ArticleFrontiers in microbiology2018
APOBEC3B Activity Is Prevalent in Urothelial Carcinoma Cells and Only Slightly Affected by LINE-1 Expression.
Article in Frontiers in microbiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- New insights into ATR inhibition in muscle invasive bladder cancer: The role of apolipoprotein B mRNA editing catalytic subunit 3B.Oncology research · 2024Article
- Proteomic and transcriptomic profiles of human urothelial cancer cells with histone deacetylase 5 overexpression.Scientific data · 2022Article
- Review
- Foamy Viruses, Bet, and APOBEC3 Restriction.Viruses · 2021Review
- Intestinal metaplasia of the urinary tract harbors potentially oncogenic genetic variants.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2021Article
- Many Different LINE-1 Retroelements Are Activated in Bladder Cancer.International journal of molecular sciences · 2020Article
- Distinctive mutational spectrum and karyotype disruption in long-term cisplatin-treated urothelial carcinoma cell lines.Scientific reports · 2019Article
- HDAC5 Expression in Urothelial Carcinoma Cell Lines Inhibits Long-Term Proliferation but Can Promote Epithelial-to-Mesenchymal Transition.International journal of molecular sciences · 2019Article
- Elephant APOBEC3A cytidine deaminase induces massive double-stranded DNA breaks and apoptosis.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The most common mutational signature in urothelial carcinoma (UC), the most common type of urinary bladder cancer is assumed to be caused by the misdirected activity of APOBEC3 (A3) cytidine deaminases, especially A3A or A3B, which are known to normally restrict the propagation of exogenous viruses and endogenous retroelements such as LINE-1 (L1). The involvement of A3 proteins in urothelial carcinogenesis is unexpected because, to date, UC is thought to be caused by chemical carcinogens rather than viral activity. Therefore, we explored the relationship between A3 expression and L1 activity, which is generally upregulated in UC. We found that UC cell lines highly express A3B and in some cases A3G, but not A3A, and exhibit corresponding cytidine deamination activity
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Registered trials
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