Evidence map›Paper›PMID 33823136›Full record

ArticleDevelopmental cell2021

An anterograde pathway for sensory axon degeneration gated by a cytoplasmic action of the transcriptional regulator P53.

David J Simon, Deanna M Belsky, Margot E Bowen, Christine Y J Ohn, Melanie K O'Rourke, Rebecca Shen, Garam Kim, Jason Pitts, Laura D Attardi, Marc Tessier-Lavigne

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Developmental cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.7field-weighted citation impact, top 27% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
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  4. Review
  5. 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

10 authors at 3 institutions in 1 country.

David J SimonLaboratory of Brain Development and Repair, Rockefeller University, New York, NY 10065, USA; Department of Biology, Stanford University, Stanford, CA 94305, USA; Department of Biochemistry, Weill Cornell Medical College, New York, NY 10065, USA. Electronic address: djs4002@med.cornell.edu.
Deanna M BelskyLaboratory of Brain Development and Repair, Rockefeller University, New York, NY 10065, USA; Department of Biology, Stanford University, Stanford, CA 94305, USA.
Margot E BowenDivision of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Christine Y J OhnDepartment of Biochemistry, Weill Cornell Medical College, New York, NY 10065, USA.
Melanie K O'RourkeDepartment of Biology, Stanford University, Stanford, CA 94305, USA.
Rebecca ShenDepartment of Biology, Stanford University, Stanford, CA 94305, USA.
Garam KimDepartment of Biology, Stanford University, Stanford, CA 94305, USA.
Jason PittsLaboratory of Brain Development and Repair, Rockefeller University, New York, NY 10065, USA.
Laura D AttardiDivision of Radiation and Cancer Biology, Department of Radiation Oncology, Stanford University School of Medicine, Stanford, CA 94305, USA; Department of Genetics, Stanford University School of Medicine, Stanford, CA 94305, USA.
Marc Tessier-LavigneLaboratory of Brain Development and Repair, Rockefeller University, New York, NY 10065, USA; Department of Biology, Stanford University, Stanford, CA 94305, USA. Electronic address: tessier3@stanford.edu.
Stanford University · USRockefeller University · USCornell University · US

Funding

Leveraging innovative technologies in basic and clinical cancer researchT32CA009302 · NCI · STANFORD UNIVERSITY · PI LAURA D ATTARDI, Aaron M Newman · 1985 to 2026
$19.1M
Integrative approaches to elucidate p53 transcriptional networks during carcinogenesisR35CA197591 · NCI · STANFORD UNIVERSITY · PI LAURA D ATTARDI · 2015 to 2026
$11.6M
Regulation of axon degeneration by the apoptotic pathwayR01NS089786 · NINDS · STANFORD UNIVERSITY · PI TESSIER-LAVIGNE, MARC · 2014 to 2018
$2.8M
NCI NIH HHS R35 CA197591NCI NIH HHS T32 CA009302NINDS NIH HHS R01 NS089786
6 · The paper itself

Abstract

Axon remodeling through sprouting and pruning contributes to the refinement of developing neural circuits. A prominent example is the pruning of developing sensory axons deprived of neurotrophic support, which is mediated by a caspase-dependent (apoptotic) degeneration process. Distal sensory axons possess a latent apoptotic pathway, but a cell body-derived signal that travels anterogradely down the axon is required for pathway activation. The signaling mechanisms that underlie this anterograde process are poorly understood. Here, we show that the tumor suppressor P53 is required for anterograde signaling. Interestingly loss of P53 blocks axonal but not somatic (i.e., cell body) caspase activation. Unexpectedly, P53 does not appear to have an acute transcriptional role in this process and instead appears to act in the cytoplasm to directly activate the mitochondrial apoptotic pathway in axons. Our data support the operation of a cytoplasmic role for P53 in the anterograde death of developing sensory axons.

Indexed as

AnimalsAxonsbcl-X ProteinCaspasesCells, CulturedCytoplasmMiceProtein DomainsSensory Receptor CellsTumor Suppressor Protein p53bcl-X ProteinCaspasesTrp53 protein, mouseTumor Suppressor Protein p53anterogradeaxonaxon degenerationBAXcaspasecytoplasmic p53neurodegenerationp53

Identifiers

PMID33823136
PMCPMC8034543
OpenAlexW3140313097

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.