| Name | G protein |
|---|---|
| Synonyms | G gamma I; Guanine nucleotide binding protein 2; G protein; GNG 2; GNG2; GNGT 2; GNGT2; Guanine nucleotide binding protein gamma 2… |
| Name | 4-aminopyridine |
|---|---|
| CAS | 4-pyridinamine |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 12208771 | Rautureau Y, Toumaniantz G, Serpillon S, Jourdon P, Trochu JN, Gauthier C: Beta 3-adrenoceptor in rat aorta: molecular and biochemical characterization and signalling pathway. Br J Pharmacol. 2002 Sep;137(2):153-61. In addition, iberotoxin (0.1 microM), glibenclamide (1 microM) and 4-aminopyridine (1 mM), selective channels blockers of K (Ca), K (ATP), and K (v) respectively, decreased the SR 58611A-mediated relaxation. 5. To identify the G protein linked to beta (3)-AR, experiments were performed in rat pre-treated with PTX (10 microg kg (-1)), a G (i/0) protein inhibitor. |
1(0,0,0,1) | Details |
| 15051151 | Fioretti B, Catacuzzeno L, Tata AM, Franciolini F: activates a background, -sensitive K channel in embryonic chick dorsal root ganglion neurons. Neuroscience. 2004;125(1):119-27. The channel was insensitive to the classical K channel blockers tetraethylammonium, charybdotoxin, 4-aminopyridine, but inhibited by millimolar Ba2+. Experiments aimed at delineating the metabotropic pathway leading to K channel activation by indicated the involvement of a pertussis toxin-insensitive G protein, and a quinacrine-sensitive cytosolic phospholipase A2. |
1(0,0,0,1) | Details |
| 11877514 | Watabe AM, Carlisle HJ, O'Dell TJ: Postsynaptic induction and presynaptic expression of group 1 mGluR-dependent LTD in the hippocampal CA1 region. J Neurophysiol. 2002 Mar;87(3):1395-403. -induced LTD was blocked when the G-protein inhibitor -5'-O-(2-thiodiphosphate) was selectively delivered into postsynaptic CA1 pyramidal cells via an intracellular recording electrode, suggesting that depresses synaptic transmission through a postsynaptic, GTP-dependent signaling pathway. Enhancing Ca (2+) influx by prolonging action potential duration with bath applications of the K (+) channel blocker 4-aminopyridine (4-AP) also strongly reduced the effects of in the presence of normal [Ca (2+)](o) (2 mM). |
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| 18073555 | Zahn PK, Straub H, Wenk M, Pogatzki-Zahn EM: A1 but not A2a receptor agonist reduces hyperalgesia caused by a surgical incision in rats: a pertussis toxin-sensitive G protein-dependent process. Anesthesiology. 2007 Nov;107(5):797-806. Furthermore, A1R-induced spinal antinociception is mediated by interactions with pertussis toxin-sensitive G proteins. In separate groups of animals, the effects of pertussis toxin, forskolin, glibenclamide, 4-aminopyridine, tetraethylammonium, apamin, charybdotoxin, or margatoxin on R-PIA-induced antinociception were examined. |
1(0,0,0,1) | Details |
| 15322267 | Choisy SC, Hancox JC, Arberry LA, Reynolds AM, Shattock MJ, James AF: Evidence for a novel K (+) channel modulated by alpha (1A)-adrenoceptors in cardiac myocytes. Mol Pharmacol. 2004 Sep;66(3):735-48. Furthermore, the PE-sensitive current was partially inhibited by external administration of high concentrations of tetraethylammonium and 4-aminopyridine, which are voltage-gated K (+) channel-blockers. I (ss,PE) resulted from PE activation of the alpha (1A)-AR subtype, involved a pertussis toxin-insensitive G-protein, and was independent of cytosolic Ca (2+). |
1(0,0,0,1) | Details |
| 10790326 | Galindo BE, Beltran C, Cragoe EJ Jr, Darszon A: Participation of a K (+) channel modulated directly by in the speract-induced signaling cascade of strongylocentrotus purpuratus sea urchin sperm. Dev Biol. 2000 May 15;221(2):285-94. The G protein activators AlF (-)(4) and mastoparan also are ineffective. |
1(0,0,0,1) | Details |
| 15034129 | Daniel H, Rancillac A, Crepel F: Mechanisms underlying cannabinoid inhibition of presynaptic Ca2+ influx at parallel fibre synapses of the rat cerebellum. J Physiol. 2004 May 15;557(Pt 1):159-74. Epub 2004 Mar 19. The present study demonstrates that the molecular mechanisms underlying the CB1 inhibitory effect involve the activation of the PTX-sensitive G (i)/G (o) subclass of G proteins, independently of any direct effect on presynaptic Ca (2+) channels (N, P/Q and R (SNX-482-sensitive) types) or on adenylate cyclase or MAPK activity, but do require the activation of G protein-gated inwardly rectifying (Ba (2+)- and tertiapin Q-sensitive) K (+) channels, in addition to 4-aminopyridine-sensitive K (+) channels. |
32(0,1,1,2) | 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. The alpha,beta-MeATP-induced inhibition was unaffected by pretreatment with atropine (10 (-6) mol/L), phentolamine (10 (-6) mol/L), (10 (-6) mol/L), nitrendipine (10 (-7) mol/L), pertussis toxin (10 (-6) mol/L) NG-nitro- (3 x 10 (-4) mol/L) and tetrodotoxin (10 (-6) mol/L), excluding an involvement of adrenergic, cholinergic, neural, nitrinergic or G-protein involvement in purinergic-mediated inhibition. 5. |
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| 10670420 | Jarolimek W, Baurle J, Misgeld U: Impaired inhibition of epileptiform activity by baclofen, but not by in the weaver hippocampus. Neuropharmacology. 2000 Jan 4;39(2):246-53. Pore mutation in a G protein-gated inwardly rectifying K+ channel subunit causes loss of K+ dependent inhibition in weaver hippocampus. |
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| 12694926 | Sayin U, Rutecki PA: Group I metabotropic glutamate receptor activation produces prolonged epileptiform neuronal synchronization and alters evoked population responses in the hippocampus. Epilepsy Res. 2003 Mar;53(3):186-95. activates a class of receptors coupled to G-proteins that initiate second messenger cascades, change ion channel function, cause release of from intracellular stores, and produce long-term changes in synaptic strength. To test the possibility that a reduction of the first evoked population spike and loss of inhibition of a second evoked population spike generated prolonged ictal discharges, we used 4-aminopyridine (4-AP 50 microM) to enhance synaptic transmission. 4-AP converted ictal discharges produced by to an interictal pattern of synchronous activity, reversed the -induced reduction in the first evoked population spike, and changed paired-pulse facilitation to inhibition. |
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| 16806307 | Schoffelmeer AN, Hogenboom F, Wardeh G, De Vries TJ: Interactions between CB1 cannabinoid and mu opioid receptors mediating inhibition of neurotransmitter release in rat nucleus accumbens core. Neuropharmacology. 2006 Sep;51(4):773-81. Epub 2006 Jun 30. It is proposed that these allosterically interacting mu and CB1 receptors in the NAc core may represent G-protein coupled heterodimeric receptor complexes. To that end, receptor-mediated inhibition of depolarization (4-aminopyridine)-induced [3H] release and (NMDA) receptor-stimulated [14C] and [3H] release was studied in superfused NAc core slices. |
1(0,0,0,1) | Details |
| 15196683 | Borasio PG, Cervellati F, Pavan B, Pareschi MC: "Low" concentrations of inhibit neurotransmitter release from the guinea-pig superior cervical ganglion. Neurosci Lett. 2004 Jul 1;364(2):86-9. -induced inhibition was counteracted by the G protein blocker sulmazole (1 mM), forskolin and alteration of influx by increasing [Ca2+] out from 2.2 to 6 mM, raising the rate of stimulation (10 Hz, 30 s), or broadening the presynaptic action potential with 10 microM 4-aminopyridine and 50 microM tetraethylammonium |
33(0,1,1,3) | 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. |
0(0,0,0,0) | Details |
| 10585528 | Gardner NM, Broadley KJ: Resistance to antagonism of atrial P (1) purinoceptor responses in the presence of K (+) channel blockade. Eur J Pharmacol. 1999 Oct 27;383(2):143-53. The rate of onset of the negative inotropic responses of guinea-pig isolated paced atria to the receptor agonist, N (6)-cyclopentyladenosine, was significantly slowed by the K (+) channel inhibitor, 4-aminopyridine (10 mM). |
0(0,0,0,0) | Details |
| 15028525 | Corti A, Mannarino C, Mazza R, Angelone T, Longhi R, Tota B: Chromogranin A N-terminal fragments vasostatin-1 and the synthetic CGA 7-57 peptide act as cardiostatins on the isolated working frog heart. Gen Comp Endocrinol. 2004 Apr;136(2):217-24. On the contrary, it was dependent from both extracellular Ca (2+) and K (+) channels, since it was abolished by pretreatment to either the Ca (2+) channel inhibitors lanthanum and or the K (+) channel inhibitors Ba (2+), 4-aminopyridine, tetraethylammonium and glibenclamide. |
0(0,0,0,0) | Details |
| 17320058 | Gotow T, Nishi T: Involvement of a Go-type G-protein coupled to guanylate cyclase in the phototransduction cascade of molluscan simple photoreceptors. Brain Res. 2007 May 4;1144:42-51. Epub 2007 Jan 26. The specific channel blocker, 4-aminopyridine (4-AP), and a GC inhibitor, LY-83583, both suppressed this hyperpolarizing photocurrent. |
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| 11489454 | Jeong HJ, Han SH, Min BI, Cho YW: 5-HT1A receptor-mediated activation of G-protein-gated inwardly rectifying K+ current in rat periaqueductal gray neurons. Neuropharmacology. 2001 Aug;41(2):175-85. I5-HT was sensitive to K+ channel blockers such as quinine and Ba2+, but insensitive to 4-aminopyridine, Cs+ and tetraethylammonium. |
2(0,0,0,2) | 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. 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. Aluminum (a G-protein activator) increased on-contraction. |
2(0,0,0,2) | Details |
| 18367171 | Lee JJ, Hahm ET, Lee CH, Cho YW: 5-HT1A receptor-mediated activation of a G-protein-coupled inwardly rectifying K+ current in rat medial preoptic area neurons. Eur J Pharmacol. 2008 May 31;586(1-3):114-22. Epub 2008 Mar 4. The -activated K+ current was sensitively blocked by Ba2+, but not by 4-aminopyridine, and was completely suppressed by N-ethylmaleimide. |
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 |
| 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. Aluminum (a G-protein activator) increased off-contraction. |
2(0,0,0,2) | Details |
| 11906950 | Wittmann S, Frohlich D, Daniels S: Characterization of the human fMLP receptor in neutrophils and in Xenopus oocytes. Br J Pharmacol. 2002 Mar;135(6):1375-82. We report functional expression in Xenopus oocytes of human fMLP-R98 cDNA, without co-expression of the promiscuous G-protein subunit, Galpha-16. 2. |
2(0,0,0,2) | Details |
| 15879679 | Matsuda T, Takeda K, Ito M, Yamagishi R, Tamura M, Nakamura H, Tsuruoka N, Saito T, Masumiya H, Suzuki T, Iida-Tanaka N, Itokawa-Matsuda M, Yamashita T, Tsuruzoe N, Tanaka H, Shigenobu K: Atria selective prolongation by NIP-142, an antiarrhythmic agent, of refractory period and action potential duration in guinea pig myocardium. J Pharmacol Sci. 2005 May;98(1):33-40. Epub 2005 May 7. In the present study, we examined the effects of NIP-142 on isolated guinea pig myocardium and on the G-protein-coupled inwardly rectifying potassium channel current -activated current; I (KACh)) expressed in Xenopus oocytes. E-4031 and 4-aminopyridine prolonged action potential duration in both left atrium and right ventricle. |
1(0,0,0,1) | Details |
| 15488297 | Hahm ET, Lee JJ, Min BI, Cho YW: Opioid inhibition of GABAergic neurotransmission in mechanically isolated rat periaqueductal gray neurons. Neurosci Res. 2004 Nov;50(3):343-54. In addition, K (+) channels blockers, Ba (2+) or 4-aminopyridine, did not affect the DAMGO effect. The present study indicates that activation of presynaptic mu-opioid receptors coupled to G-proteins inhibits release through unknown intracellular mechanisms downstream of Ca (2+) influx. |
1(0,0,0,1) | Details |
| 12742827 | Dantas AP, Igarashi J, Michel T: and control of vascular tone. Am J Physiol Heart Circ Physiol. 2003 Jun;284(6):H2045-52. Taken together, our findings demonstrate that S1P, an important intercellular mediator of platelet-vessel wall interactions, is a effective arteriolar vasodilator that acts via G protein-dependent, -sensitive, and PI3-kinase-modulated signaling pathways. S1P-induced vasodilation is abrogated by removal of endothelium or by the addition of the NOS inhibitor N (omega)-monomethyl- but is not affected by the cyclooxygenase inhibitor indomethacin, nor by the blockade of K (+) channels by using 4-aminopyridine. |
1(0,0,0,1) | Details |
| 12629172 | Gebremedhin D, Yamaura K, Zhang C, Bylund J, Koehler RC, Harder DR: Metabotropic glutamate receptor activation enhances the activities of two types of Ca2+-activated k+ channels in rat hippocampal astrocytes. J Neurosci. 2003 Mar 1;23(5):1678-87. Patch-clamp analysis of K (+) channel currents in cultured astrocytes identified the existence of 71 +/- 6 and 161 +/- 11 pS single-channel K (+) currents that were sensitive to changes in voltage and [Ca (2+)](i) and blocked by external TEA but not by charybdotoxin, iberiotoxin, apamin, or 4-aminopyridine. These results indicate that brain astrocytes contain the KCNMB4 transcript and express two novel types of K (Ca) channels that are gated by activation of a G-protein coupled metabotropic glutamate receptor functionally linked to PLC and cytochrome P450 epoxygenase activity. |
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| 15824193 | Gomez Mdel P, Nasi E: On the gating mechanisms of the light-dependent conductance in Pecten hyperpolarizing photoreceptors: does light remove inactivation in voltage-dependent K channels?. J Gen Physiol. 2005 May;125(5):455-64. Epub 2005 Apr 11. Exploiting the information that has become available on the phototransduction cascade of ciliary photoreceptors, we demonstrated that the same downstream signaling elements are implicated in the modulation of voltage-elicited currents: direct chemical stimulation both at the level of the G protein and of the final messenger that controls the light-dependent channels also attenuate the falling phase of the voltage-activated current. Although millimolar 4-aminopyridine (4-AP) suppressed both currents, at micromolar concentrations only the photocurrent was blocked. |
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| 15051158 | Wang SJ, Wang KY, Wang WC: Mechanisms underlying the riluzole inhibition of release from rat cerebral cortex nerve terminals (synaptosomes). Neuroscience. 2004;125(1):191-201. Riluzole inhibited the -dependent release of that was evoked by exposing cerebrocortical synaptosomes to the potassium channel blocker 4-aminopyridine, and this presynaptic inhibition was concentration-dependent. This release inhibition may involve a pertussis toxin-sensitive G protein signalling pathway. |
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