Evidence map›Paper›PMID 24623787›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014

TrkA in vivo function is negatively regulated by ubiquitination.

Erkan Kiris, Ting Wang, Sudhirkumar Yanpallewar, Susan G Dorsey, Jodi Becker, Sina Bavari, Mary Ellen Palko, Vincenzo Coppola, Lino Tessarollo

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.9field-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

17 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Role of the Ubiquitin System in Chronic Pain.Frontiers in molecular neuroscience · 2021
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Ubiquitin C-Terminal Hydrolase L1 (UCH-L1) Promotes Hippocampus-Dependent Memory via Its Deubiquitinating Effect on TrkB.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  13. Review
  14. Article
  15. Review
  16. In vivo regulation of NGF-mediated functions by Nedd4-2 ubiquitination of TrkA.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  17. 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

9 authors at 5 institutions in 1 country.

Erkan KirisNeural Development Section, Mouse Cancer Genetics Program, National Cancer Institute, Frederick, Maryland 21702, Department of Target Discovery and Experimental Microbiology, U.S. Army Medical Research Institute of Infectious Diseases, Frederick, Maryland 21702, University of Maryland School of Nursing and Program in Neuroscience, Baltimore, Maryland 21201, and Department of MVIMG, Wexner Medical Center Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio 43210.
Ting Wang
Sudhirkumar Yanpallewar
Susan G Dorsey
Jodi Becker
Sina Bavari
Mary Ellen Palko
Vincenzo Coppola
Lino Tessarollo
Cancer Genetics (United States) · USNational Cancer Institute · USTarget (United States) · USThe Ohio State University Wexner Medical Center · USUniversity of Maryland, Baltimore · US

Funding

Role of Neurotrophins in the Development of the Mammalian Nervous SystemZIABC010390 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI TESSAROLLO, LINO · 2009 to 2025
$14.2M
Role of Trk Receptors in the Development and Function of Non-neuronal StructuresZIABC010391 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI TESSAROLLO, LINO · 2009 to 2025
$14.0M
Intramural NIH HHS
6 · The paper itself

Abstract

TrkA is a tyrosine kinase receptor required for development and survival of the peripheral nervous system. In the adult, TrkA and its ligand NGF are peripheral pain mediators, particularly in inflammatory pain states. However, how TrkA regulates the function of nociceptive neurons and whether its activity levels may lead to sensory abnormalities is still unclear. Here we report the characterization of a 3 aa (KFG) domain that negatively regulates TrkA level and function in response to NGF. Deletion of this domain in mouse causes a reduction of TrkA ubiquitination leading to an increase in TrkA protein levels and activity. The number of dorsal root ganglia neurons is not affected by the mutation. However, mutant mice have enhanced thermal sensitivity and inflammatory pain. Together, these data suggest that ubiquitination is a mechanism used in nociceptive neurons to regulate TrkA level and function. Our results may enhance our understanding of how ubiquitination affects TrkA activation following noxious thermal stimulation and inflammatory pain.

Indexed as

AnimalsCell LineDown-RegulationEmbryonic Stem CellsFemaleGanglia, SpinalHEK293 CellsHumansHyperalgesiaInflammationMaleMiceMice, 129 StrainMice, Inbred C57BLMice, Mutant StrainsNerve Growth FactorNerve Growth FactorReceptor, trkA

Identifiers

PMID24623787
PMCPMC3951704
OpenAlexW1997759378

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.