Evidence map›Paper›PMID 9396008›Full record

ReviewMolecular neurobiology1997

RC3/neurogranin, a postsynaptic calpacitin for setting the response threshold to calcium influxes.

D D Gerendasy, J G Sutcliffe

Abstract readComparative StudyReview
PubMed Publisher
In one paragraph

Review in Molecular neurobiology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 1 pooled it
2.7field-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

71 citing papers in PubMed, 1 synthesis or guideline pooled it, 218 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
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  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Chronic CaeLife · 2022
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. The Effects of CSF Neurogranin andFrontiers in aging neuroscience · 2021
    Article
  18. StandardizedAntioxidants (Basel, Switzerland) · 2020
    Article
  19. Article
  20. Article

11 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

2 authors at 1 institution in 1 country.

D D GerendasyDepartment of Molecular Biology, Scripps Research Institute.
J G Sutcliffe
Scripps Research Institute · US

Funding

NIGMS NIH HHS GM32355
6 · The paper itself

Abstract

In this review, we attempt to cover the descriptive, biochemical and molecular biological work that has contributed to our current knowledge about RC3/neurogranin function and its role in dendritic spine development, long-term potentiation, long-term depression, learning, and memory. Based on the data reviewed here, we propose that RC3, GAP-43, and the small cerebellum-enriched peptide, PEP-19, belong to a protein family that we have named the calpacitins. Membership in this family is based on sequence homology and, we believe, a common biochemical function. We propose a model wherein RC3 and GAP-43 regulate calmodulin availability in dendritic spines and axons, respectively, and calmodulin regulates their ability to amplify the mobilization of Ca2+ in response to metabotropic glutamate receptor stimulation. PEP-19 may serve a similar function in the cerebellum, although biochemical characterization of this molecule has lagged behind that of RC3 and GAP-43. We suggest that these molecules release CaM rapidly in response to large influxes of Ca2+ and slowly in response to small increases. This nonlinear response is analogous to the behavior of a capacitor, hence the name calpacitin. Since CaM regulates the ability of RC3 to amplify the effects of metabotropic glutamate receptor agonists, this activity must, necessarily, exhibit nonlinear kinetics as well. The capacitance of the system is regulated by phosphorylation by protein kinase C, which abrogates interactions between calmodulin and RC3 or GAP-43. We further propose that the ratio of phosphorylated to unphosphorylated RC3 determines the sliding LTP/LTD threshold in concept with Ca2+/ calmodulin-dependent kinase II. Finally, we suggest that the close association between RC3 and a subset of mitochondria serves to couple energy production with the synthetic events that accompany dendritic spine development and remodeling.

Indexed as

Amino Acid SequenceAnimalsCalciumCalmodulinCalmodulin-Binding ProteinsCongenital HypothyroidismConsensus SequenceDendritesGAP-43 ProteinGene Expression RegulationHumansHypothyroidismIon TransportLearningMiceModels, NeurologicalCalciumCalmodulinCalmodulin-Binding ProteinsGAP-43 ProteinNerve Tissue ProteinsNeurograninNRGN protein, humanNrgn protein, mouseNrgn protein, ratPCP4 protein, humanPcp4 protein, mousePcp4 protein, ratPhospholipidsProtein Kinase CProtein Tyrosine PhosphatasesReceptors, Metabotropic Glutamate

Identifiers

PMID9396008
OpenAlexW2077906120

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.