ArticlePloS one2014
Cysteine string protein limits expression of the large conductance, calcium-activated K⁺ (BK) channel.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- KCurrent neuropharmacology · 2023Review
- Neurons Export Extracellular Vesicles Enriched in Cysteine String Protein and Misfolded Protein Cargo.Scientific reports · 2017Article
- Presynaptic BK channels control transmitter release: physiological relevance and potential therapeutic implications.The Journal of physiology · 2016Review
- BK Channels in the Central Nervous System.International review of neurobiology · 2016Review
- Evidence that the presynaptic vesicle protein CSPalpha is a key player in synaptic degeneration and protection in Alzheimer's disease.Molecular brain · 2015Article
- Increased Expression of the Large Conductance, Calcium-Activated K+ (BK) Channel in Adult-Onset Neuronal Ceroid Lipofuscinosis.PloS one · 2015Article
- Correction: Cysteine String Protein Limits Expression of the Large Conductance, Calcium-Activated K+ (BK) Channel.PloS one · 2015Article
- CSPα-chaperoning presynaptic proteins.Frontiers in cellular neuroscience · 2014Review
- Ion channels of the mammalian urethra.Channels (Austin, Tex.) · 2014Review
- The regulation of BK channel activity by pre- and post-translational modifications.Frontiers in physiology · 2014Review
- J protein mutations and resulting proteostasis collapse.Frontiers in cellular neuroscience · 2014Review
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Large-conductance, calcium-activated K(+) (BK) channels are widely distributed throughout the nervous system and play an essential role in regulation of action potential duration and firing frequency, along with neurotransmitter release at the presynaptic terminal. We have previously demonstrated that select mutations in cysteine string protein (CSPα), a presynaptic J-protein and co-chaperone, increase BK channel expression. This observation raised the possibility that wild-type CSPα normally functions to limit neuronal BK channel expression. Here we show by Western blot analysis of transfected neuroblastoma cells that when BK channels are present at elevated levels, CSPα acts to reduce expression. Moreover, we demonstrate that the accessory subunits, BKβ4 and BKβ1 do not alter CSPα-mediated reduction of expressed BKα subunits. Structure-function analysis reveals that the N-terminal J-domain of CSPα is critical for the observed regulation of BK channels levels. Finally, we demonstrate that CSPα limits BK current amplitude, while the loss-of-function homologue CSPαHPD-AAA increases BK current. Our observations indicate that CSPα has a role in regulating synaptic excitability and neurotransmission by limiting expression of BK channels.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.