Evidence map›Paper›PMID 23991227›Full record

ArticlePloS one2013

A loss-of-function analysis reveals that endogenous Rem2 promotes functional glutamatergic synapse formation and restricts dendritic complexity.

Anna R Moore, Amy E Ghiretti, Suzanne Paradis

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 32% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Experience-Dependent Development of Dendritic Arbors in Mouse Visual Cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  7. Article
  8. Neural architecture: from cells to circuits.Journal of neurophysiology · 2018
    Review
  9. Article
  10. Article
  11. Two Components of Aversive Memory inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  12. Review
  13. Article
  14. Rem2 is an activity-dependent negative regulator of dendritic complexity in vivo.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  15. 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

3 authors at 1 institution in 1 country.

Anna R MooreDepartment of Biology, National Center for Behavioral Genomics and Volen Center for Complex Systems, Brandeis University, Waltham, Massachusetts, USA.
Amy E Ghiretti
Suzanne Paradis
Brandeis University · US

Funding

Quantitative Neuroscience: Tools for Bridging Levels of AnalysisT32NS007292 · NINDS · BRANDEIS UNIVERSITY · PI GINA G TURRIGIANO · 1986 to 2026
$12.7M
NEUROSCIENCE: FROM CHANNELS TO BEHAVIORT32MH019929 · NIMH · BRANDEIS UNIVERSITY · PI GRIFFITH, LESLIE C · 1994 to 2023
$8.5M
Mouse CoreP30NS045713 · NINDS · BRANDEIS UNIVERSITY · PI ROSBASH, MICHAEL · 2003 to 2013
$7.8M
Semaphorin-Dependent GABAergic Synapse Formation: A Novel Approach to Increasing Inhibition in the Intact BrainR01NS065856 · NINDS · BRANDEIS UNIVERSITY · PI PARADIS, SUZANNE · 2010 to 2024
$5.4M
The Role of the Activity-Regulated GTPase Rem2 in Dendrite DevelopmentF31DA032181 · NIDA · BRANDEIS UNIVERSITY · PI GHIRETTI, AMY ELIZABETH · 2012 to 2013
$54k
NIDA NIH HHS F31 DA032181NIDA NIH HHS F31DA032181NIMH NIH HHS T32 MH019929NINDS NIH HHS P30 NS045713NINDS NIH HHS P30NS45713NINDS NIH HHS R01 NS065856NINDS NIH HHS R01NS065856NINDS NIH HHS T32 NS007292NINDS NIH HHS T32NS07292
6 · The paper itself

Abstract

Rem2 is a member of the RGK family of small Ras-like GTPases whose expression and function is regulated by neuronal activity in the brain. A number of questions still remain as to the endogenous functions of Rem2 in neurons. RNAi-mediated Rem2 knockdown leads to an increase in dendritic complexity and a decrease in functional excitatory synapses, though a recent report challenged the specificity of Rem2-targeted RNAi reagents. In addition, overexpression in a number of cell types has shown that Rem2 can inhibit voltage-gated calcium channel (VGCC) function, while studies employing RNAi-mediated knockdown of Rem2 have failed to observe a corresponding enhancement of VGCC function. To further investigate these discrepancies and determine the endogenous function of Rem2, we took a comprehensive, loss-of-function approach utilizing two independent, validated Rem2-targeted shRNAs to analyze Rem2 function. We sought to investigate the consequence of endogenous Rem2 knockdown by focusing on the three reported functions of Rem2 in neurons: regulation of synapse formation, dendritic morphology, and voltage-gated calcium channels. We conclude that endogenous Rem2 is a positive regulator of functional, excitatory synapse development and a negative regulator of dendritic complexity. In addition, while we are unable to reach a definitive conclusion as to whether the regulation of VGCCs is an endogenous function of Rem2, our study reports important data regarding RNAi reagents for use in future investigation of this issue.

Indexed as

AnimalsBase SequenceCells, CulturedDendritesDNA PrimersGlutamic AcidHEK293 CellsHippocampusHumansMonomeric GTP-Binding ProteinsRNA InterferenceSynapsesDNA PrimersGlutamic AcidMonomeric GTP-Binding ProteinsREM2 protein, human

Identifiers

PMID23991227
PMCPMC3753333
OpenAlexW2008397827

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.