Evidence map›Paper›PMID 25645366›Full record

ArticleAging cell2015

Lamin A/C-dependent interaction with 53BP1 promotes cellular responses to DNA damage.

Ian Gibbs-Seymour, Ewa Markiewicz, Simon Bekker-Jensen, Niels Mailand, Christopher J Hutchison

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

58 citing papers in PubMed, 89 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

5 authors at 3 institutions in 2 countries.

Ian Gibbs-SeymourSchool of Biological and Biomedical Sciences, Durham University, Mountjoy Science Park, Durham, DH1 3LE, UK; Ubiquitin Signaling Group, Department of Disease Biology, Novo Nordisk Foundation Center for Protein Research, University of Copenhagen, Copenhagen, DK-2200, Denmark.
Ewa Markiewicz
Simon Bekker-Jensen
Niels Mailand
Christopher J Hutchison
Durham University · GBUniversity of Copenhagen · DKNovo Nordisk Foundation · DK

Funding

Biotechnology and Biological Sciences Research Council be/ko19760/1Worldwide Cancer Research 07-0449
6 · The paper itself

Abstract

Lamins A/C have been implicated in DNA damage response pathways. We show that the DNA repair protein 53BP1 is a lamin A/C binding protein. In undamaged human dermal fibroblasts (HDF), 53BP1 is a nucleoskeleton protein. 53BP1 binds to lamins A/C via its Tudor domain, and this is abrogated by DNA damage. Lamins A/C regulate 53BP1 levels and consequently lamin A/C-null HDF display a 53BP1 null-like phenotype. Our data favour a model in which lamins A/C maintain a nucleoplasmic pool of 53BP1 in order to facilitate its rapid recruitment to sites of DNA damage and could explain why an absence of lamin A/C accelerates aging.

Indexed as

Cell Line, TumorDNA DamageDNA RepairFibroblastsHEK293 CellsHumansIntracellular Signaling Peptides and ProteinsLamin Type AProtein BindingProtein Structure, TertiaryTumor Suppressor p53-Binding Protein 1Intracellular Signaling Peptides and ProteinsLamin Type ALMNA protein, humanTP53BP1 protein, humanTumor Suppressor p53-Binding Protein 153BP1DNA damage responselaminopathylamins

Identifiers

PMID25645366
PMCPMC4364828
OpenAlexW1970417373

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.