Evidence map›Paper›PMID 9326661›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1997

Ca2+-independent inhibition of inositol trisphosphate receptors by calmodulin: redistribution of calmodulin as a possible means of regulating Ca2+ mobilization.

S Patel, S A Morris, C E Adkins, G O'Beirne, C W Taylor

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

35 citing papers in PubMed, 105 citations in OpenAlex.

  1. Calmodulin Mutations in Human Disease.Channels (Austin, Tex.) · 2023
    Review
  2. Article
  3. Article
  4. Article
  5. NCS-1 is a regulator of calcium signaling in health and disease.Biochimica et biophysica acta. Molecular cell research · 2018
    Review
  6. Article
  7. IPCellular and molecular life sciences : CMLS · 2017
    Review
  8. Sense and specificity in neuronal calcium signalling.Biochimica et biophysica acta · 2015
    Review
  9. Visualizing CaMKII and CaM activity: a paradigm of compartmentalized signaling.Journal of molecular medicine (Berlin, Germany) · 2013
    Review
  10. CaBP1, a neuronal Ca2+ sensor protein, inhibits inositol trisphosphate receptors by clamping intersubunit interactions.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  11. Calmodulin binds HER2 and modulates HER2 signaling.Biochimica et biophysica acta · 2011
    Article
  12. Review
  13. IP(3) receptors: toward understanding their activation.Cold Spring Harbor perspectives in biology · 2010
    Review
  14. STIM2 protein mediates distinct store-dependent and store-independent modes of CRAC channel activation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2008
    Article
  15. Review
  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

5 authors at 1 institution in 1 country.

S PatelDepartment of Pharmacology, Tennis Court Road, Cambridge CB2 1QJ, England, United Kingdom.
S A Morris
C E Adkins
G O'Beirne
C W Taylor
Amersham Hospital · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

The interactions between calmodulin, inositol 1,4,5-trisphosphate (InsP3), and pure cerebellar InsP3 receptors were characterized by using a scintillation proximity assay. In the absence of Ca2+, 125I-labeled calmodulin reversibly bound to multiple sites on InsP3 receptors and Ca2+ increased the binding by 190% +/- 10%; the half-maximal effect occurred when the Ca2+ concentration was 184 +/- 14 nM. In the absence of Ca2+, calmodulin caused a reversible, concentration-dependent (IC50 = 3.1 +/- 0.2 microM) inhibition of [3H]InsP3 binding by decreasing the affinity of the receptor for InsP3. This effect was similar at all Ca2+ concentrations, indicating that the site through which calmodulin inhibits InsP3 binding has similar affinities for calmodulin and Ca2+-calmodulin. Calmodulin (10 microM) inhibited the Ca2+ release from cerebellar microsomes evoked by submaximal, but not by maximal, concentrations of InsP3. Tonic inhibition of InsP3 receptors by the high concentrations of calmodulin within cerebellar Purkinje cells may account for their relative insensitivity to InsP3 and limit spontaneous activation of InsP3 receptors in the dendritic spines. Inhibition of InsP3 receptors by calmodulin at all cytosolic Ca2+ concentrations, together with the known redistribution of neuronal calmodulin evoked by protein kinases and Ca2+, suggests that calmodulin may also allow both feedback control of InsP3 receptors and integration of inputs from other signaling pathways.

Indexed as

AnimalsBinding, CompetitiveBrainCalciumCalcium ChannelsCalmodulinCattleCerebellumInositol 1,4,5-TrisphosphateInositol 1,4,5-Trisphosphate ReceptorsKineticsMicrosomesModels, NeurologicalModels, StructuralRatsReceptors, Cytoplasmic and NuclearCalciumCalcium ChannelsCalmodulinInositol 1,4,5-TrisphosphateInositol 1,4,5-Trisphosphate ReceptorsReceptors, Cytoplasmic and Nuclear

Identifiers

PMID9326661
PMCPMC23558
OpenAlexW1986684354

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.