Evidence map›Paper›PMID 23516305›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013

Protein tyrosine phosphatase receptor type O inhibits trigeminal axon growth and branching by repressing TrkB and Ret signaling.

Graziana Gatto, Irina Dudanova, Philipp Suetterlin, Alun M Davies, Uwe Drescher, John L Bixby, Rüdiger Klein

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

19 citing papers in PubMed, 27 citations in OpenAlex.

  1. Long-read whole-genome sequencing of SHR rat substrains with distinct substance use phenotypes.Mammalian genome : official journal of the International Mammalian Genome Society · 2025
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  8. Protein Tyrosine Phosphatase Receptor Type J (PTPRJ) Regulates Retinal Axonal Projections by Inhibiting Eph and Abl Kinases in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  9. Identification of Protein Tyrosine Phosphatase Receptor Type O (PTPRO) as a Synaptic Adhesion Molecule that Promotes Synapse Formation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
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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 3 countries.

Graziana GattoDepartment of Molecules-Signaling-Development, Max Planck Institute of Neurobiology, D-82152, Martinsried, Germany.
Irina Dudanova
Philipp Suetterlin
Alun M Davies
Uwe Drescher
John L Bixby
Rüdiger Klein
Max Planck Society · DEMedical Research Council · GBUniversity of Miami · US

Funding

Novel Compounds That Overcome Glial Inhibition of Axonal RegenerationR01NS059866 · NINDS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI BIXBY, JOHN L · 2009 to 2013
$1.7M
NINDS NIH HHS R01 NS059866Wellcome Trust
6 · The paper itself

Abstract

Axonal branches of the trigeminal ganglion (TG) display characteristic growth and arborization patterns during development. Subsets of TG neurons express different receptors for growth factors, but these are unlikely to explain the unique patterns of axonal arborizations. Intrinsic modulators may restrict or enhance cellular responses to specific ligands and thereby contribute to the development of axon growth patterns. Protein tyrosine phosphatase receptor type O (PTPRO), which is required for Eph receptor-dependent retinotectal development in chick and for development of subsets of trunk sensory neurons in mouse, may be such an intrinsic modulator of TG neuron development. PTPRO is expressed mainly in TrkB-expressing (TrkB(+)) and Ret(+) mechanoreceptors within the TG during embryogenesis. In PTPRO mutant mice, subsets of TG neurons grow longer and more elaborate axonal branches. Cultured PTPRO(-/-) TG neurons display enhanced axonal outgrowth and branching in response to BDNF and GDNF compared with control neurons, indicating that PTPRO negatively controls the activity of BDNF/TrkB and GDNF/Ret signaling. Mouse PTPRO fails to regulate Eph signaling in retinocollicular development and in hindlimb motor axon guidance, suggesting that chick and mouse PTPRO have different substrate specificities. PTPRO has evolved to fine tune growth factor signaling in a cell-type-specific manner and to thereby increase the diversity of signaling output of a limited number of receptor tyrosine kinases to control the branch morphology of developing sensory neurons. The regulation of Eph receptor-mediated developmental processes by protein tyrosine phosphatases has diverged between chick and mouse.

Indexed as

AnimalsAnimals, NewbornAxonsCells, CulturedFemaleGreen Fluorescent ProteinsHEK293 CellsHeLa CellsHumansMaleMembrane GlycoproteinsMiceMice, 129 StrainMice, Inbred C57BLMice, TransgenicMotor NeuronsGreen Fluorescent ProteinsMembrane GlycoproteinsNtrk2 protein, mouseProtein-Tyrosine KinasesProto-Oncogene Proteins c-retPtpro protein, mouseReceptor, EphA1Receptor-Like Protein Tyrosine Phosphatases, Class 3Receptor, trkAReceptor, trkBReceptor, trkCRet protein, mouse

Identifiers

PMID23516305
PMCPMC3667612
OpenAlexW2096616785

What OpenQuestion holds

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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.