Evidence map›Paper›PMID 20538594›Full record

ArticleThe Journal of biological chemistry2010

Modulation of endoplasmic reticulum Ca2+ store filling by cyclic ADP-ribose promotes inositol trisphosphate (IP3)-evoked Ca2+ signals.

Michiko Yamasaki-Mann, Angelo Demuro, Ian Parker

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
2.9field-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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Emerging potential benefits of modulating NADAmerican journal of physiology. Heart and circulatory physiology · 2018
    Review
  8. Inhibition of Sarco-Endoplasmic Reticulum CaFrontiers in pharmacology · 2018
    Article
  9. Article
  10. Article
  11. Endoplasmic Reticulum Stress and Associated ROS.International journal of molecular sciences · 2016
    Review
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  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
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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.

Michiko Yamasaki-MannDepartment of Neurobiology and Behavior, University of California, Irvine, California 92697, USA. michikomann@ucla.edu
Angelo Demuro
Ian Parker
University of California, Irvine · US

Funding

Elementary Events of Intracellular Calcium SignalingR37GM048071 · NIGMS · UNIVERSITY OF CALIFORNIA-IRVINE · PI PARKER, IAN · 2011 to 2020
$5.3M
SPATIAL AND TEMPORAL ASPECTS OF INSP3 SIGNALLINGR01GM048071 · NIGMS · UNIVERSITY OF CALIFORNIA-IRVINE · PI PARKER, IAN · 1992 to 2010
$3.9M
NIGMS NIH HHS GM48071NIGMS NIH HHS R01 GM048071NIGMS NIH HHS R37 GM048071
6 · The paper itself

Abstract

In addition to its well established function in activating Ca(2+) release from the endoplasmic reticulum (ER) through ryanodine receptors (RyR), the second messenger cyclic ADP-ribose (cADPR) also accelerates the activity of SERCA pumps, which sequester Ca(2+) into the ER. Here, we demonstrate a potential physiological role for cADPR in modulating cellular Ca(2+) signals via changes in ER Ca(2+) store content, by imaging Ca(2+) liberation through inositol trisphosphate receptors (IP(3)R) in Xenopus oocytes, which lack RyR. Oocytes were injected with the non-metabolizable analog 3-deaza-cADPR, and cytosolic [Ca(2+)] was transiently elevated by applying voltage-clamp pulses to induce Ca(2+) influx through expressed plasmalemmal nicotinic channels. We observed a subsequent potentiation of global Ca(2+) signals evoked by strong photorelease of IP(3), and increased numbers of local Ca(2+) puffs evoked by weaker photorelease. These effects were not evident with cADPR alone or following cytosolic Ca(2+) elevation alone, indicating that they did not arise through direct actions of cADPR or Ca(2+) on the IP(3)R, but likely resulted from enhanced ER store filling. Moreover, the appearance of a new population of puffs with longer latencies, prolonged durations, and attenuated amplitudes suggests that luminal ER Ca(2+) may modulate IP(3)R function, in addition to simply determining the size of the available store and the electrochemical driving force for release.

Indexed as

AnimalsCalciumCalcium SignalingCyclic ADP-RiboseCytosolElectrochemistryEndoplasmic ReticulumInositol 1,4,5-TrisphosphateKineticsModels, BiologicalOocytesPatch-Clamp TechniquesRyanodine Receptor Calcium Release ChannelTime FactorsXenopus laevisCalciumCyclic ADP-RiboseInositol 1,4,5-TrisphosphateRyanodine Receptor Calcium Release Channel

Identifiers

PMID20538594
PMCPMC2915741
OpenAlexW2018200055

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.