HIV-1 CONSENSUS B VIF Fragments
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HIV-1 CONSENSUS B VIF Fragments

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Cat. # Product Name Price
H09598 HIV - 1 CONSENSUS B VIF - 9 Inquiry
H09614 HIV - 1 CONSENSUS B VIF - 8 Inquiry
H09509 HIV - 1 CONSENSUS B VIF - 7 Inquiry
H09503 HIV - 1 CONSENSUS B VIF - 6 Inquiry
H09651 HIV - 1 CONSENSUS B VIF - 5 Inquiry
H09016 HIV - 1 CONSENSUS B VIF - 46 Inquiry
H09205 HIV - 1 CONSENSUS B VIF - 45 Inquiry
H09551 HIV - 1 CONSENSUS B VIF - 44 Inquiry
H09575 HIV - 1 CONSENSUS B VIF - 43 Inquiry
H09566 HIV - 1 CONSENSUS B VIF - 42 Inquiry
H09440 HIV - 1 CONSENSUS B VIF - 41 Inquiry
H09294 HIV - 1 CONSENSUS B VIF - 40 Inquiry
H09639 HIV - 1 CONSENSUS B VIF - 4 Inquiry
H09202 HIV - 1 CONSENSUS B VIF - 39 Inquiry
H09107 HIV - 1 CONSENSUS B VIF - 38 Inquiry

HIV-1 (human immunodeficiency virus type-1) virus infection factor Vif (viral infectivity factor) is a highly conserved alkaline phosphorylated protein, which is one of the auxiliary regulatory proteins of HIV-1. The main function of Vif protein is to mediate the degradation of polypeptide-like protein 3G (apolipoprotein B mRNA editing enzyme catalytic polypeptide like 3G (APOBEC3G) catalyzed by apolipoprotein B mRNA editing enzyme in host cells, thus enhancing the infectivity of the virus. In addition, it also has the function of regulating the late reverse transcription and replication of the virus and inducing cell G2 phase arrest.

The mechanism proposed for protection of the virus by HIV-1 Vif

Vif protein binds to the Cul5 E3 ubiquitin binding complex of host cells, and then modifies APOBEC3 protein by polyubiquitin, so that the latter is degraded and inactivated by proteasome. In recent years, it has been found that HIV-1 Vif needs to hijack the cell protein CBF- β (Core binding factor beta) in the process of binding Cul5 E3 complex. CBF- β is a key regulator of HIV-1 virus invasion into host cells. CBF- β not only improves the stability of Vif protein, but also promotes the assembly of Vif-Cul5 E3 ligase. Vif hijacks CBF- β to defeat the host antiviral system, both at the protein level and at the transcriptional level.

Conclusion

In summary, we can make the assumption that both HIV and other lentivirus viruses actually need the help of the APOBEC3 protein family to increase their spontaneous mutation rates in order to survive well. In fact, it is easy to test this hypothesis by experiments. As long as the function of A3G protein is completely inhibited, we will find that the spontaneous mutation of HIV virus in the process of replication is significantly reduced and they become more genetically stable. However, even a small reduction in the spontaneous mutation rate of HIV virus will make it attacked by the body’s adaptive immune response. Therefore, it seems contradictory, but inhibiting the antiretroviral activity of A3G protein is indeed an effective way to treat AIDS patients. For the survival of HIV virus, whether A3G protein is better to improve the mutation rate of its replication or reduce the mutation rate of its replication is better, which will become a research hotspot in the next few years.

References
1. Doehle, B. P., Schäfer, A., & Cullen, B. R. (2005). Human APOBEC3B is a potent inhibitor of HIV-1 infectivity and is resistant to HIV-1 Vif. Virology339(2), 281-288.
2. Richards, C. M., Li, M., Perkins, A. L., Rathore, A., Harki, D. A., & Harris, R. S. (2017). Reassessing APOBEC3G inhibition by HIV-1 Vif-derived peptides. Journal of molecular biology, 429(1), 88-96.

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