| Name | myelin basic protein |
|---|---|
| Synonyms | HMBP; MBP; Myelin A1 protein; Myelin basic protein; Myelin membrane encephalitogenic protein; Myelin A1 proteins; Myelin basic proteins; Myelin membrane encephalitogenic proteins |
| Name | 4-aminopyridine |
|---|---|
| CAS | 4-pyridinamine |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 15378653 | Bacia A, Wollmann R, Soliven B: K+ channel blockade impairs remyelination in the cuprizone model. Glia. 2004 Nov 1;48(2):156-65. We found that treatment with 4-aminopyridine (4-AP), a broad-spectrum K (+) channel antagonist, results in: (1) decreased number of oligodendroglial progenitors (OP) and OLGs; (2) diminished astrogliosis; and (3) decreased remyelination in the corpus callosum based on the immunoreactivity to myelin basic protein (MBP), Rip monoclonal antibody, and by electron microscopy. |
31(0,1,1,1) | Details |
| 15869936 | Eftekharpour E, Karimi-Abdolrezaee S, Sinha K, Velumian AA, Kwiecien JM, Fehlings MG: Structural and functional alterations of spinal cord axons in adult Long Evans Shaker (LES) dysmyelinated rats. Exp Neurol. 2005 Jun;193(2):334-49. These rats have a spontaneous mutation of the gene encoding myelin basic protein which results in severe dysmyelination of the central nervous system (CNS), providing a unique model for demyelinating/dysmyelinating disorders. Abnormal electrophysiological properties including attenuation of CAP amplitude and conduction velocity, high frequency conduction failure and enhanced sensitivity to K+ channel blockers 4-aminopyridine and dendrotoxin-I were observed in spinal cord axons from LES rats. |
1(0,0,0,1) | Details |
| 10822089 | Strauss U, Wissel K, Jung S, Wulff H, Hansel W, Zhu J, Rolfs A, Mix E: K (+) channel-blocking alkoxypsoralens inhibit the immune response of encephalitogenic T line cells and lymphocytes from Lewis rats challenged for experimental autoimmune encephalomyelitis. Immunopharmacology. 2000 Jun;48(1):51-63. Alkoxypsoralens, known as DNA photomodifying agents, have been shown to block voltage-dependent K (+) channels (Kv) as well as to alleviate functional deficits in certain multiple sclerosis (MS) patients in a manner similar to 4-aminopyridine. Since Kv channel blockers are known to inhibit T cell-mediated immune responses both in vitro and in vivo, we investigated the effects of three alkoxypsoralens, 5-methoxypsoralen (5-MOP), 8-methoxypsoralen (8-MOP), and 5,8-diethoxypsoralen (H37), on the following parameters: (1) whole-cell K (+) currents of encephalitogenic, myelin basic protein-specific memory T cell line cells (MBP-TCLC) derived from Lewis rats as measured by patch-clamp technique, (2) proliferation of MBP-TCLC and lymph node cells (LNC) from Lewis rats challenged for experimental autoimmune encephalomyelitis (EAE) by immunisation with spinal cord homogenate as measured by 3H- incorporation, (3) interferon-gamma (IFN-gamma) secretion of MBP-TCLC as measured by ELISA, and (4) IFN-gamma gene expression of LNC as measured by quantitative reverse transcription polymerase chain reaction (RT-PCR) with ELISA-detection. |
1(0,0,0,1) | Details |
| 16319208 | Sinha K, Karimi-Abdolrezaee S, Velumian AA, Fehlings MG: Functional changes in genetically dysmyelinated spinal cord axons of shiverer mice: role of juxtaparanodal Kv1 family K+ channels. J Neurophysiol. 2006 Mar;95(3):1683-95. Epub 2005 Nov 30. In this study, gap electrophysiology using selective and nonselective K+ channel blockers, confocal immunohistochemistry, and Western blotting were used to study the role of Kv1.1 and Kv1.2 K+ channel subunits in dysmyelination-induced spinal cord axonal dysfunction in shiverer mice, which lack the gene encoding myelin basic protein (MBP) and exhibit incomplete myelin sheath formation on CNS axons. The "fast" K+ channel blocker 4-aminopyridine, the toxin DTX-I, which targets the Kv1.1 and Kv1.2, but not DTX- K, which has higher selectivity for Kv1.1, increased the amplitude and area of CAPs of shiverer mice spinal cord axons but had insignificant effects in wild-type mice. |
1(0,0,0,1) | Details |
| 19607977 | Milanese M, Bonifacino T, Zappettini S, Usai C, Tacchetti C, Nobile M, Bonanno G: release from astrocytic gliosomes under physiological and pathological conditions. Int Rev Neurobiol. 2009;85:295-318. Finally, gliosomes represent functional organelles that actively export when subjected to releasing stimuli, such as ionomycin, high KCl, veratrine, 4-aminopyridine, AMPA, or ATP by mechanisms involving extracellular Ca2+, Ca2+ release from intracellular stores as well as reversal of transporters. |
0(0,0,0,0) | Details |