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1. |
When recognition loop of 9-11 amino acids is grafted from the donor APOBEC3F or 3G proteins into the acceptor scaffold of AID, the mutational signature of AID changes toward that of the donor proteins. |
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2. |
APOBEC3G and APOBEC3F gene expression in immune system and hematopoietic system cells |
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3. |
Thus, (21)WxSLVK(26) is a novel functional domain that regulates Vif activity toward both APOBEC3F and APOBEC3G and is a potential drug target to inhibit Vif activity and block HIV-1 replication. |
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4. |
results here have indicated that at least two distinct regions in the N-terminal half of HIV-1 Vif are critical for binding and exclusion of APOBEC3G/F |
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5. |
relationship between the human immunodeficiency virus type 1 viral infectivity factor (Vif) and the human APOBEC-3G and APOBEC-3F restriction factors [Review] |
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6. |
analysis of genetic editing of HBV DNA by monodomain human APOBEC3G and F cytidine deaminases |
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7. |
The Chinese population had a higher frequency of small alleles and showed a difference in allelic structure and frequency distribution in apolipoprotein B from European and American in this populations. |
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8. |
Distinct determinants in HIV-1 Vif and human APOBEC3 proteins are required for the suppression of diverse host anti-viral proteins. |
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9. |
The APOBEC3F domain that interacts with the Vif DRMR region was located between amino acids 283 and 300 of A3F. |
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10. |
A VxIPLx(4-5)LxPhix(2)YWxL motif in HIV-1 Vif is identified, which is required for efficient interaction between Vif and APOBEC3G (A3G), Vif-mediated A3G degradation and virion exclusion, and functional suppression of the A3G antiviral activity. |
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11. |
define a number of subtle differences between the ribonucleoprotein complexes associated with APOBEC3F and APOBEC3G and speculate |
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12. |
Studies focused mainly on APOBEC3F imply that it occurs associated with mRNA-PABP1 in translationally active polysomes and to a lesser extent in mRNA processing bodies (P-bodies). |
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13. |
Vif binding to RNA and DNA offers several non-exclusive ways to counteract APOBEC3G/3F factors, in addition to the well documented Vif-induced degradation by the proteasome and to the Vif-mediated repression of translation of these antiviral factors |
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14. |
Small interfering RNA-mediated depletion of APOBEC3F, but not TRIM5alpha, enhances HIV-1 infection of immature dendritic cells (iDCs), indicating that APOBEC3F controls the sensitivity of iDCs to HIV-1 infection |
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15. |
Results reveal two distinct Vif determinants, amino acids Y(40)RHHY(44) and D(14)RMR(17), which are essential for binding to APOBEC3G and APOBEC3F, respectively. |
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16. |
only the C-terminal domain of APOBEC3F and -3G dictates the retroviral minus strand 5'-TC and 5'-CC dinucleotide hypermutation preferences. |
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17. |
separation of function of the cytidine deaminase domains is maintained in hA3B and hA3F, but roles of the two domains are reversed in mouse A3 |
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18. |
The fact that several highly conserved tryphtophan residues in Vif are specifically required for the suppression of APOBEC3F (A3F) but not that of APOBEC3G (A3G) suggests a critical role for A3F in the restriction of HIV-1 in vivo. |
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19. |
APOBEC3F was less potent than APOBEC3G in inhibitinhg HIV-1; Vif proteins appeared more potent & specific when APOBEC3G is the target rather than APOBEC3F |
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20. |
APOBEC3B and APOBEC3F have roles in inhibiting L1 retrotransposition by a DNA deamination-independent mechanism |
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21. |
Findings highlight a role for APOBEC3G/3F in explaining the resistance of most dendritic cells to HIV-1 infection, as well as the susceptibility of a fraction of immature dendritic cells. |
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22. |
APOBEC3F and APOBEC3G complexes undergo dynamic conversion during HIV-1 infection |
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23. |
novel link between innate immunity against retroviruses and P-bodies suggesting that APOBEC3G and APOBEC3F could function in the context of P-bodies to restrict HIV-1 replication. |