Evidence map›Paper›PMID 25352783›Full record

ArticleFrontiers in cellular neuroscience2014

Regulation of Kv4.2 A-Type Potassium Channels in HEK-293 Cells by Hypoxia.

Yu-Qiang Liu, Wen-Xian Huang, Russell M Sanchez, Jia-Wei Min, Jiang-Jian Hu, Xiao-Hua He, Bi-Wen Peng

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.3field-weighted citation impact, top 41% of its field
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

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.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Design of Ultrapotent Genetically Encoded Inhibitors of Kv4.2 for Gating Neural Plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  4. Article
  5. Endogenous ion channels expressed in human embryonic kidney (HEK-293) cells.Pflugers Archiv : European journal of physiology · 2022
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
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 at 1 institution in 1 country.

Yu-Qiang LiuDepartment of Physiology, Hubei Provincial Key Laboratory of Developmentally Originated Disorder, School of Basic Medical Sciences, Wuhan University , Wuhan , China.
Wen-Xian HuangDepartment of Physiology, Hubei Provincial Key Laboratory of Developmentally Originated Disorder, School of Basic Medical Sciences, Wuhan University , Wuhan , China.
Russell M SanchezDepartment of Surgery, College of Medicine, Texas A&M Health Science Center, Neuroscience Institute, Scott and White Hospital, Central Texas Veterans Health Care System , Temple, TX , USA.
Jia-Wei MinDepartment of Physiology, Hubei Provincial Key Laboratory of Developmentally Originated Disorder, School of Basic Medical Sciences, Wuhan University , Wuhan , China.
Jiang-Jian HuDepartment of Physiology, Hubei Provincial Key Laboratory of Developmentally Originated Disorder, School of Basic Medical Sciences, Wuhan University , Wuhan , China.
Xiao-Hua HeDepartment of Physiology, Hubei Provincial Key Laboratory of Developmentally Originated Disorder, School of Basic Medical Sciences, Wuhan University , Wuhan , China.
Bi-Wen PengDepartment of Physiology, Hubei Provincial Key Laboratory of Developmentally Originated Disorder, School of Basic Medical Sciences, Wuhan University , Wuhan , China.
Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We previously observed that A-type potassium currents were decreased and membrane excitability increased in hippocampal dentate granule cells after neonatal global hypoxia associated with seizures. Here, we studied the effects of hypoxia on the function and expression of Kv4.2 and Kv4.3 α subunit channels, which encode rapidly inactivating A-type K currents, in transfected HEK-293 cells to determine if hypoxia alone could regulate IA in vitro. Global hypoxia in neonatal rat pups resulted in early decreased hippocampal expression of Kv4.2 mRNA and protein with 6 or 12 h post-hypoxia. Whole-cell voltage-clamp recordings revealed that similar times after hypoxia (1%) in vitro decreased peak currents mediated by recombinant Kv4.2 but not Kv4.3 channels. Hypoxia had no significant effect on the voltage-dependencies of activation and inactivation of Kv4.2 channels, but increased the time constant of activation. The same result was observed when Kv4.2 and Kv4.3 channels were co-expressed in a 1:1 ratio. These data suggested that hypoxia directly modulates A-type potassium channels of the subfamily typically expressed in principal hippocampal neurons, and does so in a manner to decrease function. Given the role of IA to slow action potential firing, these data are consistent with a direct effect of hypoxia to decrease IA as a mechanism of increased neuronal excitability and promotion of seizures.

Indexed as

A-currenthypoxiain vitropatch-clamp

Identifiers

PMID25352783
PMCPMC4196569
OpenAlexW2029157440

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

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.