Evidence map›Paper›PMID 23665919›Full record

ArticleThe EMBO journal2013

Attenuation of insulin signalling contributes to FSN-1-mediated regulation of synapse development.

Wesley L Hung, Christine Hwang, Shangbang Gao, Edward H Liao, Jyothsna Chitturi, Ying Wang, Hang Li, Christian Stigloher, Jean-Louis Bessereau, Mei Zhen

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 26% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

  1. Pooled it
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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

10 authors at 3 institutions in 2 countries.

Wesley L HungSamuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada.
Christine Hwang
Shangbang Gao
Edward H Liao
Jyothsna Chitturi
Ying Wang
Hang Li
Christian Stigloher
Jean-Louis Bessereau
Mei Zhen
Mount Sinai Hospital · CAInstitut de Biologie de l'École Normale Supérieure · FRLunenfeld-Tanenbaum Research Institute · CA

Funding

Canadian Institutes of Health Research MOP93619
6 · The paper itself

Abstract

A neuronal F-box protein FSN-1 regulates Caenorhabditis elegans neuromuscular junction development by negatively regulating DLK-mediated MAPK signalling. In the present study, we show that attenuation of insulin/IGF signalling also contributes to FSN-1-dependent synaptic development and function. The aberrant synapse morphology and synaptic transmission in fsn-1 mutants are partially and specifically rescued by reducing insulin/IGF-signalling activity in postsynaptic muscles, as well as by reducing the activity of EGL-3, a prohormone convertase that processes agonistic insulin/IGF ligands INS-4 and INS-6, in neurons. FSN-1 interacts with, and potentiates the ubiquitination of EGL-3 in vitro, and reduces the EGL-3 level in vivo. We propose that FSN-1 may negatively regulate insulin/IGF signalling, in part, through EGL-3-dependent insulin-like ligand processing.

Indexed as

AnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsF-Box ProteinsHEK293 CellsHumansInsulinMAP Kinase Kinase KinasesMAP Kinase Signaling SystemMusclesMutationProprotein Convertase 2SomatomedinsSynapsesUbiquitinationCaenorhabditis elegans ProteinsDLK-1 protein, C elegansEGL-3 proprotein convertase, C elegansF-Box ProteinsFSN-1 protein, C elegansInsulinMAP Kinase Kinase KinasesProprotein Convertase 2Somatomedins

Identifiers

PMID23665919
PMCPMC3680742
OpenAlexW2134498383

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.