The Ca(2+)-Activated K(+) Channel KCNN4/KCa3.1 Contributes to Microglia Activation and Nitric Oxide-Dependent Neurodegeneration

Brain damage and disease involve activation of microglia and production of potentially neurotoxic molecules, but there are no treatments that effectively target their harmful properties. We present evidence that the small-conductance Ca(2+)/calmodulin-activated K(+) channel KCNN4/ KCa3.1/SK4/IK1 is...

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Vydáno v:J Neurosci
Hlavní autoři: Kaushal, Vikas, Koeberle, Paulo D., Wang, Yimin, Schlichter, Lyanne C.
Médium: Artigo
Jazyk:Inglês
Vydáno: Society for Neuroscience 2007
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Articles
On-line přístup:https://ncbi.nlm.nih.gov/pmc/articles/PMC6672279/
https://ncbi.nlm.nih.gov/pubmed/17202491
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1523/JNEUROSCI.3593-06.2007
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