Evidence map›Paper›PMID 33495326›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2021

SIRT7-dependent deacetylation of NPM promotes p53 stabilization following UV-induced genotoxic stress.

Alessandro Ianni, Poonam Kumari, Shahriar Tarighi, Nicolas G Simonet, Daniela Popescu, Stefan Guenther, Soraya Hölper, Andreas Schmidt, Christian Smolka, Shijing Yue and 5 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. 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
6.1field-weighted citation impact, top 3% 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, 64 citations in OpenAlex.

  1. Aging and cancer: current understandings and future perspectives.Signal transduction and targeted therapy · 2026
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  17. SIRT7 promotes lung cancer progression by destabilizing the tumor suppressor ARF.Proceedings of the National Academy of Sciences of the United States of America · 2024
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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

15 authors at 6 institutions in 4 countries.

Alessandro IanniDepartment of Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, 61231 Bad Nauheim, Germany; alessandro.ianni@mpi-bn.mpg.de thomas.braun@mpi-bn.mpg.de.
Poonam KumariDepartment of Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, 61231 Bad Nauheim, Germany.ORCID 0000-0001-9646-2426
Shahriar TarighiDepartment of Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, 61231 Bad Nauheim, Germany.ORCID 0000-0003-3807-9212
Nicolas G SimonetChromatin Biology Laboratory, Josep Carreras Leukaemia Research Institute (IJC), 08916 Barcelona, Spain.ORCID 0000-0001-9921-7645
Daniela PopescuDepartment of Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, 61231 Bad Nauheim, Germany.
Stefan GuentherDepartment of Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, 61231 Bad Nauheim, Germany.
Soraya HölperDepartment of Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, 61231 Bad Nauheim, Germany.
Andreas SchmidtCologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), Universität zu Köln, 50931 Köln, Germany.
Christian SmolkaDepartment of Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, 61231 Bad Nauheim, Germany.ORCID 0000-0003-2341-2406
Shijing YueThe State International Science & Technology Cooperation Base of Tumor Immunology and Biological Vaccines, Nankai University, Tianjin 300071, China.
Marcus KrügerCologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), Universität zu Köln, 50931 Köln, Germany.ORCID 0000-0002-5846-6941
Claudia FiorilloDepartment of Experimental and Clinical Biomedical Sciences "Mario Serio," University of Firenze, Firenze 50139, Italy.
Alejandro VaqueroChromatin Biology Laboratory, Josep Carreras Leukaemia Research Institute (IJC), 08916 Barcelona, Spain.ORCID 0000-0002-8735-4156
Eva BoberDepartment of Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, 61231 Bad Nauheim, Germany.
Thomas BraunDepartment of Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, 61231 Bad Nauheim, Germany; alessandro.ianni@mpi-bn.mpg.de thomas.braun@mpi-bn.mpg.de.ORCID 0000-0002-6165-4804
Max Planck Institute for Heart and Lung Research · DEJosep Carreras Leukaemia Research Institute · ESUniversity of Cologne · DENankai University · CNUniversity Medical Center Freiburg · DEUniversity of Florence · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adaptation to different forms of environmental stress is crucial for maintaining essential cellular functions and survival. The nucleolus plays a decisive role as a signaling hub for coordinating cellular responses to various extrinsic and intrinsic cues. p53 levels are normally kept low in unstressed cells, mainly due to E3 ubiquitin ligase MDM2-mediated degradation. Under stress, nucleophosmin (NPM) relocates from the nucleolus to the nucleoplasm and binds MDM2, thereby preventing degradation of p53 and allowing cell-cycle arrest and DNA repair. Here, we demonstrate that the mammalian sirtuin SIRT7 is an essential component for the regulation of p53 stability during stress responses induced by ultraviolet (UV) irradiation. The catalytic activity of SIRT7 is substantially increased upon UV irradiation through ataxia telangiectasia mutated and Rad3 related (ATR)-mediated phosphorylation, which promotes efficient deacetylation of the SIRT7 target NPM. Deacetylation is required for stress-dependent relocation of NPM into the nucleoplasm and MDM2 binding, thereby preventing ubiquitination and degradation of p53. In the absence of SIRT7, stress-dependent stabilization of p53 is abrogated, both in vitro and in vivo, impairing cellular stress responses. The study uncovers an essential SIRT7-dependent mechanism for stabilization of the tumor suppressor p53 in response to genotoxic stress.

Indexed as

DNA DamageUltraviolet RaysAcetylationAnimalsAtaxia Telangiectasia Mutated ProteinsCatalysisCell Line, TumorCell NucleolusHumansLysineMiceMice, Inbred C57BLNuclear ProteinsNucleophosminPhosphorylationProtein StabilityAtaxia Telangiectasia Mutated ProteinsAtr protein, mouseLysineNPM1 protein, humanNuclear ProteinsNucleophosminProto-Oncogene Proteins c-mdm2Sirt7 protein, mouseSirtuinsTumor Suppressor Protein p53acetylationnucleolusnucleophosminp53sirtuins

Identifiers

PMID33495326
PMCPMC7865150
OpenAlexW3121945144

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.