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IL-4 type 1 receptor signaling up-regulates KCNN4 expression, and increases the KCa3.1 current and its contribution to migration of alternative-activated microglia
The Ca(2+)-activated K(+) channel, KCa3.1 (KCNN4/IK1/SK4), contributes to “classical,” pro-inflammatory activation of microglia, and KCa3.1 blockers have improved the outcome in several rodent models of CNS damage. For instance, blocking KCa3.1 with TRAM-34 rescued retinal ganglion neurons after opt...
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| Autors principals: | , , |
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| Format: | Artigo |
| Idioma: | Inglês |
| Publicat: |
Frontiers Media S.A.
2014
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| Matèries: | |
| Accés en línia: | https://ncbi.nlm.nih.gov/pmc/articles/PMC4077126/ https://ncbi.nlm.nih.gov/pubmed/25071444 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.3389/fncel.2014.00183 |
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