Evidence map›Paper›PMID 8038377›Full record

ArticleBiophysical journal1994

Calcium-dependent inactivation of L-type calcium channels in planar lipid bilayers.

J A Haack, R L Rosenberg

Open access · greenAbstract read
In one paragraph

Article in Biophysical journal, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

25 citing papers in PubMed, 64 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Mitochondrial CaMolecules and cells · 2020
    Article
  5. L-type CaJournal of physiology and biochemistry · 2019
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Caffeine-sensitive calcium stores regulate synaptic transmission from retinal rod photoreceptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1999
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Ca2+- and voltage-dependent inactivation of Ca2+ channels in nerve terminals of the neurohypophysis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1997
    Article
  20. 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

2 authors at 1 institution in 1 country.

J A HaackDepartment of Pharmacology and Physiology, University of North Carolina at Chapel Hill 27599.
R L Rosenberg
University of North Carolina at Chapel Hill · US

Funding

CALCIUM DEPENDENT INACTIVATION OF CALCIUM CHANNELSF32HL008820 · NHLBI · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI HAACK, JULIE A · 1993 to 1994
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MODULATION OF CARDIAC CALCIUM CHANNELS IN VITROR01HL049449 · NHLBI · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI ROSENBERG, ROBERT L · 1993 to 1997
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RECONSTITUTION OF NEURONAL CALCIUM CHANNELSR29NS026660 · NINDS · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI ROSENBERG, ROBERT L · 1989 to 1993
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NHLBI NIH HHS HL08820NHLBI NIH HHS HL49449NINDS NIH HHS NS26660
6 · The paper itself

Abstract

Intracellular Ca2+ can inhibit the activity of voltage-gated Ca channels by modulating the rate of channel inactivation. Ca(2+)-dependent inactivation of these channels may be a common negative feedback process important for regulating Ca2+ entry under physiological and pathological conditions. This article demonstrates that the inactivation of cardiac L-type Ca channels, reconstituted into planar lipid bilayers and studied in the presence of a dihydropyridine agonist, is sensitive to Ca2+. The rates and extents of inactivation, determined from ensemble averages of unitary Ba2+ currents, decreased when the calcium concentration facing the intracellular surface of the channel ([Ca2+]i) was lowered from approximately 10 microM to 20 nM by the addition of Ca2+ chelators. The rates and extents of Ba2+ current inactivation could also be increased by subsequent addition of Ca2+ raising the [Ca2+]i to 15 microM, thus demonstrating that the Ca2+ dependence of inactivation could be reversibly regulated by changes in [Ca2+]i. In addition, reconstituted Ca channels inactivated more quickly when the inward current was carried by Ca2+ than when it was carried by Ba2+, suggesting that local increases in [Ca2+]i could activate Ca(2+)-dependent inactivation. These data support models in which Ca2+ binds to the channel itself or to closely associated regulatory proteins to control the rate of channel inactivation, and are inconsistent with purely enzymatic models for channel inactivation.

Indexed as

Calcium Channel BlockersAnimalsBariumBiophysical PhenomenaBiophysicsCalciumFeedbackIn Vitro TechniquesKineticsLipid BilayersMyocardiumPermeabilitySarcolemmaSwineBariumCalciumCalcium Channel BlockersLipid Bilayers

Identifiers

PMID8038377
PMCPMC1275812
OpenAlexW1971351715

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.