ArticleOncogene2009
Familial breast cancer screening reveals an alteration in the RAP80 UIM domain that impairs DNA damage response function.
Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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.
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.
Who cites it
42 citing papers in PubMed, 64 citations in OpenAlex.
- RAP80 phase separation at DNA double-strand break promotes BRCA1 recruitment.Nucleic acids research · 2023Article
- Panel of Engineered Ubiquitin Variants Targeting the Family of Human Ubiquitin Interacting Motifs.ACS chemical biology · 2022Article
- Construction and validation of a novel and superior protein risk model for prognosis prediction in esophageal cancer.Frontiers in genetics · 2022Article
- Review
- FANCJ compensates for RAP80 deficiency and suppresses genomic instability induced by interstrand cross-links.Nucleic acids research · 2020Article
- 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 · 2020Article
- Structural Basis of BRCC36 Function in DNA Repair and Immune Regulation.Molecular cell · 2019Article
- Analysis of mutational signatures in primary and metastatic endometrial cancer reveals distinct patterns of DNA repair defects and shifts during tumor progression.Gynecologic oncology · 2019Article
- Active Site Gate Dynamics Modulate the Catalytic Activity of the Ubiquitination Enzyme E2-25K.Scientific reports · 2018Article
- Molecular Basis for K63-Linked Ubiquitination Processes in Double-Strand DNA Break Repair: A Focus on Kinetics and Dynamics.Journal of molecular biology · 2017Review
- RAP80, ubiquitin and SUMO in the DNA damage response.Journal of molecular medicine (Berlin, Germany) · 2017Review
- ZMYM3 regulates BRCA1 localization at damaged chromatin to promote DNA repair.Genes & development · 2017Article
- RAP80 regulates epithelial-mesenchymal transition related with metastasis and malignancy of cancer.Cancer science · 2016Article
- Genetic evaluation of BRCA1 associated a complex genes with triple-negative breast cancer susceptibility in Chinese women.Oncotarget · 2016Article
- Choreographing the Double Strand Break Response: Ubiquitin and SUMO Control of Nuclear Architecture.Frontiers in genetics · 2016Review
- A BRCA1-interacting lncRNA regulates homologous recombination.EMBO reports · 2015Article
- MERIT40 cooperates with BRCA2 to resolve DNA interstrand cross-links.Genes & development · 2015Article
- Deciphering the BRCA1 Tumor Suppressor Network.The Journal of biological chemistry · 2015Review
- PARP1-driven poly-ADP-ribosylation regulates BRCA1 function in homologous recombination-mediated DNA repair.Cancer discovery · 2014Article
- PALB2: the hub of a network of tumor suppressors involved in DNA damage responses.Biochimica et biophysica acta · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Germline mutations in two major susceptibility genes, BRCA1 and BRCA2, account for nearly 20% of familial breast cancers. A majority of the remaining genetic factors involved in heritable breast cancer susceptibility are, however, unknown. Recently, a new BRCA1-interacting protein, receptor associated protein 80 (RAP80), was identified. RAP80 plays an important role in BRCA1-mediated DNA damage responses (DDRs) by recruiting BRCA1 to DNA double-strand breaks (DSBs). A comprehensive screening of DNA from affected index cases of 112 BRCA1/BRCA2 mutation-negative Finnish breast cancer families revealed altogether 10 alterations in RAP80, one of which, c.241-243delGAA, resulted in a single glutamic acid deletion at residue 81 in a highly conserved region of ubiquitin interaction motif 1. The resultant delE81 protein product displayed significantly reduced ubiquitin binding and DSB localization. Expression of the RAP80 delE81 allele impaired both BRCA1 and ABRA1 DSB recruitment, thus compromising BRCA1-mediated DDR signaling. Compared with wild-type RAP80, expression of the delE81 allele was associated with a significant increase in cytogenetically detectable chromosomal aberrations, particularly chromatid breaks. Although evidently quite rare, these results suggest that critical constitutional mutations in RAP80 abrogate DDR function and may be involved in genetic predisposition to cancer.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.