ArticleBiochemistry2022
Design, Synthesis, and Evaluation of a Cross-Linked Oligonucleotide as the First Nanomolar Inhibitor of APOBEC3A.
Article in Biochemistry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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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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.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Controlling Topology of a Telomeric G-quadruplex DNA With a Chemical Cross-link.Chemistry (Weinheim an der Bergstrasse, Germany) · 2025Article
- Next generation APOBEC3 inhibitors: optimally designed for potency and nuclease stability.Nucleic acids research · 2025Article
- The cytidine deaminase APOBEC3A regulates nucleolar function to promote cell growth and ribosome biogenesis.PLoS biology · 2024Article
- Synthesis of 1,4-azaphosphinine nucleosides and evaluation as inhibitors of human cytidine deaminase and APOBEC3A.Beilstein journal of organic chemistry · 2024Article
- Structure-guided inhibition of the cancer DNA-mutating enzyme APOBEC3A.Nature communications · 2023Article
- Seven-membered ring nucleobases as inhibitors of human cytidine deaminase and APOBEC3A.Organic & biomolecular chemistry · 2023Article
- Structure-guided inhibition of the cancer DNA-mutating enzyme APOBEC3A.bioRxiv : the preprint server for biology · 2023Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Drug resistance is a major problem associated with anticancer chemo- and immunotherapies. Recent advances in the understanding of resistance mechanisms have revealed that enzymes of the APOBEC3 (A3) family contribute to the development of drug resistance in multiple cancers. A3 enzymes are polynucleotide cytidine deaminases that convert cytosine to uracil (C→U) in single-stranded DNA (ssDNA) and in this way protect humans against viruses and mobile retroelements. On the other hand, cancer cells use A3s, especially A3A and A3B, to mutate human DNA, and thus by increasing rates of evolution, cancer cells escape adaptive immune responses and resist drugs. However, as A3A and A3B are non-essential for primary metabolism, their inhibition opens up a strategy to augment existing anticancer therapies and suppress cancer evolution. To test our hypothesis that pre-shaped ssDNA mimicking the
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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.