ArticleCell cycle (Georgetown, Tex.)2012
Alteration/deficiency in activation-3 (Ada3) plays a critical role in maintaining genomic stability.
Article in Cell cycle (Georgetown, Tex.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 24 citations in OpenAlex.
- The Crosstalk of Long Non-Coding RNA and MicroRNA in Castration-Resistant and Neuroendocrine Prostate Cancer: Their Interaction and Clinical Importance.International journal of molecular sciences · 2021Review
- Peripheral Blood RNA Sequencing Unravels a Differential Signature of Coding and Noncoding Genes by Types of Kidney Allograft Rejection.Kidney international reports · 2020Article
- Evaluation of the impact of bioaccumulation of PAH from the marine environment on DNA integrity and oxidative stress in marine rock oyster (Saccostrea cucullata) along the Arabian sea coast.Ecotoxicology (London, England) · 2017Article
- Epidermal Growth Factor Receptor activation promotes ADA3 acetylation through the AKT-p300 pathway.Cell cycle (Georgetown, Tex.) · 2017Article
- KAT2-mediated PLK4 acetylation contributes to genomic stability by preserving centrosome number.Molecular & cellular oncology · 2017Article
- ADA3 regulates normal and tumor mammary epithelial cell proliferation through c-MYC.Breast cancer research : BCR · 2016Article
- Acetylation of Mammalian ADA3 Is Required for Its Functional Roles in Histone Acetylation and Cell Proliferation.Molecular and cellular biology · 2016Article
- Tale of a multifaceted co-activator, hADA3: from embryogenesis to cancer and beyond.Open biology · 2016Review
- Alteration/Deficiency in Activation 3 (ADA3) Protein, a Cell Cycle Regulator, Associates with the Centromere through CENP-B and Regulates Chromosome Segregation.The Journal of biological chemistry · 2015Article
- Co-expression analysis of fetal weight-related genes in ovine skeletal muscle during mid and late fetal development stages.International journal of biological sciences · 2014Article
- Cytoplasmic localization of alteration/deficiency in activation 3 (ADA3) predicts poor clinical outcome in breast cancer patients.Breast cancer research and treatment · 2013Article
- Genomic instability: Ada3 and HPV E6-acetyltransferase connections?Cell cycle (Georgetown, Tex.) · 2013Article
- Alteration/deficiency in activation 3 (ADA3): Regulator of DNA repair and genome stability.Cell cycle (Georgetown, Tex.) · 2012Article
Corrections and comments
- Commented on by
- Commented on by
Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
Cell cycle regulation and DNA repair following damage are essential for maintaining genome integrity. DNA damage activates checkpoints in order to repair damaged DNA prior to exit to the next phase of cell cycle. Recently, we have shown the role of Ada3, a component of various histone acetyltransferase complexes, in cell cycle regulation, and loss of Ada3 results in mouse embryonic lethality. Here, we used adenovirus-Cre-mediated Ada3 deletion in Ada3(fl/fl) mouse embryonic fibroblasts (MEFs) to assess the role of Ada3 in DNA damage response following exposure to ionizing radiation (IR). We report that Ada3 depletion was associated with increased levels of phospho-ATM (pATM), γH2AX, phospho-53BP1 (p53BP1) and phospho-RAD51 (pRAD51) in untreated cells; however, radiation response was intact in Ada3(-/-) cells. Notably, Ada3(-/-) cells exhibited a significant delay in disappearance of DNA damage foci for several critical proteins involved in the DNA repair process. Significantly, loss of Ada3 led to enhanced chromosomal aberrations, such as chromosome breaks, fragments, deletions and translocations, which further increased upon DNA damage. Notably, the total numbers of aberrations were more clearly observed in S-phase, as compared with G₁ or G₂ phases of cell cycle with IR. Lastly, comparison of DNA damage in Ada3(fl/fl) and Ada3(-/-) cells confirmed higher residual DNA damage in Ada3(-/-) cells, underscoring a critical role of Ada3 in the DNA repair process. Taken together, these findings provide evidence for a novel role for Ada3 in maintenance of the DNA repair process and genomic stability.
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.