ArticleCancer research2012
RAP80 is critical in maintaining genomic stability and suppressing tumor development.
Article in Cancer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 27 citations in OpenAlex.
- Complexes Formed by the K63-Specific Deubiquitinating Enzyme BRCC36: New Promising Therapeutic Targets in Human Disease.Biomolecules · 2025Review
- Article
- Review
- UBC13-Mediated Ubiquitin Signaling Promotes Removal of Blocking Adducts from DNA Double-Strand Breaks.iScience · 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
- Article
- RAP80 is an independent prognosis biomarker for the outcome of patients with esophageal squamous cell carcinoma.Cell death & disease · 2018Article
- BRE plays an essential role in preventing replicative and DNA damage-induced premature senescence.Scientific reports · 2016Article
- RAP80 regulates epithelial-mesenchymal transition related with metastasis and malignancy of cancer.Cancer science · 2016Article
- 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
- Repair versus Checkpoint Functions of BRCA1 Are Differentially Regulated by Site of Chromatin Binding.Cancer research · 2015Article
- Fine-tuning the ubiquitin code at DNA double-strand breaks: deubiquitinating enzymes at work.Frontiers in genetics · 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
- Molecular basis for impaired DNA damage response function associated with the RAP80 ΔE81 defect.The Journal of biological chemistry · 2014Article
- 53BP1, BRCA1, and the choice between recombination and end joining at DNA double-strand breaks.Molecular and cellular biology · 2014Review
- Ubiquitin-dependent recruitment of the Bloom syndrome helicase upon replication stress is required to suppress homologous recombination.The EMBO journal · 2013Article
- RNA splicing: a new player in the DNA damage response.International journal of cell biology · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
The ubiquitin interaction motif-containing protein RAP80 was recently found to play a key role in DNA damage response (DDR) signaling by facilitating the translocation of several DDR mediators, including BRCA1, to ionizing irradiation (IR)-induced foci. In this study, we examine the effect of the loss of RAP80 on genomic stability and the susceptibility to cancer development in RAP80 null (RAP80(-/-)) mice. RAP80(-/-) mice are viable and did not exhibit any apparent developmental defects. Mouse embryonic fibroblasts (MEF) derived from RAP80(-/-) mice underwent premature senescence compared with wild-type (WT) MEFs, were more sensitive to IR, and exhibited a higher level of spontaneous and IR-induced genomic instability. RAP80(-/-) thymocytes were more sensitive to IR-induced cell death than WT thymocytes. RAP80(-/-) mice were more susceptible to spontaneous lymphoma development and the development of 7,12-dimethylbenz(a)anthracene-induced mammary gland tumors. Moreover, the loss of RAP80 accelerated tumor formation in both p53(-/-) and p53(+/-) mice. Our data indicate that RAP80-deficiency promotes genomic instability and causes an increase in cancer risk consistent with the concept that RAP80 exhibits a tumor suppressor function.
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.