Evidence map›Paper›PMID 11790804›Full record

ArticleThe Journal of physiology2002

Stimulation of recombinant Ca(v)3.2, T-type, Ca(2+) channel currents by CaMKIIgamma(C).

Joshua T Wolfe, Hongge Wang, Edward Perez-Reyes, Paula Q Barrett

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

33 citing papers in PubMed, 76 citations in OpenAlex.

  1. The T-type calcium channelosome.Pflugers Archiv : European journal of physiology · 2024
    Review
  2. Review
  3. Effects of progesterone on T-type-CaNeural regeneration research · 2022
    Article
  4. Article
  5. Review
  6. Article
  7. Fast in vivo detection of myocardial norepinephrine levels in the beating porcine heart.American journal of physiology. Heart and circulatory physiology · 2020
    Article
  8. Article
  9. Regulation of T-type CaJournal of neurochemistry · 2019
    Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Leukemia inhibitory factor regulates trafficking of T-type Ca2+ channels.American journal of physiology. Cell physiology · 2011
    Article
  18. Article
  19. Article
  20. 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

4 authors at 1 institution in 1 country.

Joshua T WolfeDepartment of Pharmacology, University of Virginia School of Medicine, Charlottesville, VA 22908, USA.
Hongge Wang
Edward Perez-Reyes
Paula Q Barrett
University of Virginia · US

Funding

BASIC CARDIOVASCULAR RESEARCH TRAINING GRANTT32HL007284 · NHLBI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI Brant E Isakson, Gary K Owens · 1985 to 2026
$19.6M
T TYPE CALCIUM CHANNELS AND ALDOSTERONE SECRETIONR01HL036977 · NHLBI · YALE UNIVERSITY · PI BARRETT, PAULA Q · 1987 to 2013
$4.2M
NHLBI NIH HHS HL07284NHLBI NIH HHS HL36977NHLBI NIH HHS R01 HL036977NHLBI NIH HHS T32 HL007284
6 · The paper itself

Abstract

Molecular cloning of low-voltage activated (LVA) T-type calcium channels has enabled the study of their regulation in heterologous expression systems. Here we investigate the regulation of Ca(v)3.2 alpha(1)-subunits (alpha1H) by calcium- and/or calmodulin-dependent protein kinase II (CaMKII). 293 cells stably expressing alpha1H were transiently transfected with CaMKIIgamma(C). Using the whole-cell recording configuration, we observed that elevation of pipette free Ca(2+) (1 microM) in the presence of CaM (2 microM) increases T-type channel activity selectively at negative potentials, evoking an 11 mV hyperpolarizing shift in the half-maximal potential (V(1/2)) for activation. The V(1/2) of channel inactivation is not altered by Ca(2+)/CaM. These effects reproduced modulation observed in adrenal zona glomerulosa cells. The potentiation by Ca(2+)/CaM was dependent on the co-expression of CaMKIIgamma(C) and required Ca(2+)/CaM-dependent kinase activity. Peptide (AIP) and lipophilic (KN-62) protein kinase inhibitors prevented the Ca(2+)/CaM-induced changes in channel gating without altering basal Ca(v)3.2 channel activity (27 nM free Ca(2+)) as did replacing pipette ATP with adenylyl imidodiphosphate (AMP-PNP), a non-hydrolysable analogue. CaMKII-dependent potentiation of channel opening resulted in significant increases in apparent steady-state open probability (P(o)) and sustained channel current at negative voltages. Under identical conditions, CaMKII activation did not regulate the activity of Ca(v)3.1 channels, the first cloned member (alpha1G) of the T-type Ca(2+) channel family. Our results provide the first evidence for the differential regulation of two members of the Ca(v)3 family by protein kinase activation and the first report reconstituting CaMKII-dependent regulation of any cloned Ca(2+) channel.

Indexed as

Amino Acid SequenceAnimalsCalcium-Calmodulin-Dependent Protein KinasesCalcium-Calmodulin-Dependent Protein Kinase Type 2Calcium Channels, T-TypeCattleCell LineEnzyme ActivationHomeostasisHumansIon Channel GatingMolecular Sequence DataProtein IsoformsRecombinant ProteinsRNA, MessengerZona GlomerulosaCalcium-Calmodulin-Dependent Protein KinasesCalcium-Calmodulin-Dependent Protein Kinase Type 2Calcium Channels, T-TypeProtein IsoformsRecombinant ProteinsRNA, Messenger

Identifiers

PMID11790804
PMCPMC2290082
OpenAlexW2106343821

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.