Abstract

The APOBEC3 family of enzymes are DNA cytosine deaminases, some of which restrict replication of HIV-­‐1. This viral restriction is caused by deamination of cytosines to uracils in the viral cDNA, resulting in lethal mutation. HIV-­‐1 counteracts this deamination by producing the protein Vif, which targets the restricting APOBEC3 enzymes for proteosomal degradation. Previous studies have demonstrated that HIV-­‐1 Vif mediates degradation of APOBEC3D (A3D), APOBEC3F (A3F), APOBEC3G (A3G), and APOBEC3H (A3H). Other lentiviruses may also encode a Vif protein, however not all Vif proteins can degrade the same APOBEC3 proteins. For example, SIVmac (simian immunodeficiency virus that infects rhesus macaques) Vif was reported to mediate degradation of APOBEC3B (A3B), but not A3F. A3B does not restrict HIV, but is highly expressed in multiple cancers (bladder, cervical, lung squamous cell carcinoma, lung adenocarcinoma, head and neck, and breast) and is thought to contribute to tumor evolution. My goal is to determine the binding region between SIVmac Vif and A3B.

Advisor

Allison Land

Committee Member

Timothy Secott

Committee Member

Rachel Cohen

Date of Degree

2018

Language

english

Document Type

Thesis

Degree

Master of Science (MS)

Department

Biological Sciences

College

Science, Engineering and Technology

Creative Commons License

Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License.

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