Protein Kinase A Phosphorylation Activates Vpr-Induced Cell Cycle Arrest during Human Immunodeficiency Virus Type 1 Infection
Author:
Affiliation:
1. Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892
2. Immunology Graduate Group, University of Pennsylvania, Philadelphia, Pennsylvania 19104
Abstract
Publisher
American Society for Microbiology
Subject
Virology,Insect Science,Immunology,Microbiology
Link
https://journals.asm.org/doi/pdf/10.1128/JVI.02273-09
Reference83 articles.
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3. Altfeld, M., M. M. Addo, R. L. Eldridge, X. G. Yu, S. Thomas, A. Khatri, D. Strick, M. N. Phillips, G. B. Cohen, S. A. Islam, S. A. Kalams, C. Brander, P. J. Goulder, E. S. Rosenberg, and B. D. Walker. 2001. Vpr is preferentially targeted by CTL during HIV-1 infection. J. Immunol.167:2743-2752.
4. Bachand, F., X. J. Yao, M. Hrimech, N. Rougeau, and E. A. Cohen. 1999. Incorporation of Vpr into human immunodeficiency virus type 1 requires a direct interaction with the p6 domain of the p55 gag precursor. J. Biol. Chem.274:9083-9091.
5. Belzile, J. P., G. Duisit, N. Rougeau, J. Mercier, A. Finzi, and E. A. Cohen. 2007. HIV-1 Vpr-mediated G2 arrest involves the DDB1-CUL4AVPRBP E3 ubiquitin ligase. PLoS Pathog.3:e85.
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