Evidence map›Paper›PMID 12533600›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003

Modulation of type 1 inositol (1,4,5)-trisphosphate receptor function by protein kinase a and protein phosphatase 1alpha.

Tie-Shan Tang, Huiping Tu, Zhengnan Wang, Ilya Bezprozvanny

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

74 citing papers in PubMed, 155 citations in OpenAlex.

  1. Trial
  2. Pacemaking in the lymphatic system.The Journal of physiology · 2026
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  5. A cellular atlas of calcineurin signaling.Biochimica et biophysica acta. Molecular cell research · 2023
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  9. Review
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  12. Targeting Bcl-2-IPBiochimica et biophysica acta. Molecular cell research · 2018
    Review
  13. Altered Synaptic Vesicle Release and CaFrontiers in molecular neuroscience · 2018
    Article
  14. Article
  15. Article
  16. Review
  17. Regulation of IPCell calcium · 2017
    Review
  18. Review
  19. Article
  20. Article

14 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

4 authors at 1 institution in 1 country.

Tie-Shan TangDepartment of Physiology, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9040, USA.
Huiping Tu
Zhengnan Wang
Ilya Bezprozvanny
The University of Texas Southwestern Medical Center · US

Funding

STRUCTURE/FUNCTION OF INOSITOL TRISPHOSPHATE RECEPTORR01NS038082 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI BEZPROZVANNY, ILYA B · 1999 to 2009
$2.6M
NINDS NIH HHS R01 NS038082NINDS NIH HHS R01 NS38082
6 · The paper itself

Abstract

Type 1 inositol (1,4,5)-trisphosphate receptors (InsP3R1s) play a major role in neuronal calcium (Ca2+) signaling. The InsP3R1s are phosphorylated by protein kinase A (PKA), but the functional consequences of InsP3R1 phosphorylation and the mechanisms that control the phosphorylated state of neuronal InsP3R1s are poorly understood. In a yeast two-hybrid screen of rat brain cDNA library with the InsP3R1-specific bait, we isolated the protein phosphatase 1alpha (PP1alpha). In biochemical experiments, we confirmed the specificity of the InsP3R1-PP1alpha association and immunoprecipitated the InsP3R1-PP1 complex from rat brain synaptosomes and from the neostriatal lysate. We also established that the association with PP1 facilitates dephosphorylation of PKA-phosphorylated InsP3R1 by the endogenous neostriatal PP1 and by the recombinant PP1alpaha. We demonstrated that exposure of neostriatal slices to 8-bromo-cAMP, dopamine, calyculin A, or cyclosporine A, but not to 10 nM okadaic acid, promotes the phosphorylation of neostriatal InsP3R1 by PKA in vivo. We discovered that PKA activates and PP1alpha inhibits the activity of recombinant InsP3R1 reconstituted into planar lipid bilayers. We found that phosphorylation of InsP3R1 by PKA induces at least a fourfold increase in the sensitivity of InsP3R1 to activation by InsP3 without shifting the peak of InsP3R1 bell-shaped Ca2+ dependence. Based on these data, we suggest that InsP3R1 may participate in cross talk between cAMP and Ca2+ signaling in the neostriatum and possibly in other regions of the brain.

Indexed as

AnimalsCalciumCalcium ChannelsCalcium SignalingCyclic AMPCyclic AMP-Dependent Protein KinasesDopamineInositol 1,4,5-Trisphosphate ReceptorsNeostriatumPhosphoprotein PhosphatasesPhosphorylationPrecipitin TestsProtein BindingRatsReceptors, Cytoplasmic and NuclearSubstrate SpecificityCalciumCalcium ChannelsCyclic AMPCyclic AMP-Dependent Protein KinasesDopamineInositol 1,4,5-Trisphosphate ReceptorsPhosphoprotein PhosphatasesReceptors, Cytoplasmic and Nuclear

Identifiers

PMID12533600
PMCPMC6741879
OpenAlexW2165292955

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.