Journal
MOLECULAR AND CELLULAR NEUROSCIENCE
Volume 42, Issue 1, Pages 33-44Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.mcn.2009.05.003
Keywords
-
Categories
Funding
- Clare Boothe Luce Program of the Henry Luce Foundation
- National Institutes of Health [R01 GM083335]
Ask authors/readers for more resources
Shal K+ (K(v)4) channels across species carry the major A-type K+ current present in neurons. Shal currents are activated by small EPSPs and modulate post-synaptic potentials, backpropagation of action potentials, and induction of LTP. Fast inactivation of Shal channels regulates the impact of this post-synaptic modulation. Here, we introduce SKIP3, as the first protein interactor of Drosophila Shal K+ channels. The SKIP gene encodes three isoforms with multiple protein-protein interaction domains. SKIP3 is nervous system specific and co-localizes with Shal channels in neuronal cell bodies, and in puncta along processes. Using a genetic deficiency of SKIP, we show that the proportion of neurons displaying a very fast inactivation, consistent with Shal channels exclusively in a fast gating mode, is increased in the absence of SKIP3. As a scaffold-like protein, SKIP3 is likely to lead to the identification of a novel regulatory complex that modulates Shal channel inactivation. (C) 2009 Elsevier Inc. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available