Evidence map›Paper›PMID 38234684›Full record

ArticleFrontiers in cell and developmental biology2023

SIRT7 and p53 interaction in embryonic development and tumorigenesis.

Berta N Vazquez, Irene Fernández-Duran, Yurdiana Hernandez, Shahriar Tarighi, Joshua K Thackray, Maria Espinosa-Alcantud, Poonam Kumari, Alessandro Ianni, Lionel Cesaire, Thomas Braun and 4 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed, 5 citations in OpenAlex.

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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

14 authors at 6 institutions in 3 countries.

Berta N VazquezChromatin Biology Laboratory, Josep Carreras Leukaemia Research Institute (IJC), Badalona, Spain.
Irene Fernández-Duran *Chromatin Biology Laboratory, Josep Carreras Leukaemia Research Institute (IJC), Badalona, Spain.
Yurdiana Hernandez *Department of Genetics, Human Genetics Institute of New Jersey (HGINJ), Rutgers University, Piscataway, NJ, United States.
Shahriar TarighiDepartment of Cardiac Development and Remodeling, Max-Planck-Institute for Heart and Lung Research, Bad Nauheim, Germany.
Joshua K ThackrayDepartment of Genetics, Human Genetics Institute of New Jersey (HGINJ), Rutgers University, Piscataway, NJ, United States.
Maria Espinosa-AlcantudChromatin Biology Laboratory, Josep Carreras Leukaemia Research Institute (IJC), Badalona, Spain.
Poonam KumariDepartment of Cardiac Development and Remodeling, Max-Planck-Institute for Heart and Lung Research, Bad Nauheim, Germany.
Alessandro IanniChromatin Biology Laboratory, Josep Carreras Leukaemia Research Institute (IJC), Badalona, Spain.
Lionel CesaireDepartment of Science, Borough of Manhattan Community College (BMCC), The City University of New York (CUNY), New York, NY, United States.
Thomas BraunDepartment of Cardiac Development and Remodeling, Max-Planck-Institute for Heart and Lung Research, Bad Nauheim, Germany.
Manel EstellerCancer Epigenetics Group, Josep Carreras Leukaemia Research Institute (IJC), Barcelona, Spain.
Jay TischfieldDepartment of Genetics, Human Genetics Institute of New Jersey (HGINJ), Rutgers University, Piscataway, NJ, United States.
Alejandro VaqueroChromatin Biology Laboratory, Josep Carreras Leukaemia Research Institute (IJC), Badalona, Spain.
Lourdes SerranoDepartment of Science, Borough of Manhattan Community College (BMCC), The City University of New York (CUNY), New York, NY, United States.
Josep Carreras Leukaemia Research Institute · ESMax Planck Institute for Heart and Lung Research · DERutgers, The State University of New Jersey · USBorough of Manhattan Community College · USCentro de Investigación Biomédica en Red de Cáncer · ESCity University of New York · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

p53 is a hallmark tumor suppressor due in part to its role in cell cycle progression, DNA damage repair, and cellular apoptosis; its protein activity interrelates with the Sirtuin family of proteins, major regulators of the cellular response to metabolic, oxidative, and genotoxic stress. In the recent years, mammalian Sirtuin 7 (SIRT7) has emerged as a pivotal regulator of p53, fine-tuning its activity in a context dependent manner. SIRT7 is frequently overexpressed in human cancer, yet its precise role in tumorigenesis and whether it involves p53 regulation is insufficiently understood. Depletion of SIRT7 in mice results in impaired embryo development and premature aging. While p53 activity has been suggested to contribute to tissue specific dysfunction in adult

Indexed as

embryonic developmentepithelial to mesenchymal transitiongene expressionp53Sirt7SIRTUINtumor suppressor

Identifiers

PMID38234684
PMCPMC10791984
OpenAlexW4390570593

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.