ArticleMolecular and cellular neurosciences2009
Fast inactivation of Shal (K(v)4) K+ channels is regulated by the novel interactor SKIP3 in Drosophila neurons.
Article in Molecular and cellular neurosciences, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed, 17 citations in OpenAlex.
- Deficiency in transmitter release triggers homeostatic transcriptional changes that increase presynaptic excitability.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Age-related changes in Kv4/Shal and Kv1/Shaker expression in Drosophila and a role for reactive oxygen species.PloS one · 2021Article
- Cholinergic Synaptic Homeostasis Is Tuned by an NFAT-Mediated α7 nAChR-KCell reports · 2020Article
- The mirtron miR-1010 functions in concert with its host gene SKIP to balance elevation of nAcRβ2.Scientific reports · 2020Article
- Specialized eRpL22 paralogue-specific ribosomes regulate specific mRNA translation in spermatogenesis inMolecular biology of the cell · 2019Article
- Linking aβ42-induced hyperexcitability to neurodegeneration, learning and motor deficits, and a shorter lifespan in an Alzheimer's model.PLoS genetics · 2015Article
- Putative excitatory and putative inhibitory inputs are localised in different dendritic domains in a Drosophila flight motoneuron.The European journal of neuroscience · 2013Article
- A screen for genes expressed in the olfactory organs of Drosophila melanogaster identifies genes involved in olfactory behaviour.PloS one · 2012Article
- Inactivity-induced increase in nAChRs upregulates Shal K(+) channels to stabilize synaptic potentials.Nature neuroscience · 2011Article
- Shal/K(v)4 channels are required for maintaining excitability during repetitive firing and normal locomotion in Drosophila.PloS one · 2011Article
- SIDL interacts with the dendritic targeting motif of Shal (K(v)4) K+ channels in Drosophila.Molecular and cellular neurosciences · 2010Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
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.
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