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APOBEC3A is a member of the cytidine deaminase gene family. Additionally we are shipping APOBEC3A Antibodies (64) and many more products for this protein.
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The findings demonstrate that DNA replication provides ssDNA substrate that is susceptible to deamination by A3A. Thus, aberrant A3A activity leading to genomic damage may specifically impact rapidly replicating cells
results suggest that the APOBEC3A/3B deletion polymorphism is not significantly associated with cancer risk in our study population
Our results suggest that genetic variations in driver and APOBEC3 (show APOBEC3F Proteins) genes were associated with the risk of BC and may have impact on clinical outcome.
APOBEC3A and APOBEC3B (show APOBEC3B Proteins) preferentially deaminate the lagging strand template during DNA replication.
Germline variant and deletion polymorphism in APOBEC3A gene are not associated with breast cancer risk.
These results indicate that the mechanisms of APOBEC3 (show APOBEC3F Proteins) restriction of Koala Retro Virus by humanA3G and mouseA3 differ (deamination dependent vs. independent) and glyco-gag does not play a role in the restriction.
The role of APOBEC3A in mediating this change was confirmed by A3A overexpression in Fujioka cells, which led to a significant increase in WT1 (show WT1 Proteins) c.1303G>A mRNA editing.
This study demonstrates the cellular RNA editing activity of a member of the APOBEC3 (show APOBEC3F Proteins) family of innate restriction factors and expands the understanding of C>U RNA editing in mammals.
Structural studies show that specific binding of single-stranded DNA is regulated by the cooperative dimerization of APOBEC3A.
AFM image analyses reveal A3A binding to single-stranded DNA, and that this interaction becomes most evident ( approximately 80% complex yield) at high protein-to-DNA ratios (at least 100ratio1). A3A is predominantly monomeric when bound to single-stranded DNA.
This gene is a member of the cytidine deaminase gene family. It is one of seven related genes or pseudogenes found in a cluster, thought to result from gene duplication, on chromosome 22. Members of the cluster encode proteins that are structurally and functionally related to the C to U RNA-editing cytidine deaminase APOBEC1. The protein encoded by this gene lacks the zinc binding activity of other family members. The protein plays a role in immunity, by restricting transmission of foreign DNA such as viruses. One mechanism of foreign DNA restriction is deamination of foreign double-stranded DNA cytidines to uridines, which leads to DNA degradation. However, other mechanisms are also thought to be involved, as anti-viral effect is not dependent on deaminase activity. Two transcript variants encoding different isoforms have been found for this gene.
DNA dC->dU-editing enzyme APOBEC-3A
, phorbolin 1
, probable DNA dC->dU-editing enzyme APOBEC-3A
, apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like 3A
, similar to ARP10 protein