Apolipoprotein B mRNA Editing Enzyme, Catalytic Polypeptide-Like 3C Proteins (APOBEC3C)

Human Apolipoprotein B mRNA Editing Enzyme, Catalytic Polypeptide-Like 3C (APOBEC3C) interaction partners

1. A3C-Ile188 is capable of inhibiting Vif-deficient HIV-1 replication in T cells

2. 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.

3. our results suggest that APOBEC3C is in fact involved in protecting hosts from lentiviruses.

4. Antiviral functions of APOBEC3C against HIV-1 and APOBEC3C binding capacity

5. These results suggest that functional potential of APOBEC3B and APOBEC3C involved in cancer mutagenesis is associated with estrogen receptor status.

6. High APOBEC3C is associated with the pathogenesis of primary effusion lymphoma.

7. Expression of APOBEC3A or 3C in 293FT cells reduced the infectivity of HPV16 pseudovirions. The reduced infectivity of virions assembled in the presence of APOBEC3A, but not 3C, was attributed to decreased copy number of the encapsidated reporter plasmid.

8. APOBEC3 deaminases upregulated by IFN-beta induce E2 hypermutation of HPV16 in cervical keratinocytes.

9. The mechanism of APOBEC3C (A3C)-mediated LINE-1 inhibition was found to be deaminase independent, required an intact dimerization site and the RNA-binding pocket mutation R122A abolished L1 restriction by A3C.

10. This study confirmed the association of the APOBEC3 deletion with breast cancer risk among women of European ancestry.

11. Decreases in APOBAC3A and APOBAC3C in the cortex of psychotic patients support the hypothesis that an epigenetic misregulation of gene expression may be operative in the pathogenesis of psychotic disorders.

12. a high-resolution crystal structure of APOBEC3C with the HIV-1 viral infectivity factor (Vif)-interaction interface.

13. Findings suggest that APOBEC3-mediated editing of HIV-1 could be modulated by host and virus genetic characteristics in the context of pediatric infection.

14. The result suggest that Core-A3C may be a candidate as a novel antiviral agent against human HBV infection.

15. The authors identified a single cysteine at position 320 (C320) that disrupts A3DE activity.

16. Somatic hypermutation of human mitochondrial and nuclear DNA by APOBEC3 cytidine deaminases, a pathway for DNA catabolism.

17. The basic biology of the interactions between human APOBEC3 proteins and HIV-1 Vif, is reviewed.

18. Studies indicate the APOBEC family consists of 11 members: APOBEC-1 (Apo1), APOBEC-2 (Apo2), activation induced cytidine deaminase (AID), APOBEC- 3A, -3B, -3C, -3DE, -3F, -3H (Apo3A-H) and APOBEC- 4 (Apo4).

19. different APOBEC3 family members function to neutralize specific lentiviruses

20. APOBEC3 proteins may help prevent the zoonotic infection of humans by simple retroviruses and provide a mechanism for how simple retroviruses can avoid inhibition by APOBEC3 family members.