Evidence map›Paper›PMID 16473932›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2006

Depletion "skraps" and dynamic buffering inside the cellular calcium store.

Bradley S Launikonis, Jingsong Zhou, Leandro Royer, Thomas R Shannon, Gustavo Brum, Eduardo Ríos

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
–field-weighted citation impact
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

48 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Pathological mechanisms of vacuolar aggregate myopathy arising from a Casq1 mutation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  6. Review
  7. Review
  8. Store-operated CaCommunications biology · 2018
    Article
  9. Ambiguous interactions between diastolic and SR CaThe Journal of general physiology · 2017
    Review
  10. Calsequestrin depolymerizes when calcium is depleted in the sarcoplasmic reticulum of working muscle.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. 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

6 authors.

Bradley S LaunikonisSection of Cellular Signaling, Department of Molecular Biophysics and Physiology, Rush University, 1750 West Harrison Street, Suite 1279JS, Chicago, IL 60612, USA.
Jingsong Zhou
Leandro Royer
Thomas R Shannon
Gustavo Brum
Eduardo Ríos

Funding

Skeletal Muscle. Ca Release Control Inside the Sarcoplasmic Reticulum.R01AR049184 · NIAMS · RUSH UNIVERSITY MEDICAL CENTER · PI RIOS, EDUARDO · 2003 to 2013
$3.1M
CALCIUM MOVEMENTS IN EXCITATION-CONTRACTION COUPLINGR01AR032808 · NIAMS · RUSH UNIVERSITY MEDICAL CENTER · PI RIOS, EDUARDO · 1986 to 2011
$1.6M
NIAMS NIH HHS R01 AR032808NIAMS NIH HHS R01 AR049184
6 · The paper itself

Abstract

Ca2+ signals, produced by Ca2+ release from cellular stores, switch metabolic responses inside cells. In muscle, Ca2+ sparks locally exhibit the rapid start and termination of the cell-wide signal. By imaging Ca2+ inside the store using shifted excitation and emission ratioing of fluorescence, a surprising observation was made: Depletion during sparks or voltage-induced cell-wide release occurs too late, continuing to progress even after the Ca2+ release channels have closed. This finding indicates that Ca2+ is released from a "proximate" compartment functionally in between store lumen and cytosol. The presence of a proximate compartment also explains a paradoxical surge in intrastore Ca2+, which was recorded upon stimulation of prolonged, cell-wide Ca2+ release. An intrastore surge upon induction of Ca2+ release was first reported in subcellular store fractions, where its source was traced to the store buffer, calsequestrin. The present results update the evolving concept, largely due to N. Ikemoto and C. Kang, of calsequestrin as a dynamic store. Given the strategic location and reduction of dimensionality of Ca2+-adsorbing linear polymers of calsequestrin, they could deliver Ca2+ to the open release channels more efficiently than the luminal store solution, thus constituting the proximate compartment. When store depletion becomes widespread, the polymers would collapse to increase store [Ca2+] and sustain the concentration gradient that drives release flux.

Indexed as

Calcium SignalingAnimalsCalciumCytosolMuscle Fibers, SkeletalMuscle, SkeletalRana pipiensCalcium

Identifiers

PMID16473932
PMCPMC1413852

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.