ArticleCell cycle (Georgetown, Tex.)2017
Cytidine deaminase deficiency impairs sister chromatid disjunction by decreasing PARP-1 activity.
Article in Cell cycle (Georgetown, Tex.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 13 citations in OpenAlex.
- Regulation of mitotic chromosome architecture and resolution of ultrafine anaphase bridges by PICH.Cell cycle (Georgetown, Tex.) · 2021Article
- A decrease in NAMPT activity impairs basal PARP-1 activity in cytidine deaminase deficient-cells, independently of NADScientific reports · 2020Article
- CDA as a predictive marker for life-threatening toxicities in patients with AML treated with cytarabine.Blood advances · 2018Observational
- CDA gene silencing regulated the proliferation and apoptosis of chronic myeloid leukemia K562 cells.Cancer cell international · 2018Article
- Proper sister chromatid disjunction requires CDA and PARP-1.Cell cycle (Georgetown, Tex.) · 2017Article
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5 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Bloom Syndrome (BS) is a rare genetic disease characterized by high levels of chromosomal instability and an increase in cancer risk. Cytidine deaminase (CDA) expression is downregulated in BS cells, leading to an excess of cellular dC and dCTP that reduces basal PARP-1 activity, compromising optimal Chk1 activation and reducing the efficiency of downstream checkpoints. This process leads to the accumulation of unreplicated DNA during mitosis and, ultimately, ultrafine anaphase bridge (UFB) formation. BS cells also display incomplete sister chromatid disjunction when depleted of cohesin. Using a combination of fluorescence in situ hybridization and chromosome spreads, we investigated the possible role of CDA deficiency in the incomplete sister chromatid disjunction in cohesin-depleted BS cells. The decrease in basal PARP-1 activity in CDA-deficient cells compromised sister chromatid disjunction in cohesin-depleted cells, regardless of BLM expression status. The observed incomplete sister chromatid disjunction may be due to the accumulation of unreplicated DNA during mitosis in CDA-deficient cells, as reflected in the changes in centromeric DNA structure associated with the decrease in basal PARP-1 activity. Our findings reveal a new function of PARP-1 in sister chromatid disjunction during mitosis.
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