ArticleMolecular brain2014
Synaptotagmin I delays the fast inactivation of Kv1.4 channel through interaction with its N-terminus.
Article in Molecular brain, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 9 citations in OpenAlex.
- Selective reduction of KCNA4 in vulnerable glutamatergic-serotonin neurons of the dorsal raphe nucleus in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Potential roles of voltage-gated ion channel disruption in Tuberous Sclerosis Complex.Frontiers in molecular neuroscience · 2024Article
- The Effects of 4-Hydroxybenzoic Acid Identified from Bamboo (The Malaysian journal of medical sciences : MJMS · 2018Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe voltage-gated potassium channel Kv1.4 is an important A-type potassium channel and modulates the excitability of neurons in central nervous system. Analysis of the interaction between Kv1.4 and its interacting proteins is helpful to elucidate the function and mechanism of the channel.
resultsIn the present research, synaptotagmin I was for the first time demonstrated to be an interacting protein of Kv1.4 and its interaction with Kv1.4 channel did not require the mediation of other synaptic proteins. Using patch-clamp technique, synaptotagmin I was found to delay the inactivation of Kv1.4 in HEK293T cells in a Ca2+-dependent manner, and this interaction was proven to have specificity. Mutagenesis experiments indicated that synaptotagmin I interacted with the N-terminus of Kv1.4 and thus delayed its N-type fast inactivation.
conclusionThese data suggest that synaptotagmin I is an interacting protein of Kv1.4 channel and, as a negative modulator, may play an important role in regulating neuronal excitability and synaptic efficacy.
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