ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Dipeptidyl peptidase-like protein 6 is required for normal electrophysiological properties of cerebellar granule cells.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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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.
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Who cites it
24 citing papers in PubMed, 33 citations in OpenAlex.
- Kv4.2The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Neuronal Roles of the Multifunctional Protein Dipeptidyl Peptidase-like 6 (DPP6).International journal of molecular sciences · 2022Review
- Article
- Light-regulated voltage-gated potassium channels for acute interrogation of channel function in neurons and behavior.PloS one · 2021Article
- FMRP(1-297)-tat restores ion channel and synaptic function in a model of Fragile X syndrome.Nature communications · 2020Article
- Activity-dependent isomerization of Kv4.2 by Pin1 regulates cognitive flexibility.Nature communications · 2020Article
- The sockeye salmon genome, transcriptome, and analyses identifying population defining regions of the genome.PloS one · 2020Article
- A-Type KFrontiers in molecular neuroscience · 2018Review
- KThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Kv4.2 and accessory dipeptidyl peptidase-like protein 10 (DPP10) subunit preferentially form a 4:2 (Kv4.2:DPP10) channel complex.The Journal of biological chemistry · 2015Article
- Transient outward potassium channel: a heart failure mediator.Heart failure reviews · 2015Review
- DPP6 domains responsible for its localization and function.The Journal of biological chemistry · 2014Article
- The expression pattern of a Cav3-Kv4 complex differentially regulates spike output in cerebellar granule cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- IA channels: diverse regulatory mechanisms.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2014Review
- T-type channels buddy up.Pflugers Archiv : European journal of physiology · 2014Review
- Modulatory mechanisms and multiple functions of somatodendritic A-type K (+) channel auxiliary subunits.Frontiers in cellular neuroscience · 2014Review
- Functional stoichiometry underlying KChIP regulation of Kv4.2 functional expression.Journal of neurochemistry · 2013Article
- Dipeptidyl-peptidase-like-proteins confer high sensitivity to the scorpion toxin AmmTX3 to Kv4-mediated A-type K+ channels.The Journal of physiology · 2013Article
- A new TASK for Dipeptidyl Peptidase-like Protein 6.PloS one · 2013Article
- Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
In cerebellar granule (CG) cells and many other neurons, A-type potassium currents play an important role in regulating neuronal excitability, firing patterns, and activity-dependent plasticity. Protein biochemistry has identified dipeptidyl peptidase-like protein 6 (DPP6) as an auxiliary subunit of Kv4-based A-type channels and thus a potentially important regulator of neuronal excitability. In this study, we used an RNA interference (RNAi) strategy to examine the role DPP6 plays in forming and shaping the electrophysiological properties of CG cells. DPP6 RNAi delivered by lentiviral vectors effectively disrupts DPP6 protein expression in CG cells. In response to the loss of DPP6, I(SA) peak conductance amplitude is reduced by >85% in parallel with a dramatic reduction in the level of I(SA) channel protein complex found in CG cells. The I(SA) channels remaining in CG cells after suppression of DPP6 show alterations in gating similar to Kv4 channels expressed in heterologous systems without DPP6. In addition to these effects on A-type current, we find that loss of DPP6 has additional effects on input resistance and Na(+) channel conductance that combine with the effects on I(SA) to produce a global change in excitability. Overall, DPP6 expression seems to be critical for the expression of a high-frequency electrophysiological phenotype in CG cells by increasing leak conductance, A-type current levels and kinetics, and Na(+) current amplitude.
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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.