Evidence map›Paper›PMID 10973476›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2000

Mitochondrial control of calcium-channel gating: a mechanism for sustained signaling and transcriptional activation in T lymphocytes.

M Hoth, D C Button, R S Lewis

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

102 citing papers in PubMed, 263 citations in OpenAlex.

  1. Review
  2. The ubiquitin-activating enzyme inhibitor TAK-243 activates store-operated CaBiochimica et biophysica acta. Molecular cell research · 2026
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Mitochondrial Regulation of CD8⁺ T Cells: Mechanisms and Therapeutic Modulation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  8. Review
  9. Review
  10. House dust mite allergens, store-operated CaThe Journal of physiology · 2024
    Review
  11. Targeting mitochondrial CaThe Journal of physiology · 2024
    Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Plasma Membrane CaFunction (Oxford, England) · 2022
    Article
  17. Article
  18. Maintaining social contacts: The physiological relevance of organelle interactions.Biochimica et biophysica acta. Molecular cell research · 2020
    Review
  19. Calcium regulation of T cell metabolismCurrent opinion in physiology · 2020
    Article
  20. Review

42 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

M HothDepartment of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA 94305-5426, USA.
D C Button
R S Lewis
Stanford University · US

Funding

ION CHANNELS AND SIGNALING MECHANISMS IN T LYMPHOCYTESR01GM045374 · NIGMS · STANFORD UNIVERSITY · PI LEWIS, RICHARD S · 1991 to 2011
$5.0M
NIGMS NIH HHS R01 GM045374
6 · The paper itself

Abstract

In addition to their well-known functions in cellular energy transduction, mitochondria play an important role in modulating the amplitude and time course of intracellular Ca(2+) signals. In many cells, mitochondria act as Ca(2+) buffers by taking up and releasing Ca(2+), but this simple buffering action by itself often cannot explain the organelle's effects on Ca(2+) signaling dynamics. Here we describe the functional interaction of mitochondria with store-operated Ca(2+) channels in T lymphocytes as a mechanism of mitochondrial Ca(2+) signaling. In Jurkat T cells with functional mitochondria, prolonged depletion of Ca(2+) stores causes sustained activation of the store-operated Ca(2+) current, I(CRAC) (CRAC, Ca(2+) release-activated Ca(2+)). Inhibition of mitochondrial Ca(2+) uptake by compounds that dissipate the intramitochondrial potential unmasks Ca(2+)-dependent inactivation of I(CRAC). Thus, functional mitochondria are required to maintain CRAC-channel activity, most likely by preventing local Ca(2+) accumulation near sites that govern channel inactivation. In cells stimulated through the T-cell antigen receptor, acute blockade of mitochondrial Ca(2+) uptake inhibits the nuclear translocation of the transcription factor NFAT in parallel with CRAC channel activity and [Ca(2+)](i) elevation, indicating a functional link between mitochondrial regulation of I(CRAC) and T-cell activation. These results demonstrate a role for mitochondria in controlling Ca(2+) channel activity and signal transmission from the plasma membrane to the nucleus.

Indexed as

Calcium ChannelsHumansIon Channel GatingJurkat CellsMitochondriaSignal TransductionT-LymphocytesTranscriptional ActivationCalcium Channels

Identifiers

PMID10973476
PMCPMC27072
OpenAlexW2138760035

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.