Recombinant Human DNA dC->dU-editing enzyme APOBEC-3G (APOBEC3G)

1. It has been shown that HCMV has evolved mutational robustness against IFN-beta by limiting the presence of APOBEC3G hot spots in essential open reading frames of its genome. PMID: 30045985
2. We found that A3G regulates the expression of several cellular proteins, which influences the capacity of the host cell to replicate measles virus. PMID: 29925665
3. Low APOBEC3G expression is associated with HIV-1 replication. PMID: 29677220
4. study concludes that hA3G may restrict porcine endogenous retrovirus (PERV) by both deamination-dependent mechanisms and inhibition of DNA strand transfer during PERV reverse transcription. PMID: 29610985
5. two stem-loop structures within the 5'-untranslated region of A3G mRNA are crucial for translation inhibition by Vif in HIV-infected cells, and most Vif alleles neutralize A3G translation efficiently PMID: 27996044
6. DNA substrate selection by APOBEC3G PMID: 29596531
7. these findings indicate that A3G is associated with cervical intraepithelial neoplasia , suggesting its important roles in human papillomavirus-induced pathophysiological processes such as cervical intraepithelial neoplasia progression and viral elimination PMID: 28590025
8. These findings report genetic variants possibly associated with susceptibility to HIV-1 infection (CUL5 rs11212495, rs7103534, rs7117111) and partial viral load control (APOBEC3G rs2294367). PMID: 28302043
9. analysis indicated that IL-6 also increased the expression of A3B through JAK1/STAT3 signaling pathway, which formed a positive feedback to maintain the continuous expression of A3B and IL-6, and thereby promoted the prolonged non-resolving inflammation PMID: 28646470
10. The goal of this methods review is through example of our research on APOBEC3G, describe the application of cross-linking methods to characterize and quantify macromolecular interactions and their functional implications PMID: 26988126
11. Our results identify APOBEC3G as a new candidate biomarker for tumor-infiltrating T lymphocytes and favorable prognoses for HGSOC. PMID: 27016308
12. propose that APOBEC3G has the ability to induce T cell plasticity and modulate immune response. PMID: 27282578
13. The results show for the first time the nuclear translocation of A3G in activated-proliferating CD4(+) T cells. PMID: 26987686
14. Mouse mammary tumour virus only moderately susceptible to inhibition by the human APOBEC3G. PMID: 28809145
15. Data suggest that heat shock proteins, in particular Hsp90, stimulate APOBEC3-mediated DNA deamination activity toward hepatitis B viral DNA, suggesting a potential physiological role in mutagenesis/carcinogenesis and viral innate immunity; Hsp90 stimulates deamination activity of APOBEC3G, APOBEC3B, and APOBEC3C during co-expression in human liver HepG2 cells. PMID: 28637869
16. Study indicates that the A3G rs8177832 polymorphism is associated with a decreased risk of chronic hepatitis B virus infection and hepatocellular carcinoma (HCC), while the rs2011861 polymorphism is associated with an increased risk of HCC. PMID: 28127197
17. APOBEC3G through its variants rs6001417, rs8177832, and rs35228531, in this study interferes with HIV-1/HBV co-infection could be due the HIV-1 mono-infection in a population from Burkina Faso. PMID: 27449138
18. APOBEC3DE binds to itself, APOBEC3F, and APOBEC3G and antagonizes APOBEC3F and, to a lesser extent, APOBEC3G restriction of hepatitis B virus replication. PMID: 27289067
19. cyclin F functions as an intrinsic cellular regulator of HIV-1 Vif and has a negative regulatory effect on the maintenance of viral infectivity by restoring APOBEC3G expression. Gene Indexing Project Expand All Collapse All PMID: 28184007
20. These results indicate that APOBEC3 proteins can be copackaged and can comutate the same genomes, and can cooperate to inhibit HIV replication. PMID: 27439715
21. Here, the authors show that APOBEC3G polyubiquitination is essential for its HIV-1 vif-induced degradation. PMID: 27297094
22. DNA mutagenic activity and capacity for HIV-1 restriction of the cytidine deaminase APOBEC3G depend on whether DNA or RNA binds to tyrosine 315 PMID: 28381554
23. The findings suggest that APOBEC3G polymorphisms alone may not have significant predictive power for inferring genetic susceptibility to vertical transmission of HIV in children perinatally exposed to HIV PMID: 27245545
24. APOBEC3G binds viral RNA and DNA in vitro; this binding may constitute the basis of APOBEC3G antiviral activity. PMID: 28029777
25. an APOBEC3F/APOBEC3G hetero-oligomer can form that has unique properties compared to each APOBEC3 alone. This hetero-oligomer has increased efficiency of virus hypermutation, raising the idea that we still may not fully realize the antiviral mechanisms of endogenous APOBEC3 enzymes. Hetero-oligomerization may be a mechanism to increase their antiviral activity in the presence of Vif. PMID: 27881650
26. using novel human A3G transgenic mouse models that express varying levels of A3G as is seen in humans, this study clearly demonstrates that polymorphic vif alleles can have differential anti-A3G activity in vivo PMID: 27363431
27. thousands of mutation clusters introduced along primate evolution which exhibit features that strongly fit the known patterns of APOBEC3G mutagenesis. These results suggest that APOBEC3G-induced mutations have contributed to the evolution of all genomes PMID: 27056836
28. the effect of APOBEC3G over-expression upon AATF gene expression, was examined. PMID: 27611213
29. The results disclosed no association between the single nucleotide polymorphisms of APOBEC3G and susceptibility to HIV-1, or effects of these polymorphisms on the CD4(+) T cell count or clinical phase of disease. PMID: 27730383
30. APOBEC-3G serves as a suppressor of cervical cancer cell proliferation and invasion. PMID: 26722417
31. Findings support a role for APOBEC3G/F proteins in the generation of plasma drug-resistant minority human immunodeficiency virus type 1 variants (DRMVs). However, this role seems to be limited to a small subset of mutations and does not explain most of the DRMVs evaluated. PMID: 26482266
32. STAT3 plays an important role in IFN-induced A3G production, and HBsAg may correlated with poor response to IFN treatment PMID: 27003258
33. Atomic Force spectroscopy revealed two distinct binding modes by which A3G interacts with ssDNA. One mode requires sequence specificity, as demonstrated by stronger and more stable complexes with deaminase specific ssDNA than with nonspecific ssDNA. PMID: 26503602
34. results demonstrate that the up-regulation of A3G in pancreatic cancer cells induces anoikis resistance, and they provide novel insight into the mechanism by which A3G affects the malignant behavior of pancreatic cancer cells PMID: 26178819
35. Data show that restriction factor APOBEC3G (A3G) is susceptible to degradation by the HIV-1 Vif protein, whereas restriction factor APOBEC3B (A3B) is resistant to Vif. PMID: 26668372
36. This study demonstrates an association of rs6001417, rs8177832, and rs35228531 of APOBEC3G with HIV-1 infection in a population from Burkina Faso. PMID: 26741797
37. Results were consistent with Pokeweed antiviral protein activity inhibiting translation of Vif, which in turn reduces the effect of Vif to inactivate the host restriction factor APOBEC3G. PMID: 26275799
38. USF1 gene can take part in basal transcription regulation of the human A3G gene in hepatocyte, and the identified E-box represented a binding site for the USF1. PMID: 26772882
39. Incomplete APOBEC3G/F neutralization by a single Vif amino acid substitution. PMID: 26055363
40. This study identifies a new cellular complex, HDAC6/A3G, involved in the autophagic degradation of Vif, and suggests that HDAC6 represents a new antiviral factor capable of controlling HIV-1 infectiveness by counteracting Vif and its functions. PMID: 26105074
41. Human APOBEC3G C-terminal directly binds hepatitis C virus non-structural protein NS3 at its C-terminus. PMID: 25811715
42. The data predicts a mechanistic model of RNA inhibition of ssDNA binding to APOBEC3G in which competitive and allosteric interactions determine RNA-bound versus ssDNA-bound conformational states. PMID: 26424853
43. This study showed a high level of APOBEC3F/3G editing in HIV-2 sequences from antiretroviral-naive patients. PMID: 25985400
44. upregulated in the skin of Lichen planus patients PMID: 25384438
45. APOBEC3G is more efficient at mutating retroviral DNA than APOBEC3F. PMID: 26048885
46. A3G and A3F inhibit porcine endogenous retrovirus replication. PMID: 26016442
47. These results highlight that the N-terminal domain of the full length A3G protein has an important influence on its DNA sequence specificity and mutator activity. PMID: 25974865
48. Vif continues to protect HIV-1 from the deleterious effects of APOBEC3G, even after packaging of APOBEC3G has occurred. PMID: 25304135
49. The rather indiscriminate RNA binding characteristics of A3G and A3F promote functionality by enabling recruitment into a wide range of retroviral particles whose packaged RNA genomes comprise divergent sequences. PMID: 25590131
50. It may be concluded hepatitis B virus up-regulates HBD-3 and A3G expression in vivo and in vitro in placental trophoblast and lack of this up-regulation is possibly associated with intrauterine transmission of hepatitis B. PMID: 25196417

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HGNC: 17357

OMIM: 607113

KEGG: hsa:60489

STRING: 9606.ENSP00000385057

UniGene: Hs.660143