Evidence map›Paper›PMID 23665224›Full record

ArticleCell reports2013

The Phr1 ubiquitin ligase promotes injury-induced axon self-destruction.

Elisabetta Babetto, Bogdan Beirowski, Emilie V Russler, Jeffrey Milbrandt, Aaron DiAntonio

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers.

0numbers the graph read from it
0cells of the map it votes in
116citing papers in PubMed
7.8field-weighted citation impact, top 2% 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

116 citing papers in PubMed, 170 citations in OpenAlex.

  1. The Repair Manual of a Fruit Fly Brain.International journal of molecular sciences · 2026
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  9. Pathogenic variants inmedRxiv : the preprint server for health sciences · 2025
    Article
  10. Stepwise activation of SARM1 for cell death and axon degeneration revealed by a biosynthetic NMN mimic.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  11. SARM1-Dependent Axon Degeneration: Nucleotide Signaling, Neurodegenerative Disorders, Toxicity, and Therapeutic Opportunities.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2024
    Review
  12. Article
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  17. A nerve-wracking buzz: lessons fromFrontiers in aging neuroscience · 2023
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  18. Review
  19. The NADeLife · 2022
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56 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Elisabetta BabettoDepartment of Developmental Biology, Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, MO 63110, USA.
Bogdan Beirowski
Emilie V Russler
Jeffrey Milbrandt
Aaron DiAntonio
Washington University in St. Louis · USHope Center for Neurological Disorders · US

Funding

PHYSIOLOGY AND GENETICS OF THE GDNF HOMOLOG NEURTURINR01AG013730 · NIA · WASHINGTON UNIVERSITY · PI JEFFREY D MILBRANDT · 1996 to 2026
$10.6M
Regulation of axonal degeneration by the DLK kinaseR37NS065053 · NINDS · WASHINGTON UNIVERSITY · PI Aaron Diantonio · 2020 to 2026
$4.3M
MOLECULAR PATHWAYS REGULATING SYNAPTIC GROWTHR01DA020812 · NIDA · WASHINGTON UNIVERSITY · PI DIANTONIO, AARON · 2007 to 2016
$3.3M
REGULATION OF AXONAL DEGENERATION BY THE DLK KINASER01NS065053 · NINDS · WASHINGTON UNIVERSITY · PI DIANTONIO, AARON · 2010 to 2019
$3.3M
IDENTIFICATION OF AXONAL DEGENERATION PATHWAYSR01NS078007 · NINDS · WASHINGTON UNIVERSITY · PI DIANTONIO, AARON, MILBRANDT, JEFFREY D · 2012 to 2014
$1.8M
NIA NIH HHS R01 AG013730NIDA NIH HHS DA020812NIDA NIH HHS R01 DA020812NINDS NIH HHS NS065053NINDS NIH HHS NS078007NINDS NIH HHS R01 NS065053NINDS NIH HHS R01 NS078007NINDS NIH HHS R37 NS065053
6 · The paper itself

Abstract

Axon degeneration is an evolutionarily conserved process that drives the loss of damaged axons and is an early event in many neurological disorders, so it is important to identify the molecular constituents of this poorly understood mechanism. Here, we demonstrate that the Phr1 E3 ubiquitin ligase is a central component of this axon degeneration program. Loss of Phr1 results in prolonged survival of severed axons in both the peripheral and central nervous systems, as well as preservation of motor and sensory nerve terminals. Phr1 depletion increases the axonal level of the axon survival molecule nicotinamide mononucleotide adenyltransferase 2 (NMNAT2), and NMNAT2 is necessary for Phr1-dependent axon stability. The profound long-term protection of peripheral and central mammalian axons following Phr1 deletion suggests that pharmacological inhibition of Phr1 function may be an attractive therapeutic candidate for amelioration of axon loss in neurological disease.

Indexed as

AnimalsAxonsCarrier ProteinsCells, CulturedGanglia, SpinalMAP Kinase Kinase KinasesMiceMice, KnockoutNerve DegenerationNeuritesNicotinamide-Nucleotide AdenylyltransferaseRNA InterferenceRNA, Small InterferingUbiquitin-Protein LigasesVincristineCarrier ProteinsMAP Kinase Kinase Kinasesmitogen-activated protein kinase kinase kinase 12Mycbp2 protein, mouseNicotinamide-Nucleotide AdenylyltransferaseNmnat2 protein, mouseRNA, Small InterferingUbiquitin-Protein LigasesVincristine

Identifiers

PMID23665224
PMCPMC3671584
OpenAlexW2104604323

What OpenQuestion holds

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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.