Evidence map›Paper›PMID 23576435›Full record

ArticleThe Journal of biological chemistry2013

Auxiliary KChIP4a suppresses A-type K+ current through endoplasmic reticulum (ER) retention and promoting closed-state inactivation of Kv4 channels.

Yi-Quan Tang, Ping Liang, Jingheng Zhou, Yanxin Lu, Lei Lei, Xiling Bian, KeWei Wang

Abstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed.

  1. Review
  2. KCells · 2023
    Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Whole-Genome Cardiac DNA Methylation Fingerprint and Gene Expression Analysis Provide New Insights in the Pathogenesis of Chronic Chagas Disease Cardiomyopathy.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2017
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Yi-Quan TangDepartment of Neurobiology, Neuroscience Research Institute, Peking University Health Science Center, Peking University School of Pharmaceutical Sciences, Beijing 100191, China.
Ping Liang
Jingheng Zhou
Yanxin Lu
Lei Lei
Xiling Bian
KeWei Wang

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the brain and heart, auxiliary Kv channel-interacting proteins (KChIPs) co-assemble with pore-forming Kv4 α-subunits to form a native K(+) channel complex and regulate the expression and gating properties of Kv4 currents. Among the KChIP1-4 members, KChIP4a exhibits a unique N terminus that is known to suppress Kv4 function, but the underlying mechanism of Kv4 inhibition remains unknown. Using a combination of confocal imaging, surface biotinylation, and electrophysiological recordings, we identified a novel endoplasmic reticulum (ER) retention motif, consisting of six hydrophobic and aliphatic residues, 12-17 (LIVIVL), within the KChIP4a N-terminal KID, that functions to reduce surface expression of Kv4-KChIP complexes. This ER retention capacity is transferable and depends on its flanking location. In addition, adjacent to the ER retention motif, the residues 19-21 (VKL motif) directly promote closed-state inactivation of Kv4.3, thus leading to an inhibition of channel current. Taken together, our findings demonstrate that KChIP4a suppresses A-type Kv4 current via ER retention and enhancement of Kv4 closed-state inactivation.

Indexed as

Amino Acid MotifsEndoplasmic ReticulumHEK293 CellsHumansIon TransportKv Channel-Interacting ProteinsPotassiumProtein Structure, TertiaryShal Potassium ChannelsKv Channel-Interacting ProteinsPotassiumShal Potassium ChannelsClosed-state InactivationConfocal MicroscopyElectrophysiologyEndoplasmic Reticulum (ER)GatingKChIPsKv4NeurobiologyPotassium ChannelsTrafficking

Identifiers

PMID23576435
PMCPMC3663498

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.