Evidence map›Paper›PMID 24190996›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2013

TAp73 knockout mice show morphological and functional nervous system defects associated with loss of p75 neurotrophin receptor.

Maria Victoria Niklison-Chirou, Joern R Steinert, Massimiliano Agostini, Richard A Knight, David Dinsdale, Antonio Cattaneo, Tak W Mak, Gerry Melino

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

39 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Structural diversity of p63 and p73 isoforms.Cell death and differentiation · 2022
    Review
  5. Review
  6. Article
  7. Article
  8. Aging · 2021
    Article
  9. Article
  10. Article
  11. Regulation of Adult Neurogenesis in Mammalian Brain.International journal of molecular sciences · 2020
    Review
  12. Article
  13. The Non-coding Side of Medulloblastoma.Frontiers in cell and developmental biology · 2020
    Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Clinical implications of the deregulated TP73 isoforms expression in cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2018
    Review
  20. Article
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

8 authors at 4 institutions in 3 countries.

Maria Victoria Niklison-ChirouToxicology Unit, Medical Research Council, Leicester LE1 9HN, United Kingdom.
Joern R Steinert
Massimiliano Agostini
Richard A Knight
David Dinsdale
Antonio Cattaneo
Tak W Mak
Gerry Melino
Medical Research Council · GBEuropean Brain Research Institute · ITPrincess Margaret Cancer Centre · CAUniversity of Leicester · GB

Funding

Medical Research Council MC_U132670600Medical Research Council MC_U132681855Telethon GGP09133
6 · The paper itself

Abstract

Total and N-terminal isoform selective p73 knockout mice show a variety of central nervous system defects. Here we show that TAp73 is a transcriptional activator of p75 neurotrophin receptor (p75(NTR)) and that p75(NTR) mRNA and protein levels are strongly reduced in the central and peripheral nervous systems of p73 knockout mice. In parallel, primary cortical neurons from p73 knockout mice showed a reduction in neurite outgrowth and in nerve growth factor-mediated neuronal differentiation, together with reduced miniature excitatory postsynaptic current frequencies and behavioral defects. p73 null mice also have impairments in the peripheral nervous system with reduced thermal sensitivity, axon number, and myelin thickness. At least some of these morphological and functional impairments in p73 null cells can be rescued by p75(NTR) re-expression. Together, these data demonstrate that loss of p75(NTR) contributes to the neurological phenotype of p73 knockout mice.

Indexed as

AnimalsBlotting, WesternBrainComputational BiologyMiceMice, KnockoutMiniature Postsynaptic PotentialsMyelin SheathNervous System MalformationsNeuritesNuclear ProteinsReceptors, Nerve Growth FactorReverse Transcriptase Polymerase Chain ReactionTranscriptional Activationdelta Np73, mouseNgfr protein, mouseNuclear ProteinsReceptors, Nerve Growth FactorCGRPNGFp53 familysciatic nerve

Identifiers

PMID24190996
PMCPMC3839698
OpenAlexW2069519707

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.