Evidence map›Paper›PMID 24444792›Full record

ArticleMolecular and cellular neurosciences2014

Selective regulation of axonal growth from developing hippocampal neurons by tumor necrosis factor superfamily member APRIL.

Catarina Osório, Pedro J Chacón, Matthew White, Lilian Kisiswa, Sean Wyatt, Alfredo Rodríguez-Tébar, Alun M Davies

Open access · hybridAbstract read
In one paragraph

Article in Molecular and cellular neurosciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

21 citing papers in PubMed, 33 citations in OpenAlex.

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  11. How CD40L reverse signaling regulates axon and dendrite growth.Cellular and molecular life sciences : CMLS · 2021
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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

7 authors at 3 institutions in 2 countries.

Catarina OsórioSchool of Biosciences, Cardiff University, Museum Avenue, Cardiff, CF10 3AT Wales, United Kingdom.
Pedro J ChacónSchool of Biosciences, Cardiff University, Museum Avenue, Cardiff, CF10 3AT Wales, United Kingdom; Centro Andaluz de Biología Molecular y Medicina Regenerativa (CABIMER), Americo Vespucio s/n, Isla de la Cartuja, 41092 Seville, Spain.
Matthew WhiteSchool of Biosciences, Cardiff University, Museum Avenue, Cardiff, CF10 3AT Wales, United Kingdom.
Lilian KisiswaSchool of Biosciences, Cardiff University, Museum Avenue, Cardiff, CF10 3AT Wales, United Kingdom.
Sean WyattSchool of Biosciences, Cardiff University, Museum Avenue, Cardiff, CF10 3AT Wales, United Kingdom.
Alfredo Rodríguez-TébarCentro Andaluz de Biología Molecular y Medicina Regenerativa (CABIMER), Americo Vespucio s/n, Isla de la Cartuja, 41092 Seville, Spain.
Alun M DaviesSchool of Biosciences, Cardiff University, Museum Avenue, Cardiff, CF10 3AT Wales, United Kingdom. Electronic address: daviesalun@cf.ac.uk.
Cardiff University · GBCentro Andaluz de Biología Molecular y Medicina Regenerativa · ESNational Museum Wales · GB

Funding

Wellcome Trust 085984
6 · The paper itself

Abstract

APRIL (A Proliferation-Inducing Ligand, TNFSF13) is a member of the tumor necrosis factor superfamily that regulates lymphocyte survival and activation and has been implicated in tumorigenesis and autoimmune diseases. Here we report the expression and first known activity of APRIL in the nervous system. APRIL and one of its receptors, BCMA (B-Cell Maturation Antigen, TNFRSF17), are expressed by hippocampal pyramidal cells of fetal and postnatal mice. In culture, these neurons secreted APRIL, and function-blocking antibodies to either APRIL or BCMA reduced axonal elongation. Recombinant APRIL enhanced axonal elongation, but did not influence dendrite elongation. The effect of APRIL on axon elongation was inhibited by anti-BCMA and the expression of a signaling-defective BCMA mutant in these neurons, suggesting that the axon growth-promoting effect of APRIL is mediated by BCMA. APRIL promoted phosphorylation and activation of ERK1, ERK2 and Akt and serine phosphorylation and inactivation of GSK-3β in cultured hippocampal pyramidal cells. Inhibition of MEK1/MEK2 (activators of ERK1/ERK2), PI3-kinase (activator of Akt) or Akt inhibited the axon growth-promoting action of APRIL, as did pharmacological activation of GSK-3β and the expression of a constitutively active form of GSK-3β. These findings suggest that APRIL promotes axon elongation by a mechanism that depends both on ERK signaling and PI3-kinase/Akt/GSK-3β signaling.

Indexed as

NeurogenesisAnimalsAxonsB-Cell Maturation AntigenCells, CulturedDendritesGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHippocampusMAP Kinase Kinase 1MAP Kinase Kinase 2MiceMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Phosphoinositide-3 Kinase InhibitorsProtein Kinase InhibitorsB-Cell Maturation AntigenGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGsk3b protein, mouseMap2k2 protein, mouseMAP Kinase Kinase 1MAP Kinase Kinase 2Mitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Phosphoinositide-3 Kinase InhibitorsProtein Kinase InhibitorsProto-Oncogene Proteins c-aktTnfrsf17 protein, mouseTnfsf13 protein, mouseTumor Necrosis Factor Ligand Superfamily Member 13AxonHippocampal pyramidal cellTumor necrosis factor receptor superfamilyTumor necrosis factor superfamily

Identifiers

PMID24444792
PMCPMC4008386
OpenAlexW2163970556

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.