Evidence map›Paper›PMID 17349691›Full record

ReviewCell calcium2007

Recent breakthroughs in the molecular mechanism of capacitative calcium entry (with thoughts on how we got here).

James W Putney

Open access · greenAbstract readReview
In one paragraph

Review in Cell calcium, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed
11.7field-weighted citation impact, top 1% 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

93 citing papers in PubMed, 217 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Flavored e-liquids increase cytoplasmic CaAmerican journal of physiology. Lung cellular and molecular physiology · 2020
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. The functions of store-operated calcium channels.Biochimica et biophysica acta. Molecular cell research · 2017
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Lysosomal Calcium in Neurodegeneration.Messenger (Los Angeles, Calif. : Print) · 2016
    Article
  17. Phosphoinositide signaling in somatosensory neurons.Advances in biological regulation · 2016
    Review
  18. Store-operated calcium entry and diabetic complications.Experimental biology and medicine (Maywood, N.J.) · 2016
    Review
  19. Article
  20. Article

33 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

1 author at 1 institution in 1 country.

James W PutneyNational Institute of Environmental Health Sciences, NIH, P.O. Box 12233, Research Triangle Park, NC 27709, United States. putney@niehs.nih.gov
National Institute of Environmental Health Sciences · US

Funding

CAPACITATIVE CALCIUM ENTRYZ01ES090087 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI PUTNEY, JAMES W · 1997 to 2008
$5.2M
Intramural NIH HHS Z01 ES090087Intramural NIH HHS Z99 ES999999
6 · The paper itself

Abstract

Activation of phospholipase C by G-protein-coupled receptors results in release of intracellular Ca(2+) and activation of Ca(2+) channels in the plasma membrane. The intracellular release of Ca(2+) is signaled by the second messenger, inositol 1,4,5-trisphosphate. Ca(2+) entry involves signaling from depleted intracellular stores to plasma membrane Ca(2+) channels, a process referred to as capacitative calcium entry or store-operated calcium entry. The electrophysiological current associated with capacitative calcium entry is the calcium-release-activated calcium current, or I(crac). In the 20 years since the inception of the concept of capacitative calcium entry, a variety of activation mechanisms have been proposed, and there has been considerable interest in the possibility of transient receptor potential channels functioning as store-operated channels. However, in the past 2 years, two major players in both the signaling and permeation mechanisms for store-operated channels have been discovered: Stim1 (and possibly Stim2) and the Orai proteins. Activation of store-operated channels involves an endoplasmic reticulum Ca(2+) sensor called Stim1. Stim1 acts by redistributing within a small component of the endoplasmic reticulum, approaching the plasma membrane, but does not appear to translocate into the plasma membrane. Stim1, either directly or indirectly, signals to plasma membrane Orai proteins which constitute pore-forming subunits of store-operated channels.

Indexed as

AnimalsBiological TransportCalciumCalcium ChannelsMembrane ProteinsThapsigarginTransient Receptor Potential ChannelsCalciumCalcium ChannelsMembrane ProteinsThapsigarginTransient Receptor Potential Channels

Identifiers

PMID17349691
PMCPMC1986648
OpenAlexW2028226397

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.