Evidence map›Paper›PMID 32427887›Full record

ArticleCommunications biology2020

Tau affects P53 function and cell fate during the DNA damage response.

Martina Sola, Claudia Magrin, Giona Pedrioli, Sandra Pinton, Agnese Salvadè, Stéphanie Papin, Paolo Paganetti

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.9field-weighted citation impact, top 7% 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

33 citing papers in PubMed, 49 citations in OpenAlex.

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  18. Genetic Networks of Alzheimer's Disease, Aging, and Longevity in Humans.International journal of molecular sciences · 2023
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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 2 institutions in 1 country.

Martina Sola *Neurodegeneration Research Group, Laboratory for Biomedical Neurosciences, Ente Cantonale Ospedaliero, Torricella-Taverne, Switzerland.
Claudia Magrin *Neurodegeneration Research Group, Laboratory for Biomedical Neurosciences, Ente Cantonale Ospedaliero, Torricella-Taverne, Switzerland.
Giona PedrioliNeurodegeneration Research Group, Laboratory for Biomedical Neurosciences, Ente Cantonale Ospedaliero, Torricella-Taverne, Switzerland.ORCID http://orcid.org/0000-0003-4401-5995
Sandra PintonNeurodegeneration Research Group, Laboratory for Biomedical Neurosciences, Ente Cantonale Ospedaliero, Torricella-Taverne, Switzerland.
Agnese SalvadèNeurodegeneration Research Group, Laboratory for Biomedical Neurosciences, Ente Cantonale Ospedaliero, Torricella-Taverne, Switzerland.
Stéphanie PapinNeurodegeneration Research Group, Laboratory for Biomedical Neurosciences, Ente Cantonale Ospedaliero, Torricella-Taverne, Switzerland.
Paolo PaganettiNeurodegeneration Research Group, Laboratory for Biomedical Neurosciences, Ente Cantonale Ospedaliero, Torricella-Taverne, Switzerland. paolo.paganetti@eoc.ch.ORCID http://orcid.org/0000-0003-1896-6324
Laboratory for Biomedical Neurosciences · CHUniversity of Basel · CH

Funding

Swiss National Science Foundation 166612
6 · The paper itself

Abstract

Cells are constantly exposed to DNA damaging insults. To protect the organism, cells developed a complex molecular response coordinated by P53, the master regulator of DNA repair, cell division and cell fate. DNA damage accumulation and abnormal cell fate decision may represent a pathomechanism shared by aging-associated disorders such as cancer and neurodegeneration. Here, we examined this hypothesis in the context of tauopathies, a neurodegenerative disorder group characterized by Tau protein deposition. For this, the response to an acute DNA damage was studied in neuroblastoma cells with depleted Tau, as a model of loss-of-function. Under these conditions, altered P53 stability and activity result in reduced cell death and increased cell senescence. This newly discovered function of Tau involves abnormal modification of P53 and its E3 ubiquitin ligase MDM2. Considering the medical need with vast social implications caused by neurodegeneration and cancer, our study may reform our approach to disease-modifying therapies.

Indexed as

DNA RepairCell Line, TumorDNA DamageHumanstau ProteinsTumor Suppressor Protein p53MAPT protein, humantau ProteinsTumor Suppressor Protein p53

Identifiers

PMID32427887
PMCPMC7237658
OpenAlexW3027255994

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.