic inhibition. Clin Exp Pharmacol Physiol. 2000 Oct;27(10):771-9. The alpha,beta-MeATP-induced inhibition was blocked in a concentration-dependent manner in the presence of the K+ channel blocker apamin, but was unaffected by other K+ channel blockers, such as charybdotoxin (10 (-7) mol/L), 4-aminopyridine (10 (-4) mol/L), glibenclamide (10 (-5) mol/L) and tetraethylammonium (10 (-3) mol/L). 4. In order to investigate whether the internal Ca2+ stores participated in the inhibitory effect observed, we depleted internal Ca2+ stores with cyclopiazonic acid, a specific Ca2+-ATPase inhibitor. |
1(0,0,0,1) | Details |
| 12606650 | Wang XQ, Xiao AY, Yang A, LaRose L, Wei L, Yu SP: Block of Na+,K+-ATPase and induction of hybrid death by 4-aminopyridine in cultured cortical neurons. J Pharmacol Exp Ther. 2003 May;305(2):502-6. Epub 2003 Jan 21. |
33(0,1,1,3) | 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. However, substance P-induced tonic inward currents were blocked by thapsigargin, a Ca2+-ATPase inhibitor in the endoplasmic reticulum or by an external 1 mM Na+ solution. |
1(0,0,0,1) | Details |
| 15111247 | Amador FC, Santos MS, Oliveira CR: Lipid peroxidation and aluminium effects on the cholinergic system in nerve terminals. Neurotox Res. 2001 Jul;3(3):223-33. In the present study, we analyzed how aluminium and oxidative stress induced by /Fe (2+) affect the mechanisms related with the cholinergic system in a crude synaptosomal fraction isolated from rat brain. [(3) H] uptake, [(3) H] release, membrane potential and Na (+)/K (+)-ATPase activity were determined in the presence or in the absence of aluminium in control conditions and in the presence of (0.8 mM)/Fe (2+) (2.5 micro M). Additionally, aluminium potentiated the inhibition of the high-affinity [(3) H] uptake observed following lipid peroxidation and had the same effect on the Na (+)/K (+)-ATPase activity. [(3) H] release induced by 4-aminopyridine, and membrane potential were not significantly affected under oxidizing conditions, either in the absence or in the presence of aluminium. |
1(0,0,0,1) | Details |
| 14505131 | Aydin C, Sarac B, Koyuncu A, Yildirim S, Sen M, Sarioglu Y: Relaxant effect of and in guinea pig gallbladder muscle strips in vitro. J Gastroenterol. 2003;38(8):765-71. BACKGROUND: The aim of this study was to investigate the role of and H (+)-K (+) ATPase inhibitors, in gallbladder smooth muscle contractility in vitro. Pretreatment with atropine (1 microM), N (W)-nitro methyl ester (L-NAME; 30 microM), indomethacin (10 microM), ammonium (7.5 mM), (7.5 mM), tetraethylammonium (0.5 mM), glibenclamide (1 micro M), 4-aminopyridine (0.1 mM), or did not inhibit this relaxation. |
1(0,0,0,1) | Details |
| 10741431 | Wadsworth SJ, Chander A: H+-and K+-dependence of Ca2+ uptake in lung lamellar bodies. J Membr Biol. 2000 Mar 1;174(1):41-51. The inhibitors of Ca2+-activated K+-channels, tetraethylammonium, Penitrem A, and 4-aminopyridine, also inhibited the K+-dependent Ca2+ uptake at 700 nM Ca2+. At 100 nM Ca2+, the uptake was almost completely inhibited by bafilomycin A1, a selective inhibitor of vacuolar type H+-ATPase, or by NH4Cl, which raises the lamellar body pH, suggesting that the pH gradient regulates the uptake. |
1(0,0,0,1) | Details |
| 14684382 | Escobar LI, Martinez-Tellez JC, Salas M, Castilla SA, Carrisoza R, Tapia D, Vazquez M, Bargas J, Bolivar JJ: A voltage-gated K (+) current in renal inner medullary collecting duct cells. Am J Physiol Cell Physiol. 2004 Apr;286(4):C965-74. Epub 2003 Dec 18. Immunocytochemical analysis of cell culture and kidney inner medulla showed that Kv1.3 is colocalized with the Na (+)-K (+)-ATPase at the basolateral membrane, although it is also in the cytoplasm. It was inhibited by tetraethylammonium, quinidine, 4-aminopyridine, and Ba (2+) and was not Ca (2+) dependent. |
1(0,0,0,1) | Details |
| 19942549 | Ulusoy HB, Kaya MG: induced dilation in bovine coronary artery involves both inward rectifier channels and Na+ /K+ ATPase. Acta Physiol Hung. 2009 Dec;96(4):427-36. After a washout period, this procedure was repeated in presence of ouabain, a blocker of Na+ /K+ ATPase or a K+ channel blocker (tetraethylammonium, 4-aminopyridine, glibenclamide or barium). |
8(0,0,1,3) | Details |
| 19171133 | Yaktubay Dondas N, Karatas Y, Kaya D, Soylu N, Singirik E, Baysal F: Molecular mechanism of KCl-induced relaxation of the esophagus. . Eur J Pharmacol. 2009 Mar 1;605(1-3):123-8. Epub 2009 Jan 10. Similarly, potassium channel blockers such as 4-aminopyridine (4-AP; 100 microM) and tetraethylammonium (TEA; 100 microM) caused a significant inhibition on relaxations to KCl. In addition, ouabain (100 microM), a specific blocker of Na (+)-K (+)-ATPase, also caused a significant inhibition on these relaxations. |
2(0,0,0,2) | Details |
| 16330128 | Wang SJ: Facilitatory effect of on release from rat hippocampal 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. |
0(0,0,0,0) | Details |
| 19362578 | Subramaniam G, Achike FI, Mustafa MR: Effect of acidosis on the mechanism (s) of insulin-induced vasorelaxation in normal Wistar-Kyoto (WKY) rat aorta. Regul Pept. 2009 Jun 5;155(1-3):70-5. Epub 2009 Apr 10. The insulin effect was also significantly (p <0.05) inhibited by tetraethylammonium (TEA; BK (Ca) blocker), 4-Aminopyridine (4-AP; K (V) channel blocker), combined treatments (L-NAME+4-AP+TEA, in +ED tissues) or (4-AP+TEA, in -ED tissues). |
0(0,0,0,0) | Details |
| 20089711 | Zoer B, Cogolludo AL, Perez-Vizcaino F, De Mey JG, Blanco CE, Villamor E: Hypoxia sensing in the fetal chicken femoral artery is mediated by the mitochondrial electron transport chain. Am J Physiol Regul Integr Comp Physiol. 2010 Apr;298(4):R1026-34. Epub 2010 Jan 20. The relaxation was enhanced in the presence of the voltage-gated K (+) channel blocker 4-aminopyridine. |
0(0,0,0,0) | Details |
| 15464283 | Bradford SE, Nadler JV: release from rat hippocampal synaptosomes. Neuroscience. 2004;128(4):751-65. Both amino acids were released by 25 mM K (+), 300 microM 4-aminopyridine (4-AP) and 0.5 and 1 microM ionomycin in a predominantly Ca (2+)-dependent manner. |
0(0,0,0,0) | Details |
| 12110616 | Weston AH, Richards GR, Burnham MP, Feletou M, Vanhoutte PM, Edwards G: K+-induced hyperpolarization in rat mesenteric artery: identification, localization and role of Na+/K+-ATPases. Br J Pharmacol. 2002 Jul;136(6):918-26. RT-PCR, Western blotting and immunohistochemical techniques collectively showed the presence of alpha (1)-, alpha (2)- and alpha (3)-subunits of Na (+)/K (+)-ATPase in the myocytes. 6. In the presence of 10 microM (m.p. -33.7+/-3 mV), repolarization to 5 mM KCl did not occur in the presence or absence of 4-aminopyridine but was restored (-26.9+/-1.8 mV) on addition of iberiotoxin (100 nM). |
2(0,0,0,2) | Details |
| 10903955 | Jiang F, Li CG, Rand MJ: Mechanisms of -independent relaxations induced by carbachol and in rat isolated renal arteries. Br J Pharmacol. 2000 Jul;130(6):1191-200. These relaxations were not altered by 4-aminopyridine (4-AP), glibenclamide or apamin. The Na (+)-K (+) ATPase inhibitor ouabain reduced these relaxations in a concentration-dependent manner. 4. |
2(0,0,0,2) | Details |
| 12740420 | Yamanaka J, Nishimura J, Hirano K, Kanaide H: An important role for the Na+-Ca2+ exchanger in the decrease in cytosolic Ca2+ concentration induced by isoprenaline in the porcine coronary artery. J Physiol. 2003 Jun 1;549(Pt 2):553-62. Epub 2003 May 9. Various types of K+ channel blockers (iberiotoxin, 4-aminopyridine, apamin or glibenclamide) or combinations of these blockers failed to completely inhibit the Iso-induced decreases in [Ca2+] i and tension. |
0(0,0,0,0) | Details |
| 20051248 | Jin H, Hadri L, Palomeque J, Morel C, Karakikes I, Kaprielian R, Hajjar R, Lebeche D: KChIP2 attenuates cardiac hypertrophy through regulation of I (to) and intracellular signaling. J Mol Cell Cardiol. 2010 Jan 4. Interestingly, blocking I (to) with 4-aminopyridine in KChIP2-overexpressing adult cardiomyocytes significantly increased the Ca (2+) transients to control levels. |
0(0,0,0,0) | Details |
| 14978190 | Callera GE, Yogi A, Tostes RC, Rossoni LV, Bendhack LM: Ca2+-activated K+ channels underlying the impaired -induced vasodilation in 2K-1C hypertensive rats. J Pharmacol Exp Ther. 2004 Jun;309(3):1036-42. Epub 2004 Feb 20. The voltage-dependent K (+) channels inhibitor 4-aminopyridine attenuated -induced relaxation in both groups. |
0(0,0,0,0) | Details |
| 19642025 | Hiruma H, Kawakami T: Effects of 4-aminopyridine on organelle movement in cultured mouse dorsal root ganglion neurites. J Mol Neurosci. 2010 Mar;40(3):295-302. Epub 2009 Jul 30. The 4-AP-induced Brownian movement of lysosomes with vacuole formation and inhibition of axonal transport were prevented by the simultaneous treatment with vacuolar H (+) ATPase inhibitor bafilomycin A1 or in Cl (-)-free SO (4)(2-) medium. |
2(0,0,0,2) | Details |
| 11287496 | Inoue T, Lin X, Kohlmeier KA, Orr HT, Zoghbi HY, Ross WN: dynamics and electrophysiological properties of cerebellar Purkinje cells in SCA1 transgenic mice. J Neurophysiol. 2001 Apr;85(4):1750-60. receptor type 1 and the sarco/endoplasmic reticulum Ca (2+) ATPase pump, which regulate [Ca (2+)](i), are expressed at lower levels in these cells compared with the levels in cells from wild-type (WT) mice. This delay was increased by hyperpolarizing prepulses and was eliminated by 4-aminopyridine, which suggests that this delay was due to enhancement of the A-like K (+) conductance in the SCA1 PCs. |
1(0,0,0,1) | Details |
| 11030715 | Homer KL, Wanstall JC: Cyclic GMP-independent relaxation of rat pulmonary artery by a diazeniumdiolate donor. Br J Pharmacol. 2000 Oct;131(4):673-82. ODQ-resistant relaxation to (i. e. relaxation seen in the presence of 10 microM ODQ) was inhibited by (80 mM), charybdotoxin (300 nM), iberiotoxin (300 nM), apamin (100 nM), ouabain (1 mM) or thapsigargin (100 nM) but not by 4-aminopyridine (3 mM), glybenclamide (10 microM) or (10 microM). We conclude that, on rat pulmonary artery, can produce cyclic GMP-independent relaxation that involves, at least in part, activation of Na (+)/K (+)-ATPase, sarco-endoplasmic reticulum Ca (2+)-ATPase and -activated channels. |
1(0,0,0,1) | Details |
| 12763062 | Lee JH, Marcus DC: Endolymphatic homeostasis by Reissner's membrane. Neuroscience. 2003;119(1):3-8. I (sc) was also inhibited by an inhibitor of Na (+),K (+)-ATPase, ouabain, and by the K (+) channel blockers Ba (2+), 4-aminopyridine and quinine but not tetraethylammonium nor glibenclamide, consistent with the presence of a voltage-activated K (+) channel. |
0(0,0,0,0) | Details |
| 11374879 | Denda M, Ashida Y, Inoue K, Kumazawa N: Skin surface electric potential induced by ion-flux through epidermal cell layers. Biochem Biophys Res Commun. 2001 Jun 1;284(1):112-7. Disruption of mitochondrial function and inhibition of ATPase reduced the skin surface potential 50-70%. |
1(0,0,0,1) | Details |
| 11007532 | Wu L, Wang Z, Wang R: Tetraethylammonium-evoked oscillatory contractions of rat tail artery: a K-K model. Can J Physiol Pharmacol. 2000 Sep;78(9):696-707. The inhibition of Ca2+-ATPase in the sarcoplasmic reticulum with micromolar concentrations of thapsigargin or cyclopiazonic acid either abolished or enhanced, respectively, the TEA-induced oscillatory contractions. The voltage-dependent K+ (Kv) channel specific blocker, 4-aminopyridine (4-AP), induced a sustained, but not oscillated, vascular contraction. |
1(0,0,0,1) | Details |
| 11279259 | Ogita K, Hirata K, Bole DG, Yoshida S, Tamura Y, Leckenby AM, Ueda T: Inhibition of vesicular storage and exocytotic release by Rose Bengal. J Neurochem. 2001 Apr;77(1):34-42. This vesicular uptake inhibition was achieved largely without affecting H (+)-pump ATPase. We show that various degrees of reduction elicited by Rose Bengal in [(3) H] in synaptic vesicles inside the synaptosome result in a corresponding decrease in the amount of [(3) H] released in a depolarization- (induced by 4-aminopyridine) and Ca (2+)-dependent manner. |
1(0,0,0,1) | Details |
| 10658046 | Janssen LJ, Netherton SJ, Walters DK: Ca (2+)-dependent K (+) channels and Na (+)-K (+)-ATPase mediate H (2) O (2)- and -induced relaxations in canine trachealis. J Appl Physiol. 2000 Feb;88(2):745-52. These relaxations were decreased in magnitude and/or slowed by nifedipine (10 (-6) M), ouabain (10 (-6) M), or tetraethylammonium (25 mM), but not by 4-aminopyridine (5 mM), and were small or absent in tissues precontracted with 30 mM KCl. |
1(0,0,0,1) | Details |
| 17363384 | Armstrong ML, Dua AK, Murrant CL: initiates vasodilatation induced by a single skeletal muscle contraction in hamster cremaster muscle. J Physiol. 2007 Jun 1;581(Pt 2):841-52. Epub 2007 Mar 15. Muscle fibres were stimulated in the absence and presence of an inhibitor of a source of K (+), the voltage dependent K (+) channel inhibitor 3,4-diaminopyridine (DAP, 3 x 10 (-4) M) and inhibitors of the K (+) dilatory signal transduction pathway, either a Na (+) K (+)-ATPase inhibitor (ouabain; 10 (-4) M) or an inward rectifying K (+) channel inhibitor (barium BaCl (2); 5 x 10 (-5) M). |
1(0,0,0,1) | Details |