Evidence map›Paper›PMID 23613532›Full record

ReviewThe Journal of physiology2013

The role of ubiquitin-mediated pathways in regulating synaptic development, axonal degeneration and regeneration: insights from fly and worm.

Xiaolin Tian, Chunlai Wu

Abstract readReview
In one paragraph

Review in The Journal of physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Loss of the spectraplakin short stop activates the DLK injury response pathway in Drosophila.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    Article
  12. Article
  13. Advances in synapse formation: forging connections in the worm.Wiley interdisciplinary reviews. Developmental biology
    Review
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.

Xiaolin TianNeuroscience Center of Excellence, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA.
Chunlai Wu

Funding

The Role of Highwire/DFsn Ubiquitination Complex During Synaptic DevelopmentR01NS070962 · NINDS · LSU HEALTH SCIENCES CENTER · PI WU, CHUNLAI · 2010 to 2014
$1.5M
NINDS NIH HHS NS070962NINDS NIH HHS R01 NS070962
6 · The paper itself

Abstract

The covalent attachment of the 76 amino acid peptide ubiquitin to target proteins is a rapid and reversible modification that regulates protein stability, activity and localization. As such, it is a potent mechanism for sculpting the synapse. Recent studies from two genetic model organisms, Caenorhabditis elegans and Drosophila, have provided mounting evidence that ubiquitin-mediated pathways play important roles in controlling the presynaptic size, synaptic elimination and stabilization, synaptic transmission, postsynaptic receptor abundance, axonal degeneration and regeneration. While the data supporting the requirement of ubiquitination/deubiquitination for normal synaptic development and repair are compelling, detailed analyses of signalling events up- and downstream of these ubiquitin modifications are often challenging. This article summarizes the related research conducted in worms and flies and provides insight into the fundamental questions facing this field.

Indexed as

AnimalsAxonsCaenorhabditis elegansCaenorhabditis elegans ProteinsDrosophilaDrosophila ProteinsGuanine Nucleotide Exchange FactorsNerve Tissue ProteinsSynapsesUbiquitinUbiquitinationCaenorhabditis elegans ProteinsDrosophila ProteinsGuanine Nucleotide Exchange FactorsHIW protein, DrosophilaNerve Tissue ProteinsRPM-1 protein, C elegansUbiquitin

Identifiers

PMID23613532
PMCPMC3717216

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.