Genetic and mechanistic basis for APOBEC3H alternative splicing, retrovirus restriction, and counteraction by HIV-1 protease
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, whic...
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Nature Portfolio
2018
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oai:doaj.org-article:ea3b48a2ed974a7c8e6b38190a93470e2021-12-02T14:40:07ZGenetic and mechanistic basis for APOBEC3H alternative splicing, retrovirus restriction, and counteraction by HIV-1 protease10.1038/s41467-018-06594-32041-1723https://doaj.org/article/ea3b48a2ed974a7c8e6b38190a93470e2018-10-01T00:00:00Zhttps://doi.org/10.1038/s41467-018-06594-3https://doaj.org/toc/2041-1723Human 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.Diako EbrahimiChristopher M. RichardsMichael A. CarpenterJiayi WangTerumasa IkedaJordan T. BeckerAdam Z. ChengJennifer L. McCannNadine M. ShabanDaniel J. SalamangoGabriel J. StarrettJairam R. LingappaJeongsik YongWilliam L. BrownReuben S. HarrisNature PortfolioarticleScienceQENNature Communications, Vol 9, Iss 1, Pp 1-11 (2018) |
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Science Q 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 Genetic and mechanistic basis for APOBEC3H alternative splicing, retrovirus restriction, and counteraction by HIV-1 protease |
description |
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. |
format |
article |
author |
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 |
author_facet |
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 |
author_sort |
Diako Ebrahimi |
title |
Genetic and mechanistic basis for APOBEC3H alternative splicing, retrovirus restriction, and counteraction by HIV-1 protease |
title_short |
Genetic and mechanistic basis for APOBEC3H alternative splicing, retrovirus restriction, and counteraction by HIV-1 protease |
title_full |
Genetic and mechanistic basis for APOBEC3H alternative splicing, retrovirus restriction, and counteraction by HIV-1 protease |
title_fullStr |
Genetic and mechanistic basis for APOBEC3H alternative splicing, retrovirus restriction, and counteraction by HIV-1 protease |
title_full_unstemmed |
Genetic and mechanistic basis for APOBEC3H alternative splicing, retrovirus restriction, and counteraction by HIV-1 protease |
title_sort |
genetic and mechanistic basis for apobec3h alternative splicing, retrovirus restriction, and counteraction by hiv-1 protease |
publisher |
Nature Portfolio |
publishDate |
2018 |
url |
https://doaj.org/article/ea3b48a2ed974a7c8e6b38190a93470e |
work_keys_str_mv |
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1718390450093555712 |