Evidence map›Paper›PMID 31669485›Full record

ArticleExperimental neurology2020

Mechanism and role of the intra-axonal Calreticulin translation in response to axonal injury.

Almudena Pacheco, Tanuja T Merianda, Jeffery L Twiss, Gianluca Gallo

Open access · hybridAbstract read
In one paragraph

Article in Experimental neurology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

15 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. The Axonal Glycolytic Pathway Contributes to Sensory Axon Extension and Growth Cone Dynamics.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  10. Article
  11. Review
  12. Article
  13. A CaCurrent biology : CB · 2020
    Article
  14. Review
  15. 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

4 authors at 3 institutions in 1 country.

Almudena PachecoTemple University School of Medicine, Shriners Pediatric Research Center, Department of Anatomy and Cell Biology, 3500 North Broad St, Philadelphia, PA 19140, United States of America. Electronic address: apacheco.garcia@gmail.com.
Tanuja T MeriandaDrexel University, Department of Biology, Philadelphia, PA 19104, United States of America.
Jeffery L TwissUniversity of South Carolina, Department of Biological Sciences, Columbia 29208, SC, United States of America. Electronic address: twiss@mailbox.sc.edu.
Gianluca GalloTemple University School of Medicine, Shriners Pediatric Research Center, Department of Anatomy and Cell Biology, 3500 North Broad St, Philadelphia, PA 19140, United States of America. Electronic address: tue86088@temple.edu.
Temple University · USDrexel University · USUniversity of South Carolina · US

Funding

Localized translation of cytoskeletal proteins in axonal morphogenesisR01NS078030 · NINDS · TEMPLE UNIV OF THE COMMONWEALTH · PI GALLO, GIANLUCA · 2013 to 2017
$1.7M
NINDS NIH HHS R01 NS078030
6 · The paper itself

Abstract

Following injury, sensory axons locally translate mRNAs that encode proteins needed for the response to injury, locally and through retrograde signaling, and for regeneration. In this study, we addressed the mechanism and role of axotomy-induced intra-axonal translation of the ER chaperone Calreticulin. In vivo peripheral nerve injury increased Calreticulin levels in sensory axons. Using an in vitro model system of sensory neurons amenable to mechanistic dissection we provide evidence that axotomy induces local translation of Calreticulin through PERK (protein kinase RNA-like endoplasmic reticulum kinase) mediated phosphorylation of eIF2α by a mechanism that requires both 5' and 3'UTRs (untranslated regions) elements in Calreticulin mRNA. ShRNA mediated depletion of Calreticulin or inhibition of PERK signaling increased axon retraction following axotomy. In contrast, expression of axonally targeted, but not somatically restricted, Calreticulin mRNA decreased retraction and promoted axon regeneration following axotomy in vitro. Collectively, these data indicate that the intra-axonal translation of Calreticulin in response to axotomy serves to minimize the ensuing retraction, and overexpression of axonally targeted Calreticulin mRNA promotes axon regeneration.

Indexed as

AnimalsAxonsAxotomyCalreticulineIF-2 KinaseMaleNerve RegenerationPeripheral Nerve InjuriesProtein BiosynthesisRatsRats, Sprague-DawleyCalreticulineIF-2 KinaseAxonal injuryCalreticulineIF2α phosphorylationTranslational control

Identifiers

PMID31669485
PMCPMC6909931
OpenAlexW2982029461

What OpenQuestion holds

Textmetadata
LicenceTDM
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.