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APOBEC3A is a member of the cytidine deaminase gene family.
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Human Polyclonal APOBEC3A Primary Antibody pour WB - ABIN1881066
Thielen, McNevin, McElrath, Hunt, Klein, Lingappa: Innate immune signaling induces high levels of TC-specific deaminase activity in primary monocyte-derived cells through expression of APOBEC3A isoforms. dans The Journal of biological chemistry 2010
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Human Polyclonal APOBEC3A Primary Antibody pour ELISA, IHC - ABIN408686
Zahoor, Xue, Sato, Murakami, Takeshima, Aida: HIV-1 Vpr induces interferon-stimulated genes in human monocyte-derived macrophages. dans PLoS ONE 2014
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direct evidence that both A3A and HPV16 E7 interact with CUL2, suggesting that the E7-CUL2 complex formed during HPV infection may regulate A3A protein levels in the cell.
review of current understanding of APOBEC3A and APOBEC3B (Montrer APOBEC3B Anticorps) biology in human papillomavirus Infection restriction, evolution, and associated cancer mutagenesis
p53 (Montrer TP53 Anticorps) activation alters APOBECA3 gene regulation.Activated p53 (Montrer TP53 Anticorps) binds transcriptional regulatory regions of APOBECA3 gene.
These results highlight the fundamental impact of APOBEC3A overexpression on human transcriptome by widespread RNA editing.
High-level APOBEC3A expression is associated with better overall survival, especially among patients carrying APOBEC3B (Montrer APOBEC3B Anticorps)-deletion alleles in Taiwanese oral squamous cell carcinoma patients.
Our study demonstrates that 20% of C-->T and C-->G mutations in the TpCpW context-where W denotes A or T, segregating as polymorphisms in human population-or 1.4% of all heritable mutations are attributable to APOBEC3A/B activity.
findings reveal the role of A3A as a potent anti-Human cytomegalovirus (HCMV) innate barrier, activated by HCMV infection in the authentic tissues of the maternal-fetal interface. These findings pave the way to new insights into the potential impact of APOBEC proteins on HCMV pathogenesis.
APOBEC3A/B and HLA-DQA1 (Montrer HLA-DQA2 Anticorps) are powerful biomarkers for systemic sclerosis risk evaluation and contribute to the susceptibility to systemic sclerosis.
High APOBEC3A expression is associated with acute myelogenous leukemia.
Steady-state kinetic analysis reveals that APOBEC3A (A3A) discriminates against all ox-mCs by 3700-fold, arguing that ox-mC deamination does not contribute substantially to demethylation. A3A is, by contrast, highly proficient at C/mC deamination.
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