| Name | ERK1 |
|---|---|
| Synonyms | ERK 1; ERK1; ERT 2; ERT2; Extracellular signal regulated kinase 1; Extracellular signal related kinase 1b; Extracellular signal related kinase 1c; HS44KDAP… |
| Name | 4-aminopyridine |
|---|---|
| CAS | 4-pyridinamine |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 15086522 | Merlo D, Cifelli P, Cicconi S, Tancredi V, Avoli M: 4-Aminopyridine-induced epileptogenesis depends on activation of mitogen-activated protein kinase ERK. J Neurochem. 2004 May;89(3):654-9. Here, we studied the activation state of ERK1/2 in rat hippocampal slices during application of the K (+) channel blocker 4-aminopyridine (4AP, 50 micro m), a procedure that enhances synaptic transmission and leads to the appearance of epileptiform activity. |
34(0,1,1,4) | Details |
| 17537430 | Han W, Tang X, Wu H, Liu Y, Zhu D: Role of ERK1/2 signaling pathways in 4-aminopyridine-induced rat pulmonary vasoconstriction. Eur J Pharmacol. 2007 Aug 13;569(1-2):138-44. Epub 2007 Apr 30. |
9(0,0,1,4) | Details |
| 18845540 | Tauskela JS, Fang H, Hewitt M, Brunette E, Ahuja T, Thivierge JP, Comas T, Mealing GA: Elevated synaptic activity preconditions neurons against an in vitro model of ischemia. J Biol Chem. 2008 Dec 12;283(50):34667-76. Epub 2008 Oct 9. Specifically, exposing cultures to a K (+)-channel blocker, 4-aminopyridine (20-2500 microm), and a (A) receptor antagonist, bicuculline (50 microm) (4-AP/bic), for 1-2 days resulted in potent tolerance to normally lethal OGD applied up to 3 days later. Preconditioning induced phosphorylation of ERK1/2 and CREB which, along with Ca (2+) spiking and OGD tolerance, was eliminated by tetrodotoxin. |
4(0,0,0,4) | Details |
| 17005865 | Kalita K, Kharebava G, Zheng JJ, Hetman M: Role of megakaryoblastic acute leukemia-1 in ERK1/2-dependent stimulation of serum response factor-driven transcription by BDNF or increased synaptic activity. J Neurosci. 2006 Sep 27;26(39):10020-32. |
3(0,0,0,3) | Details |
| 15800056 | Guo TB, Lu J, Li T, Lu Z, Xu G, Xu M, Lu L, Dai W: Insulin-activated, K+-channel-sensitive Akt pathway is primary mediator of ML-1 cell proliferation. Am J Physiol Cell Physiol. 2005 Aug;289(2):C257-63. Epub 2005 Mar 30. Here we report that suppression of a voltage-gated K (+) channel with 4-aminopyridine (4-AP), barium, and tetraethylammonium inhibited both EGF- and insulin-stimulated myeloblastic leukemia ML-1 cell proliferation in a concentration-dependent manner. In serum-starved ML-1 cells, insulin rapidly stimulated phosphorylation of ERK1/2 and Akt, and the phosphorylation levels peaked approximately 30 min after treatment. |
2(0,0,0,2) | Details |
| 16183639 | Lenz G, Avruch J: Glutamatergic regulation of the p70S6 kinase in primary mouse neurons. . J Biol Chem. 2005 Nov 18;280(46):38121-4. Epub 2005 Sep 22. Brief glutamatergic stimulation of neurons from fetal mice, cultured in vitro for 6 days, activates the mTOR-S6 kinase, ERK1/2 and Akt pathways, to an extent approaching that elicited by brain-derived neurotrophic factor. After 12 days in culture, the response to direct glutamatergic activation is attenuated but can be uncovered by suppression of interneurons with bicuculline in the presence of the weak K (+) channel blocker 4-aminopyridine (4-AP). |
1(0,0,0,1) | Details |