Evidence map›Paper›PMID 23503728›Full record

ArticlePflugers Archiv : European journal of physiology2013

Surface expression and function of Cav3.2 T-type calcium channels are controlled by asparagine-linked glycosylation.

Norbert Weiss, Stefanie A G Black, Chris Bladen, Lina Chen, Gerald W Zamponi

Abstract read
PubMed Publisher
In one paragraph

Article in Pflugers Archiv : European journal of physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

60 citing papers in PubMed, 104 citations in OpenAlex.

  1. Review
  2. Sialylation in the nervous system: Functions and mechanisms.The Journal of biological chemistry · 2026
    Review
  3. Article
  4. Regulatory Action of Calcium and Calcium Channels in Pain Pathways.International journal of biological sciences · 2025
    Review
  5. CaThe journal of headache and pain · 2024
    Article
  6. Structural basis for human CaCell research · 2024
    Article
  7. The T-type calcium channelosome.Pflugers Archiv : European journal of physiology · 2024
    Review
  8. Electrophysiological characterization of a CaPflugers Archiv : European journal of physiology · 2023
    Article
  9. Article
  10. Review
  11. Regulation of CaPflugers Archiv : European journal of physiology · 2022
    Article
  12. Voltage-dependent CaPflugers Archiv : European journal of physiology · 2022
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Targeting T-type/CaV3.2 channels for chronic pain.Translational research : the journal of laboratory and clinical medicine · 2021
    Review
  18. Article
  19. The life cycle of voltage-gated CaNeuronal signaling · 2021
    Review
  20. Golgi-Dependent Copper Homeostasis Sustains Synaptic Development and Mitochondrial Content.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    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

5 authors at 1 institution in 1 country.

Norbert WeissHotchkiss Brain Institute, Department of Physiology and Pharmacology, University of Calgary, 3330 Hospital Drive N.W, AB, Calgary, T2N 4N1, Canada.
Stefanie A G Black
Chris Bladen
Lina Chen
Gerald W Zamponi
University of Calgary · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Low-voltage-activated T-type calcium channels play important roles in neuronal physiology where they control cellular excitability and synaptic transmission. Alteration in T-type channel expression has been linked to various pathophysiological conditions such as pain arising from diabetic neuropathy. In the present study, we looked at the role of asparagine (N)-linked glycosylation on human Cav3.2 T-type channel expression and function. Manipulation of N-glycans on cells expressing a recombinant Cav3.2 channel revealed that N-linked glycosylation is critical for proper functional expression of the channel. Using site-directed mutagenesis to disrupt the canonical N-linked glycosylation sites of Cav3.2 channel, we show that glycosylation at asparagine N192 is critical for channel expression at the surface, whereas glycosylation at asparagine N1466 controls channel activity. Moreover, we demonstrate that N-linked glycosylation of Cav3.2 not only controls surface expression and activity of the channel but also underlies glucose-dependent potentiation of T-type Ca(2+) current. Our data suggest that N-linked glycosylation of T-type channels may play an important role in aberrant upregulation of T-type channel activity in response to glucose elevations.

Indexed as

AsparagineCalciumCalcium Channels, T-TypeCells, CulturedGlucoseGlycosylationHumansUp-RegulationAsparagineCACNA1H protein, humanCalciumCalcium Channels, T-TypeGlucose

Identifiers

PMID23503728
OpenAlexW2105893174

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.