ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2002
Protein kinase modulation of a neuronal cation channel requires protein-protein interactions mediated by an Src homology 3 domain.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 96 citations in OpenAlex.
- Cholinergic depolarization recruits a persistent CaJournal of neurophysiology · 2023Article
- A Closely Associated Phospholipase C Regulates Cation Channel Function through Phosphoinositide Hydrolysis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Regulation of neuronal excitability by interaction of fragile X mental retardation protein with slack potassium channels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Evolutionary conservation of the signaling proteins upstream of cyclic AMP-dependent kinase and protein kinase C in gastropod mollusks.Brain, behavior and evolution · 2009Review
- Identification of a functional interaction between Kv4.3 channels and c-Src tyrosine kinase.Biochimica et biophysica acta · 2008Article
- Ca2+-dependent regulation of a non-selective cation channel from Aplysia bag cell neurones.The Journal of physiology · 2006Article
- Kinases bicker over an ion channel.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2006Article
- Association/dissociation of a channel-kinase complex underlies state-dependent modulation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005Article
- Regulation of recombinant and native hyperpolarization-activated cation channels.Molecular neurobiology · 2004Review
- Regulation of an Aplysia bag-cell neuron cation channel by closely associated protein kinase A and a protein phosphatase.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004Article
- Prolonged activation of Ca2+-activated K+ current contributes to the long-lasting refractory period of Aplysia bag cell neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulating evidence suggests that many ion channels reside within a multiprotein complex that contains kinases and other signaling molecules. The role of the adaptor proteins that physically link these complexes together for the purposes of ion channel modulation, however, has been little explored. Here, we examine the protein-protein interactions required for regulation of an Aplysia bag cell neuron cation channel by a closely associated protein kinase C (PKC). In inside-out patches, the PKC-dependent enhancement of cation channel open probability could be prevented by the src homology 3 (SH3) domain, presumably by disrupting a link between the channel and the kinase. SH3 and PDZ domains from other proteins were ineffective. Modulation was also prevented by an SH3 motif peptide that preferentially binds the SH3 domain of src. Furthermore, whole-cell depolarizations elicited by cation channel activation were decreased by the src SH3 domain. These data suggest that the cation channel-PKC association may require SH3 domain-mediated interactions to bring about modulation, promote membrane depolarization, and initiate prolonged changes in bag cell neuron excitability. In general, protein-protein interactions between ion channels and protein kinases may be a prominent mechanism underlying neuromodulation.
Indexed as
Identifiers
11756482PMC6757624W2098381765What OpenQuestion holds
Registered trials
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