ArticleCell cycle (Georgetown, Tex.)2016
BCL10 is recruited to sites of DNA damage to facilitate DNA double-strand break repair.
Article in Cell cycle (Georgetown, Tex.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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
10 citing papers in PubMed, 17 citations in OpenAlex.
- Targeting racial disparities in breast cancer: mechanistic insights and therapeutic potential of African medicinal plants.Medical oncology (Northwood, London, England) · 2025Review
- High-expression of BCL10 inhibits cell-mediated immunity within the tumor immune microenvironment.Frontiers in immunology · 2025Article
- Bcl10 phosphorylation-dependent droplet-like condensation positively regulates DNA virus-induced innate immune signaling.Science China. Life sciences · 2023Article
- Epigenetic Determinants of Racial Disparity in Breast Cancer: Looking beyond Genetic Alterations.Cancers · 2022Review
- Establishment and Validation of a Peroxisome-related Gene Signature for Prognostic Prediction and Immune Distinction in Hepatocellular Carcinoma.Journal of Cancer · 2022Article
- Contribution of nuclear BCL10 expression to tumor progression and poor prognosis of advanced and/or metastatic pancreatic ductal adenocarcinoma by activating NF-κB-related signaling.Cancer cell international · 2021Article
- Differential Expression Profile of NLRs and AIM2 in Glioma and Implications for NLRP12 in Glioblastoma.Scientific reports · 2019Article
- RNF126 Quenches RNF168 Function in the DNA Damage Response.Genomics, proteomics & bioinformatics · 2018Article
- BCL10 - Bridging CARDs to Immune Activation.Frontiers in immunology · 2018Review
- Ubc13: the Lys63 ubiquitin chain building machine.Oncotarget · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 2 countries.
Funding
Abstract
Recent studies have found BCL10 can localize to the nucleus and that this is linked to tumor aggression and poorer prognosis. These studies suggest that BCL10 localization plays a novel role in the nucleus that may contribute to cellular transformation and carcinogenesis. In this study, we show that BCL10 functions as part of the DNA damage response (DDR). We found that BCL10 facilitates the rapid recruitment of RPA, BRCA1 and RAD51 to sites of DNA damage. Furthermore, we also found that ATM phosphorylates BCL10 in response to DNA damage. Functionally, BCL10 promoted DNA double-strand breaks repair, enhancing cell survival after DNA damage. Taken together our results suggest a novel role for BCL10 in the repair of DNA lesions.
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.