Nature Communications (Oct 2018)
Genetic and mechanistic basis for APOBEC3H alternative splicing, retrovirus restriction, and counteraction by HIV-1 protease
- Diako Ebrahimi,
- Christopher M. Richards,
- Michael A. Carpenter,
- Jiayi Wang,
- Terumasa Ikeda,
- Jordan T. Becker,
- Adam Z. Cheng,
- Jennifer L. McCann,
- Nadine M. Shaban,
- Daniel J. Salamango,
- Gabriel J. Starrett,
- Jairam R. Lingappa,
- Jeongsik Yong,
- William L. Brown,
- Reuben S. Harris
Affiliations
- Diako Ebrahimi
- Department of Biochemistry, Molecular Biology and Biophysics, Masonic Cancer Center, Institute for Molecular Virology, Center for Genome Engineering, University of Minnesota
- Christopher M. Richards
- Department of Biochemistry, Molecular Biology and Biophysics, Masonic Cancer Center, Institute for Molecular Virology, Center for Genome Engineering, University of Minnesota
- Michael A. Carpenter
- Department of Biochemistry, Molecular Biology and Biophysics, Masonic Cancer Center, Institute for Molecular Virology, Center for Genome Engineering, University of Minnesota
- Jiayi Wang
- Department of Biochemistry, Molecular Biology and Biophysics, Masonic Cancer Center, Institute for Molecular Virology, Center for Genome Engineering, University of Minnesota
- Terumasa Ikeda
- Department of Biochemistry, Molecular Biology and Biophysics, Masonic Cancer Center, Institute for Molecular Virology, Center for Genome Engineering, University of Minnesota
- Jordan T. Becker
- Department of Biochemistry, Molecular Biology and Biophysics, Masonic Cancer Center, Institute for Molecular Virology, Center for Genome Engineering, University of Minnesota
- Adam Z. Cheng
- Department of Biochemistry, Molecular Biology and Biophysics, Masonic Cancer Center, Institute for Molecular Virology, Center for Genome Engineering, University of Minnesota
- Jennifer L. McCann
- Department of Biochemistry, Molecular Biology and Biophysics, Masonic Cancer Center, Institute for Molecular Virology, Center for Genome Engineering, University of Minnesota
- Nadine M. Shaban
- Department of Biochemistry, Molecular Biology and Biophysics, Masonic Cancer Center, Institute for Molecular Virology, Center for Genome Engineering, University of Minnesota
- Daniel J. Salamango
- Department of Biochemistry, Molecular Biology and Biophysics, Masonic Cancer Center, Institute for Molecular Virology, Center for Genome Engineering, University of Minnesota
- Gabriel J. Starrett
- Department of Biochemistry, Molecular Biology and Biophysics, Masonic Cancer Center, Institute for Molecular Virology, Center for Genome Engineering, University of Minnesota
- Jairam R. Lingappa
- Departments of Global Health, Medicine and Pediatrics, University of Washington
- Jeongsik Yong
- Department of Biochemistry, Molecular Biology and Biophysics, Masonic Cancer Center, Institute for Molecular Virology, Center for Genome Engineering, University of Minnesota
- William L. Brown
- Department of Biochemistry, Molecular Biology and Biophysics, Masonic Cancer Center, Institute for Molecular Virology, Center for Genome Engineering, University of Minnesota
- Reuben S. Harris
- Department of Biochemistry, Molecular Biology and Biophysics, Masonic Cancer Center, Institute for Molecular Virology, Center for Genome Engineering, University of Minnesota
- DOI
- https://doi.org/10.1038/s41467-018-06594-3
- Journal volume & issue
-
Vol. 9,
no. 1
pp. 1 – 11
Abstract
Human APOBEC3H has several haplotypes and splice variants with distinct anti-HIV-1 activities, but the genetics underlying the expression of these variants are unclear. Here, the authors identify an intronic deletion in A3H haplotype II resulting in production of the most active splice variant, which is counteracted by HIV-1 protease.
