Evidence map›Paper›PMID 23776520›Full record

ArticlePloS one2013

The SAX-3 receptor stimulates axon outgrowth and the signal sequence and transmembrane domain are critical for SAX-3 membrane localization in the PDE neuron of C. elegans.

Jia Li, Pu Pu, Weidong Le

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 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 48% 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

2 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. 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 2 institutions in 1 country.

Jia LiThe Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.
Pu Pu
Weidong Le
Shanghai Institutes for Biological Sciences · CNChinese Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

SAX-3, a receptor for Slit in C. elegans, is well characterized for its function in axonal development. However, the mechanism that regulates the membrane localization of SAX-3 and the role of SAX-3 in axon outgrowth are still elusive. Here we show that SAX-3::GFP caused ectopic axon outgrowth, which could be suppressed by the loss-of-function mutation in unc-73 (a guanine nucleotide exchange factor for small GTPases) and unc-115 (an actin binding protein), suggesting that they might act downstream of SAX-3 in axon outgrowth. We also examined genes related to axon development for their possible involvement in the subcellular localization of SAX-3. We found the unc-51 mutants appeared to accumulate SAX-3::GFP in the neuronal cell body of the posterior deirid (PDE) neuron, indicating that UNC-51 might play a role in SAX-3 membrane localization. Furthermore, we demonstrate that the N-terminal signal sequence and the transmembrane domain are essential for the subcellular localization of SAX-3 in the PDE neurons.

Indexed as

Analysis of VarianceAnimalsAxonsCaenorhabditis elegansCaenorhabditis elegans ProteinsCell MembraneDNA PrimersGreen Fluorescent ProteinsMicroscopy, FluorescenceNerve Tissue ProteinsProtein Serine-Threonine KinasesProtein Structure, TertiaryReal-Time Polymerase Chain ReactionReceptors, ImmunologicRNA InterferenceRoundabout ProteinsCaenorhabditis elegans ProteinsDNA PrimersGreen Fluorescent ProteinsNerve Tissue ProteinsProtein Serine-Threonine KinasesReceptors, ImmunologicRoundabout ProteinsUNC-51 protein, C elegans

Identifiers

PMID23776520
PMCPMC3680500
OpenAlexW2048161959

What OpenQuestion holds

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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.