Evidence map›Paper›PMID 19716796›Full record

ArticleMolecular cell2009

A selective requirement for 53BP1 in the biological response to genomic instability induced by Brca1 deficiency.

Liu Cao, Xioaling Xu, Samuel F Bunting, Jie Liu, Rui-Hong Wang, Longyue L Cao, J Julie Wu, Tie-Nan Peng, Junjie Chen, Andre Nussenzweig and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 197 papers.

0numbers the graph read from it
0cells of the map it votes in
197citing papers in PubMed
8.8field-weighted citation impact, top 2% 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

197 citing papers in PubMed, 301 citations in OpenAlex.

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137 more citing papers are in PubMed but not listed here.

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

12 authors at 5 institutions in 2 countries.

Liu CaoTranslational Medicine Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA. liu.cao@nih.gov
Xioaling Xu
Samuel F Bunting
Jie Liu
Rui-Hong Wang
Longyue L Cao
J Julie Wu
Tie-Nan Peng
Junjie Chen
Andre Nussenzweig
Chu-Xia Deng
Toren Finkel
National Institutes of Health · USJilin University · CNNational Cancer Institute · USNational Heart Lung and Blood Institute · USYale University · US

Funding

The role of autophagy in aging and metabolismZIAHL005012 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI FINKEL, TOREN · 2009 to 2017
$11.8M
Reactive Oxygen Species, Stem cells and AgingZ01HL005012 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI FINKEL, TOREN · 1997 to 2008
$5.5M
Chemoprevention and therapeutic treatment of BRCA1 associated mammary tumorsZIADK056009 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI DENG, CHUXIA · 2009 to 2014
$4.0M
Roles of BRCA1 transcription target genes in tumorigenesis and agingZIADK056011 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI DENG, CHUXIA · 2009 to 2014
$3.9M
Genomic instability in aging and cancerZIAHL006036 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI FINKEL, TOREN · 2010 to 2012
$2.6M
Intramural NIH HHS Z01 HL005012
6 · The paper itself

Abstract

The molecular pathways leading from genomic instability to cellular senescence and/or cell death remain incompletely characterized. Using mouse embryonic fibroblasts with constitutively increased DNA damage due to the absence of the full-length form of the tumor suppressor Brca1 (Brca1(Delta 11/Delta 11)), we show that deletion of p53 binding protein 1 (53BP1) selectivity abrogates senescence and cell death stimulated by reduced Brca1 activity. Furthermore, the embryonic lethality induced by Brca1 mutation can be alleviated by 53BP1 deletion. Adult Brca1(Delta 11/Delta 11)53BP1(-/-) manifest constitutively high levels of genomic instability, yet age relatively normally, with a surprisingly low incidence of overall tumor formation. Together, these in vitro and in vivo data suggest that 53BP1 is specifically required for the development of premature senescence and apoptosis induced by Brca1 deficiency. These observations may have important implications for Brca1-mediated tumor formation as well as for the molecular pathway leading from genomic instability to organismal aging.

Indexed as

Genomic InstabilityAgingAnimalsApoptosisAtaxia Telangiectasia Mutated ProteinsBRCA1 ProteinCell Cycle ProteinsCells, CulturedCell Transformation, NeoplasticCellular SenescenceCheckpoint Kinase 2Chromosomal Proteins, Non-HistoneDNA-Binding ProteinsDoxorubicinFibroblastsGamma RaysAtaxia Telangiectasia Mutated ProteinsAtm protein, mouseBRCA1 ProteinCell Cycle ProteinsCheckpoint Kinase 2Chek2 protein, mouseChromosomal Proteins, Non-HistoneDNA-Binding ProteinsDoxorubicingamma-H2AX protein, mouseHistonesHydrogen PeroxideIntracellular Signaling Peptides and ProteinsProtein Serine-Threonine KinasesTrp53bp1 protein, mouseTumor Suppressor p53-Binding Protein 1Tumor Suppressor Proteins

Identifiers

PMID19716796
PMCPMC3392030
OpenAlexW1970266671

What OpenQuestion holds

Textmetadata
LicenceTDM
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.