ArticleThe Journal of biological chemistry2013
A biochemical analysis linking APOBEC3A to disparate HIV-1 restriction and skin cancer.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 48 citations in OpenAlex.
- Chemiluminescent Deoxyribozyme Sensors for DNA-Editing Enzymes.ACS chemical biology · 2026Article
- An overview of the functions and mechanisms of APOBEC3A in tumorigenesis.Acta pharmaceutica Sinica. B · 2024Review
- The role of distinct APOBEC/ADAR mRNA levels in mutational signatures linked to aging and ultraviolet radiation.Scientific reports · 2024Article
- Single-stranded DNA binding proteins influence APOBEC3A substrate preference.Scientific reports · 2021Article
- Structure-Based Design of First-Generation Small Molecule Inhibitors Targeting the Catalytic Pockets of AID, APOBEC3A, and APOBEC3B.ACS pharmacology & translational science · 2021Article
- Review
- APOBEC3A Loop 1 Is a Determinant for Single-Stranded DNA Binding and Deamination.Biochemistry · 2019Article
- APOBEC3s: DNA-editing human cytidine deaminases.Protein science : a publication of the Protein Society · 2019Review
- Nucleotide Weight Matrices Reveal Ubiquitous Mutational Footprints of AID/APOBEC Deaminases in Human Cancer Genomes.Cancers · 2019Article
- Evolutionary effects of the AID/APOBEC family of mutagenic enzymes on human gamma-herpesviruses.Virus evolution · 2019Article
- Crystal structure of the catalytic domain of HIV-1 restriction factor APOBEC3G in complex with ssDNA.Nature communications · 2018Article
- Substrate sequence selectivity of APOBEC3A implicates intra-DNA interactions.Scientific reports · 2018Article
- Correlation of gene expression and associated mutation profiles of APOBEC3A, APOBEC3B, REV1, UNG, and FHIT with chemosensitivity of cancer cell lines to drug treatment.Human genomics · 2018Article
- Expansions, diversification, and interindividual copy number variations of AID/APOBEC family cytidine deaminase genes in lampreys.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Conformational Switch Regulates the DNA Cytosine Deaminase Activity of Human APOBEC3B.Scientific reports · 2017Article
- Enzyme cycling contributes to efficient induction of genome mutagenesis by the cytidine deaminase APOBEC3B.Nucleic acids research · 2017Article
- Family-Wide Comparative Analysis of Cytidine and Methylcytidine Deamination by Eleven Human APOBEC Proteins.Journal of molecular biology · 2017Article
- Activation-induced deoxycytidine deaminase: Structural basis for favoring WRC hot motif specificities unique among APOBEC family members.DNA repair · 2017Article
- NMR-based method of small changes reveals how DNA mutator APOBEC3A interacts with its single-stranded DNA substrate.Nucleic acids research · 2017Article
- Crystal structure of APOBEC3A bound to single-stranded DNA reveals structural basis for cytidine deamination and specificity.Nature communications · 2017Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Human deoxycytidine deaminase APOBEC3A (Apo3A) acts as an HIV-1 restriction factor in cells of myeloid lineage yet functions separately as a potent mutator for genomic DNA. Apo3A activity and C motif deamination specificity exhibit a striking dependence on pH that reflects these two distinct biological processes. Upon infection of macrophages, HIV-1 induces the formation of autophagosomes, and requires autophagosomes for replication, whereas inhibiting lysosomal fusion indicative of late stage autophagy. Here we show that Apo3A has optimal activity and a strict 5'-YYCR motif specificity in the pH 5.8-6.1 range, characteristic of enclosed autophagosomal membrane compartments, and reflective of the mutation pattern of HIV-1. In contrast to the high activity and narrow specificity of Apo3A at acid pH, a 13-30-fold reduction in specific activity is accompanied by relaxed C deamination specificity at pH 7.4-8. Notably, Apo3A is also expressed in keratinocytes, and is up-regulated in skin lesions. At pH 7.9, we show that Apo3A generates transcription-dependent CC → TT tandem mutations on the non-transcribed strand, a hallmark signature of skin cancer. The biochemical data taken in conjunction with the biological up-regulation of Apo3A in skin lesions suggests that enzyme-catalyzed deaminations at adjacent C sites followed by normal replication generating CC → TT mutations provides an alternative molecular basis for the initiation events in skin cancer in contrast to well established pathways in which CC dimers formed in response to UV radiation either undergo nonenzymatic spontaneous deaminations or aberrant replication.
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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.