期刊
JOURNAL OF VIROLOGY
卷 88, 期 10, 页码 5881-5887出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.00062-14
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资金
- Aihara Innovative Mathematical Modeling Projec
- Japan Society for the Promotion of Science (JSPS), through the Funding Program for World-Leading Innovative R&D on Science and Technology (FIRST Program)
- Council for Science and Technology Policy of Japan
- Takeda Science Foundation
- Sumitomo Foundation Research Grant
- Senshin Medical Research Foundation
- Kyushu University Interdisciplinary Programs in Education and Projects in Research Development
- JSPS [B25800092, B24390112, S22220007]
- Research on Innovative Areas from the Ministry of Education, Culture, Sports, Science and Technology of Japan [24115008]
- Research on HIV/AIDS from the Ministry of Health, Labor and Welfare of Japan
- Grants-in-Aid for Scientific Research [24115008, 24390112] Funding Source: KAKEN
APOBEC3F and APOBEC3G cytidine deaminases potently inhibit human immunodeficiency virus type 1 (HIV-1) replication by enzymatically inserting G-to-A mutations in viral DNA and/or impairing viral reverse transcription independently of their deaminase activity. Through experimental and mathematical investigation, here we quantitatively demonstrate that 99.3% of the antiviral effect of APOBEC3G is dependent on its deaminase activity, whereas 30.2% of the antiviral effect of APOBEC3F is attributed to deaminase-independent ability. This is the first report quantitatively elucidating how APOBEC3F and APOBEC3G differ in their anti-HIV-1 modes.
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