Evidence map›Paper›PMID 20976103›Full record

ArticlePloS one2010

Regulation of STIM1 and SOCE by the ubiquitin-proteasome system (UPS).

Jeffrey M Keil, Zhouxin Shen, Steven P Briggs, Gentry N Patrick

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.5field-weighted citation impact, top 21% 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

30 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
  2. ESCRT-0 regulates AMPA receptor currents and CabioRxiv : the preprint server for biology · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. STIM1 in tumor cell death: angel or devil?Cell death discovery · 2023
    Review
  7. Article
  8. Article
  9. Neuronal Store-Operated Calcium Channels.Molecular neurobiology · 2023
    Review
  10. Article
  11. Review
  12. Review
  13. Target Molecules of STIM Proteins in the Central Nervous System.Frontiers in molecular neuroscience · 2020
    Review
  14. Remodeling of ER-plasma membrane contact sites but not STIM1 phosphorylation inhibits CaProceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  15. Review
  16. Review
  17. Molecular physiology and pathophysiology of stromal interaction molecules.Experimental biology and medicine (Maywood, N.J.) · 2018
    Review
  18. Article
  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

4 authors at 1 institution in 1 country.

Jeffrey M KeilSection of Neurobiology, Department of Biological Sciences, University of California San Diego, La Jolla, California, United States of America.
Zhouxin Shen
Steven P Briggs
Gentry N Patrick
University of California, San Diego · US

Funding

Ubiquitin-dependent Regulation of AMPA Receptor Trafficking and TurnoverR01NS060847 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI PATRICK, GENTRY N · 2010 to 2014
$1.8M
Regulatory mechanisms of proteasome function in neuronsR21NS054732 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI PATRICK, GENTRY N · 2009 to 2010
$409k
NINDS NIH HHS NS054732NINDS NIH HHS R01 NS060847NINDS NIH HHS R21 NS054732
6 · The paper itself

Abstract

The ubiquitin proteasome system (UPS) mediates the majority of protein degradation in eukaryotic cells. The UPS has recently emerged as a key degradation pathway involved in synapse development and function. In order to better understand the function of the UPS at synapses we utilized a genetic and proteomic approach to isolate and identify novel candidate UPS substrates from biochemically purified synaptic membrane preparations. Using these methods, we have identified Stromal interacting molecule 1 (STIM1). STIM1 is as an endoplasmic reticulum (ER) calcium sensor that has been shown to regulate store-operated Ca(2+) entry (SOCE). We have characterized STIM1 in neurons, finding STIM1 is expressed throughout development with stable, high expression in mature neurons. As in non-excitable cells, STIM1 is distributed in a membranous and punctate fashion in hippocampal neurons. In addition, a population of STIM1 was found to exist at synapses. Furthermore, using surface biotinylation and live-cell labeling methods, we detect a subpopulation of STIM1 on the surface of hippocampal neurons. The role of STIM1 as a regulator of SOCE has typically been examined in non-excitable cell types. Therefore, we examined the role of the UPS in STIM1 and SOCE function in HEK293 cells. While we find that STIM1 is ubiquitinated, its stability is not altered by proteasome inhibitors in cells under basal conditions or conditions that activate SOCE. However, we find that surface STIM1 levels and thapsigargin (TG)-induced SOCE are significantly increased in cells treated with proteasome inhibitors. Additionally, we find that the overexpression of POSH (Plenty of SH3's), an E3 ubiquitin ligase recently shown to be involved in the regulation of Ca(2+) homeostasis, leads to decreased STIM1 surface levels. Together, these results provide evidence for previously undescribed roles of the UPS in the regulation of STIM1 and SOCE function.

Indexed as

AnimalsBase SequenceCalciumCell LineDNA PrimersGreen Fluorescent ProteinsHippocampusHomeostasisHumansHydrolysisIon TransportMembrane ProteinsMiceMice, TransgenicNeoplasm ProteinsNeuronsCalciumDNA PrimersGreen Fluorescent ProteinsMembrane ProteinsNeoplasm ProteinsProteasome Endopeptidase ComplexSTIM1 protein, humanStromal Interaction Molecule 1Ubiquitin

Identifiers

PMID20976103
PMCPMC2956693
OpenAlexW1967949819

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.