Evidence map›Paper›PMID 17234598›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007

The RNA-binding protein HuD binds acetylcholinesterase mRNA in neurons and regulates its expression after axotomy.

Julie Deschênes-Furry, Kambiz Mousavi, Federico Bolognani, Rachael L Neve, Robin J Parks, Nora I Perrone-Bizzozero, Bernard J Jasmin

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. 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
2.3field-weighted citation impact, top 13% 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, 39 citations in OpenAlex.

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  14. Characterization of multiple exon 1 variants in mammalian HuD mRNA and neuron-specific transcriptional control via neurogenin 2.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
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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 5 institutions in 3 countries.

Julie Deschênes-FurryDepartment of Cellular and Molecular Medicine and Centre for Neuromuscular Disease, University of Ottawa, Ottawa, Ontario, Canada K1H 8M5.
Kambiz Mousavi
Federico Bolognani
Rachael L Neve
Robin J Parks
Nora I Perrone-Bizzozero
Bernard J Jasmin
University of Ottawa · CAHarvard University · USInstitute of Cell Biology and Neurobiology · ITOttawa Hospital · CAUniversity of New Mexico · US

Funding

Mechanisms of Post-Transcriptional Control of Neuronal mRNAsR01NS030255 · NINDS · UNIVERSITY OF NEW MEXICO · PI PERRONE-BIZZOZERO, NORA IRMA · 1997 to 2011
$2.8M
MECHANISMS OF CONTROL OF THE GAP-43 GENER29NS030255 · NINDS · UNIVERSITY OF NEW MEXICO · PI PERRONE-BIZZOZERO, NORA IRMA · 1991 to 1995
–
NINDS NIH HHS NS30255NINDS NIH HHS R01 NS030255
6 · The paper itself

Abstract

After axotomy, expression of acetylcholinesterase (AChE) is greatly reduced in the superior cervical ganglion (SCG); however, the molecular events involved in this response remain unknown. Here, we first examined AChE mRNA levels in the brain of transgenic mice that overexpress human HuD. Both in situ hybridization and reverse transcription-PCR demonstrated that AChE transcript levels were increased by more than twofold in the hippocampus of HuD transgenic mice. Additionally, direct interaction between the HuD transgene product and AChE mRNA was observed. Next, we examined the role of HuD in regulating AChE expression in intact and axotomized rat SCG neurons. After axotomy of the adult rat SCG neurons, AChE transcript levels decreased by 50 and 85% by the first and fourth day, respectively. In vitro mRNA decay assays indicated that the decrease in AChE mRNA levels resulted from changes in the stability of presynthesized transcripts. A combination of approaches performed using the region that directly encompasses an adenylate and uridylate (AU)-rich element within the AChE 3'-untranslated region demonstrated a decrease in RNA-protein complexes in response to axotomy of the SCG and, specifically, a decrease in HuD binding. After axotomy, HuD transcript and protein levels also decreased. Using a herpes simplex virus construct containing the human HuD sequence to infect SCG neurons in vivo, we found that AChE and GAP-43 mRNA levels were maintained in the SCG after axotomy. Together, the results of this study demonstrate that AChE expression in neurons of the rat SCG is regulated via post-transcriptional mechanisms that involve the AU-rich element and HuD.

Indexed as

AcetylcholinesteraseAnimalsAxotomyELAV-Like Protein 4ELAV ProteinsFemaleGene Expression Regulation, EnzymologicHumansMiceMice, TransgenicNeuronsProtein BindingRatsRats, Sprague-DawleyRNA-Binding ProteinsRNA, MessengerAcetylcholinesteraseELAVL4 protein, humanELAV-Like Protein 4ELAV ProteinsRNA-Binding ProteinsRNA, Messenger

Identifiers

PMID17234598
PMCPMC6672799
OpenAlexW1977621096

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.