Evidence map›Paper›PMID 26200251›Full record

ArticleNeuroscience letters2015

ERK signaling mediates CaSR-promoted axon growth.

Thomas N Vizard, Michael Newton, Laura Howard, Sean Wyatt, Alun M Davies

Open access · hybridAbstract read
In one paragraph

Article in Neuroscience letters, 2015. 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
0.6field-weighted citation impact, top 38% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Silencing the enhancer of zeste homologue 2,Neural regeneration research · 2022
    Article
  6. Article
  7. Sensory Axon Growth Requires Spatiotemporal Integration of CaSR and TrkB Signaling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  8. Review
  9. Article
  10. PAR3-PAR6-atypical PKC polarity complex proteins in neuronal polarization.Cellular and molecular life sciences : CMLS · 2018
    Review
  11. Article
  12. Article
  13. 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

5 authors at 1 institution in 1 country.

Thomas N VizardSchool of Biosciences, Biomedical Building, Museum Avenue, Cardiff CF10 3US, UK. Electronic address: thomas.vizard@ndcn.ox.ac.uk.
Michael NewtonSchool of Biosciences, Biomedical Building, Museum Avenue, Cardiff CF10 3US, UK.
Laura HowardSchool of Biosciences, Biomedical Building, Museum Avenue, Cardiff CF10 3US, UK.
Sean WyattSchool of Biosciences, Biomedical Building, Museum Avenue, Cardiff CF10 3US, UK.
Alun M DaviesSchool of Biosciences, Biomedical Building, Museum Avenue, Cardiff CF10 3US, UK.
Cardiff University · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

The extracellular calcium-sensing receptor (CaSR) is a G-protein coupled receptor that monitors the systemic extracellular free ionized calcium level ([Ca(2+)]o) in organs involved in systemic [Ca(2+)]o homeostasis. CaSR is widely expressed in the nervous system and its activation promotes axon and dendrite growth during development, but the mechanism by which it does this is not known. Here we show that enhanced axon growth and branching from cultured embryonic sympathetic neurons by activation of the endogenous CaSR depends on the presence of nerve growth factor (NGF). Our observation that activation of overexpressed CaSR promotes axon growth in NGF-free medium has enabled us to investigate CaSR downstream signaling contributing to axon growth in the absence of NGF signaling. We show that activation of overexpressed CaSR leads to activation of ERK1 and ERK2, and pharmacological inhibition of CaSR-dependent ERK1/ERK2 activation prevents CaSR-dependent axon growth. Analysis of axon growth from cultured neurons expressing deletion mutants of the CaSR cytoplasmic tail revealed that the region between alanine 877 and glycine 907 is required for promoting axon growth that is distinct from the high-affinity filamin-A binding site that has previously been implicated in ERK1/ERK2 activation.

Indexed as

AnimalsAxonsCell LineEnzyme ActivationMiceMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Nerve Growth FactorReceptors, Calcium-SensingReceptors, G-Protein-CoupledSignal TransductionCASR protein, mouseMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Nerve Growth FactorReceptors, Calcium-SensingReceptors, G-Protein-CoupledAxon growthDevelopmentExtracellular calcium-sensing receptorExtracellular-regulated kinaseSympathetic neuron

Identifiers

PMID26200251
PMCPMC4552171
OpenAlexW1842177104

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.