Quantification of the functional expression of the Ca2+-activated K+channel KCa3.1 on microglia from adult human neocortical tissue
Author:
Affiliation:
1. Saniona A/S; Baltorpvej 154 2750 Ballerup Denmark
2. Neurobiology Research Unit; Copenhagen University Hospital, Rigshospitalet; Copenhagen Denmark
3. Epilepsy Clinic; Copenhagen University Hospital, Rigshospitalet; Copenhagen Denmark
Funder
European Union's Seventh Framework Programme, InMind
Strategic Research Council
Publisher
Wiley
Subject
Cellular and Molecular Neuroscience,Neurology
Link
http://onlinelibrary.wiley.com/wol1/doi/10.1002/glia.23040/fullpdf
Reference38 articles.
1. Chemokine modulation of high-conductance Ca2+-sensitive K+ currents in microglia from human hippocampi;Bordey;Eur J Neurosci,2003
2. Inhibition of the Ca2+-dependent K+ channel, KCNN4/KCa3.1, improves tissue protection and locomotor recovery after spinal cord injury;Bouhy;J Neurosci,2011
3. The potassium channel KCa3.1 constitutes a pharmacological target for neuroinflammation associated with ischemia/reperfusion stroke;Chen;J Cereb Blood Flow Metab,2015
4. The KCa3.1 blocker TRAM-34 reduces infarction and neurological deficit in a rat model of ischemia/reperfusion stroke;Chen;J Cereb Blood Flow Metab,2011
5. Ca2+-activated K+ channel from human erythrocyte membranes: Single channel rectification and selectivity;Christophersen;J Membr Biol,1991
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