| Name | cAMP dependent protein kinase (protein family or complex) |
|---|---|
| Synonyms | Protein kinase A; cAMP dependent protein kinase; cAMP dependent protein kinases |
| Name | 4-aminopyridine |
|---|---|
| CAS | 4-pyridinamine |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 12466248 | Wang SJ, Coutinho V, Sihra TS: Presynaptic cross-talk of beta-adrenoreceptor and 5-hydroxytryptamine receptor signalling in the modulation of release from cerebrocortical nerve terminals. Br J Pharmacol. 2002 Dec;137(8):1371-9. The presynaptic interactions between facilitatory beta-adrenoreceptors and inhibitory receptors modulating release from cerebrocortical nerve terminals were examined. 2. 4-aminopyridine (4-AP, 1 mM)-evoked release was facilitated by the membrane permeant cyclic-3',5'- (cAMP) analogue, 8-bromo-cAMP (8-Br-cAMP), used to directly activate cAMP-dependent protein kinase (PKA). 3. |
81(1,1,1,1) | 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. These results suggest that hyperthermia reduces release from pre-synaptic terminals, in part by blocking the adenylyl cyclase-protein kinase A signaling pathway and activating pre-synaptic 4-aminopyridine-sensitive K (+) channels. |
32(0,1,1,2) | Details |
| 18665350 | Ristori C, Cammalleri M, Martini D, Pavan B, Liu Y, Casini G, Dal Monte M, Bagnoli P: Involvement of the cAMP-dependent pathway in the reduction of epileptiform bursting caused by somatostatin in the mouse hippocampus. Naunyn Schmiedebergs Arch Pharmacol. 2008 Dec;378(6):563-77. Epub 2008 Jul 30. Using a well-established model of epileptiform activity induced by Mg (2+)-free medium with 4-aminopyridine [0 Mg (2+)/4-aminopyridine (4-AP)] in mouse hippocampal slices, we demonstrated that protein kinase A (PKA)-related signaling is upregulated by hippocampal bursting and that treatment with SRIF normalizes this upregulation. |
6(0,0,1,1) | Details |
| 12417644 | Xu Y, Chiamvimonvat N, Vazquez AE, Akunuru S, Ratner N, Yamoah EN: Gene-targeted deletion of neurofibromin enhances the expression of a transient outward K+ current in Schwann cells: a protein kinase A-mediated mechanism. J Neurosci. 2002 Nov 1;22(21):9194-202. However, Nf1-/- SCs showed a significant increase (approximately 1.5-fold) in a 4-aminopyridine-sensitive transient outward K+ current (I (A)). |
2(0,0,0,2) | Details |
| 15066141 | Mei YA, Vaudry D, Basille M, Castel H, Fournier A, Vaudry H, Gonzalez BJ: PACAP inhibits delayed rectifier current via a cAMP/PKA transduction pathway: evidence for the involvement of I k in the anti-apoptotic action of PACAP. Eur J Neurosci. 2004 Mar;19(6):1446-58. Addition of the specific protein kinase A inhibitor H89 in the patch pipette solution prevented the reduction of I (K) induced by both PACAP and dbcAMP. |
2(0,0,0,2) | Details |
| 18720421 | Yang TT, Wang SJ: and its human metabolite OPC14857 reduce, through a presynaptic mechanism, release in rat prefrontal cortex: possible relevance to neuroprotective interventions in schizophrenia. Synapse. 2008 Nov;62(11):804-18. Both and OPC13857 potently inhibited 4-aminopyridine (4-AP)-evoked release in a concentration-dependent manner. Moreover, or OPC13857 modulation of 4-AP-evoked release appears to involve a protein kinase A (PKA) signaling cascade, insofar as pretreatment of synaptosomes with the PKA inhibitor H89 suppressed the inhibitory effect of or OPC13857. |
1(0,0,0,1) | Details |
| 15237094 | Wu BN, Lin RJ, Lo YC, Shen KP, Wang CC, Lin YT, Chen IJ: KMUP-1, a derivative, induces relaxation of guinea-pig isolated trachea: the role of the epithelium, cyclic nucleotides and K+ channels. Br J Pharmacol. 2004 Aug;142(7):1105-14. Epub 2004 Jul 5. KMUP-1 (10 microm) increased the expression of protein kinase A (PKARI) and protein kinase G (PKG1alpha1beta) in a time-dependent manner, but this was only significant for PKG after 9 h. Tracheal relaxation induced by KMUP-1 was attenuated by epithelium removal and by pretreatment with inhibitors of soluble guanylate cyclase (sGC) (1H-[1,2,4] oxadiazolo [4,3-a] quinoxalin-1-one (ODQ), 1 microm), synthase (Nomega-nitro- methyl ester, 100 microm), K+ channels (tetraethylammonium, 10 mm), KATP channels (glibenclamide, 1 microm), voltage-dependent K+ channels (4-aminopyridine, 100 microm) and Ca2+-dependent K+ channels (charybdotoxin, 0.1 microm or apamin, 1 microm). |
1(0,0,0,1) | Details |
| 16151435 | Wu BN, Tu HF, Welsh DG, Chen IJ: KMUP-1 activates BKCa channels in basilar artery myocytes via cyclic nucleotide-dependent protein kinases. Br J Pharmacol. 2005 Nov;146(6):862-71. BKCa current activation by KMUP-1 was markedly inhibited by a soluble guanylate cyclase inhibitor (ODQ 10 microM), an adenylate cyclase inhibitor (SQ 22536 10 microM), competitive antagonists of and cAMP (Rp- 100 microM and Rp-cAMP, 100 microM), and - and cAMP-dependent protein kinase inhibitors (KT5823, 300 nM and KT5720, 300 nM). |
2(0,0,0,2) | Details |
| 17949708 | Chang Y, Huang WJ, Tien LT, Wang SJ: Ginsenosides Rg1 and Rb1 enhance release through activation of protein kinase A in rat cerebrocortical nerve terminals (synaptosomes). Eur J Pharmacol. 2008 Jan 6;578(1):28-36. Epub 2007 Oct 2. Result showed that the Ca (2+)-dependent release of evoked by 4-aminopyridine was facilitated by ginsenoside Rg1 or Rb1 in a concentration-dependent manner. |
2(0,0,0,2) | Details |
| 12782184 | Wang SJ: Cannabinoid CB1 receptor-mediated inhibition of release from rat hippocampal synaptosomes. Eur J Pharmacol. 2003 May 23;469(1-3):47-55. Using synaptosomal preparation, I show here that 2,3-dihydro-5-methyl-3-(4-morpholinyl-methyl)-pyrrolo-1,4-benzoxazin-6-yl- 1-naphthalenylmethanone (WIN 55212-2) strongly depressed 4-aminopyridine-evoked release in a concentration-dependent manner, and this effect was reversed by the selective cannabinoid CB (1) receptor antagonist 1-(2,4-dichlorophenyl)-5-(4-iodophenyl)-4-methyl-N-4-morpholinyl-1H-pyrazo le-3-carboxamide (AM 281). |
0(0,0,0,0) | Details |
| 17498241 | Xu F, Tse FW, Tse A: Pituitary adenylate cyclase-activating polypeptide (PACAP) stimulates the sensing type I (glomus) cells of rat carotid bodies via reduction of a background TASK-like K+ current. J Neurochem. 2007 Jun;101(5):1284-93. H89, a protein kinase A (PKA) inhibitor attenuated the PACAP response. In the presence of tetraethylammonium (TEA) and 4-aminopyridine (4-AP), PACAP reduced a background K (+) current. |
1(0,0,0,1) | Details |
| 12626609 | Jeong HJ, Jang IS, Nabekura J, Akaike N: Adenosine A1 receptor-mediated presynaptic inhibition of GABAergic transmission in immature rat hippocampal CA1 neurons. J Neurophysiol. 2003 Mar;89(3):1214-22. It was concluded that the activation of presynaptic Alpha (1) receptors modulates the probability of spontaneous release via cAMP- and protein kinase A dependent pathway. K (+) channel blockers, 4-aminopyridine (100 microM) and Ba (2+) (1 mM), had no effect on the inhibitory effect of CPA on GABAergic mIPSC frequency. |
1(0,0,0,1) | Details |
| 12668054 | Wang SJ, Sihra TS: Opposing facilitatory and inhibitory modulation of release elicited by cAMP production in cerebrocortical nerve terminals (synaptosomes). Neuropharmacology. 2003 Apr;44(5):686-97. Activation of cAMP-protein kinase A (PKA) is widely reported to facilitate synaptic transmission. The adenylyl cyclase (AC) activator, forskolin, failed to have any effect on 4-aminopyridine (4-AP)-evoked release, when added alone. |
1(0,0,0,1) | 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. These results suggest that ginkgolide B effects a increase in protein kinase A activation, which subsequently enhances the Ca2+ entry through voltage-dependent N- and P/Q-type Ca2+ channels to cause a increase in evoked release from rat hippocampal nerve terminals. |
1(0,0,0,1) | Details |
| 18702677 | Coutts CA, Balt LN, Ali DW: Protein kinase A modulates A-type currents of larval zebrafish (Danio rerio) white muscle fibres. Acta Physiol. 2009 Feb;195(2):259-72. Epub 2008 Sep 20. |
1(0,0,0,1) | Details |
| 17277021 | Luykenaar KD, Welsh DG: Activators of the PKA and PKG pathways attenuate RhoA-mediated suppression of the KDR current in cerebral arteries. Am J Physiol Heart Circ Physiol. 2007 Jun;292(6):H2654-63. Epub 2007 Feb 2. This study tested whether activation of protein kinase A (PKA) and G (PKG) pathways would attenuate the ability of RhoA to suppress the delayed rectifier K (+) current and limit agonist-induced depolarization and constriction. An increase in K (V) channel activity was found to partly underlie these associated changes, as constriction to 4-aminopyridine channel blocker) was greater after PKA or PKG activation. |
1(0,0,0,1) | Details |
| 17606273 | Mato S, Lafourcade M, Robbe D, Bakiri Y, Manzoni OJ: Role of the cyclic-AMP/PKA cascade and of P/Q-type Ca++ channels in endocannabinoid-mediated long-term depression in the nucleus accumbens. Neuropharmacology. 2008 Jan;54(1):87-94. Epub 2007 May 5. In contrast, eCB-LTD was blocked by treatment of the slices with the adenylyl cyclase (AC) activator forskolin (10 microM), and with the protein kinase A (PKA) inhibitor KT5720 (1 microM) (fEPSP=108.9+/-5.7% in forskolin and 110.5+/-7.7% in KT5720, compared to 80.6+/-3.9% in control conditions). |
1(0,0,0,1) | Details |
| 16234412 | Lin RJ, Wu BN, Lo YC, An LM, Dai ZK, Lin YT, Tang CS, Chen IJ: A -based epithelium-dependent airway relaxant KMUP-3 (7-[2-[4-(4-nitrobenzene) piperazinyl] ethyl]- increases respiratory performance and protects against tumor necrosis factor-alpha-induced tracheal contraction, involving release and expression of and protein kinase G. J Pharmacol Exp Ther. 2006 Feb;316(2):709-17. Epub 2005 Oct 18. In isolated trachea precontracted with carbachol, KMUP-3 (10-100 microM)-caused relaxations were attenuated by epithelium removal and by pretreatments with an inhibitor of K (+) channel, tetraethylammonium (10 mm); K (ATP) channel, glibenclamide (1 microM); voltage-dependent K (+) channel, 4-aminopyridine (100 microM); Ca (2+)-dependent K (+) channel, charybdotoxin (0.1 microM) or apamin (1 microM); soluble guanylate cyclase (sGC), 1H-[1,2,4] oxadiazolo [4,3-a] quinoxalin-1one (ODQ, 1 microM); (NO) synthase, N (omega)-nitro- methyl ester (L-NAME, 100 microM); and adenylate cyclase, SQ 22536 [9-(terahydro-2-furanyl)- (100 microM). Western blot analysis indicated that KMUP-3 (1 microM) induced expression of protein kinase A (PKA)(ri) and protein kinase G (PKG)(1alpha 1beta) in TSMCs.SQ 22536 inhibited KMUP-3-induced expression of (PKA)(ri). |
1(0,0,0,1) | Details |
| 17322023 | Moritz A, Gust R, Pertz HH: Characterization of the relaxant response to N,N'-dipropyl-1,2-bis (2,6-dichloro-4-hydroxyphenyl) ethylenediamine in porcine coronary arteries. J Pharmacol Exp Ther. 2007 May;321(2):699-706. Epub 2007 Feb 22. The relaxant response to 8 was unaffected by the estrogen receptor antagonist ICI 182,780 (7alpha-[9-[(4,4,5,5,5-pentafluoropentyl]-sulfinyl] nonyl]-estra-1,3,5 (10)- triene-3,17beta-diol) and K+ channel blockers, i.e., TEA, glibenclamide, and 4-aminopyridine. Furthermore, the vasodilatory effect of 8 was unaffected by the adenylyl cyclase inhibitor SQ 22536 [9-(tetrahydro-2-furanyl)- the guanylyl cyclase inhibitor ODQ [1H-[1,2,4] oxadiazolo [4,3-a] quinoxalin-1-one], the protein kinase A inhibitor KT 5720 [(9S,10S,12R)-2,3,9,10,11,12-hexahydro-10--9-methyl-1-oxo-9,12-epox y-1H-diindolo [1,2,3-fg: 3',2',1'-kl] pyrrolo [3,4-i][1,6] benzodiazocine-10-carboxylic acid hexyl ester], the protein kinase G inhibitor KT 5823 [(9S,10R,12R)-2,3,9,10,11,12-hexahydro-10-methoxy-2,9-dimethyl-1-oxo-9,12- epoxy-1H-diindolo [1,2,3-fg:3',2',1'-kl] pyrrolo [3,4-i][1,6] benzodiazocine-1 0-carboxylic acid methyl ester], and the p38 mitogen-activated protein kinase (MAPK) inhibitor SB 203580 [4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)- . |
1(0,0,0,1) | Details |
| 11588168 | Jovanovic JN, Sihra TS, Nairn AC, Hemmings HC Jr, Greengard P, Czernik AJ: Opposing changes in phosphorylation of specific sites in synapsin I during Ca2+-dependent release in isolated nerve terminals. J Neurosci. 2001 Oct 15;21(20):7944-53. We demonstrate that, in vitro, phosphorylation sites 1, 2, and 3 of synapsin I (P-site 1 phosphorylated by cAMP-dependent protein kinase; P-sites 2 and 3 phosphorylated by Ca (2+)-calmodulin-dependent protein kinase II) were excellent substrates for protein phosphatase 2A, whereas P-sites 4, 5, and 6 (phosphorylated by mitogen-activated protein kinase) were efficiently dephosphorylated only by Ca (2+)-calmodulin-dependent protein phosphatase 2B-calcineurin. |
1(0,0,0,1) | Details |
| 11790809 | Lien CC, Martina M, Schultz JH, Ehmke H, Jonas P: Gating, modulation and subunit composition of voltage-gated K (+) channels in dendritic inhibitory interneurones of rat hippocampus. J Physiol. 2002 Jan 15;538(Pt 2):405-19. Voltage-gated K (+) currents in nucleated patches isolated from OA interneurones consisted of three major components: a fast delayed rectifier K (+) current component that was highly sensitive to external 4-aminopyridine (4-AP) and tetraethylammonium (TEA) (half-maximal inhibitory concentrations < 0.1 mM for both blockers), a slow delayed rectifier K (+) current component that was sensitive to high concentrations of TEA, but insensitive to 4-AP, and a rapidly inactivating A-type K (+) current component that was blocked by high concentrations of 4-AP, but resistant to TEA. This inhibition was absent in the presence of the protein kinase A (PKA) inhibitor H-89, implying the involvement of PKA-mediated phosphorylation. |
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. In the present study, patch-clamp whole-cell recording and transwell-migration assays were used to examine the effects of TGF-beta1- and phorbol 12- 13- (PMA)-induced expression of I (A) channels on myofibroblast migration and its modulation by the protein kinase A (PKA) pathway. 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 |
| 12684454 | Dong Y, White FJ: D1-class receptors selectively modulate a slowly inactivating current in rat medial prefrontal cortex pyramidal neurons. J Neurosci. 2003 Apr 1;23(7):2686-95. Inhibition of protein kinase A (PKA) with either PKI or Rp-cAMP abolished D1R modulation. The A-type current (I (A)), with rapid activation and inactivation kinetics, was completely inactivated by prolonged holding of the membrane potential at -40 mV and was sensitive to the K (+) channel blocker 4-aminopyridine (4-AP) but not tetraethylammonium (TEA) or dendrotoxin (DTX). |
1(0,0,0,1) | Details |
| 11801366 | Doi A, Ishibashi H, Jinno S, Kosaka T, Akaike N: Presynaptic inhibition of GABAergic miniature currents by metabotropic glutamate receptor in the rat CNS. Neuroscience. 2002;109(2):299-311. The application of K+ channel blockers such as 4-aminopyridine, Cs+, Ba2+ or tetraethylammonium increased the mIPSC frequency, but failed to inhibit the tACPD action on mIPSC. |
0(0,0,0,0) | Details |
| 16153635 | Zhang Y, Pertens E, Janssen LJ: 8-isoprostaglandin E (2) activates Ca (2+)-dependent K (+) current via cyclic AMP signaling pathway in murine renal artery. Eur J Pharmacol. 2005 Sep 27;520(1-3):22-8. This augmentation was observed in the presence of 4-aminopyridine (4-AP, 10 (-3) M) but not that of charybdotoxin (Ch Tx, 10 (-7) M). |
0(0,0,0,0) | Details |
| 10564084 | van Den Abbeele T, Teulon J, Huy PT: Two types of voltage-dependent channels in outer hair cells from the guinea pig cochlea. Am J Physiol. 1999 Nov;277(5 Pt 1):C913-25. It was not sensitive to internal Ca (2+), was inhibited by 4-aminopyridine, was activated by depolarization above -30 mV, and exhibited a rundown after excision. |
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 |
| 12548092 | Andre E, Malheiros A, Cechinel-Filho V, Yunes RA, Calixto JB: Role of and K+ channels in relaxation induced by polygodial in rabbit corpus cavernosum in vitro. J Cardiovasc Pharmacol. 2003 Feb;41(2):300-6. In contrast, apamin, charybdotoxin, and 4-aminopyridine or the protein kinase A inhibitor KT 5720 all failed to affect either polygodial or -mediated relaxation in these preparations. |
0(0,0,0,0) | Details |