Evidence map›Paper›PMID 24142877›Full record

ArticleGenes & development2013

Physiological modulation of endogenous BRCA1 p220 abundance suppresses DNA damage during the cell cycle.

Stoil D Dimitrov, David Lu, Nana Naetar, Yiduo Hu, Shailja Pathania, Chryssa Kanellopoulou, David M Livingston

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
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

17 citing papers in PubMed, 22 citations in OpenAlex.

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  7. RAP80 and BRCA1 PARsylation protect chromosome integrity by preventing retention of BRCA1-B/C complexes in DNA repair foci.Proceedings of the National Academy of Sciences of the United States of America · 2020
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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.

Stoil D DimitrovDepartment of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA;
David Lu
Nana Naetar
Yiduo Hu
Shailja Pathania
Chryssa Kanellopoulou
David M Livingston
Dana-Farber Cancer Institute · USHarvard University · US

Funding

Use of Organotypic and Mammary Gland Models to Investigate the Outcomes of ClonalP01CA080111 · NCI · WHITEHEAD INSTITUTE FOR BIOMEDICAL RES · PI DILLON, DEBORAH · 1999 to 2018
$36.0M
BEHAVIORAL INTERVENTION FOR CHILDREN WITH CANCERK04CA000938 · NCI · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI ZELTZER, LONNIE K · 1985 to 1985
–
NCI NIH HHS 5 P01CA80111NCI NIH HHS 5T32CA00938-30NCI NIH HHS P01 CA080111
6 · The paper itself

Abstract

Endogenous BRCA1 p220 expression peaks in S and G2 when it is activated, and the protein participates in certain key DNA damage responses. In contrast, its expression is markedly reduced in G0/G1. While variations in transcription represent a significant part of p220 expression control, there is at least one other relevant process. We found that a microRNA, miR-545, that is expressed throughout the cell cycle down-modulates endogenous p220 mRNA and protein abundance directly in both G0/G1 and S/G2. When miR-545 function was inhibited by a specific antagomir, endogenous p220 expression increased in G0/G1, and aberrant p220-associated DNA damage responses and de novo DNA strand breaks accumulated. Analogous results were observed upon inhibition of miR-545 function in S/G2. Both sets of antagomir effects were mimicked by infecting cells with a p220 cDNA-encoding adenoviral vector. Thus, strand breaks were a product of p220 overexpression, and their prevention by miR-545 depends on its modulation of p220 expression. Breaks were also dependent on aberrant, overexpressed p220-driven recruitment of RAD51 to either spontaneously arising or mutagen-based DNA damage sites. Hence, when its level is not physiologically maintained, endogenous p220 aberrantly directs at least one DNA repair protein, RAD51, to damage sites, where their action contributes to the development of de novo DNA damage. Thus, like its loss, a surfeit of endogenous p220 function represents a threat to genome integrity.

Indexed as

Gene Expression RegulationBinding SitesBRCA1 ProteinCell CycleCell Line, TumorDNA DamageDNA RepairHEK293 CellsHumansMicroRNAsProtein BindingRad51 RecombinaseRNA, MessengerUltraviolet RaysBRCA1 ProteinBRCA1 protein, humanMicroRNAsRad51 RecombinaseRNA, MessengerBRCA1cell cycleDNA damageG0/G1miR-545

Identifiers

PMID24142877
PMCPMC3814647
OpenAlexW2133518321

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.