Journal article
Use of ATP analogs to inhibit HIV-1 transcription
Virology (New York, N.Y.), v 432(1), pp 219-231
10 Oct 2012
PMID: 22771113
Featured in Collection : UN Sustainable Development Goals @ Drexel
Abstract
Human immunodeficiency virus type 1 (HIV-1) is the etiological agent of AIDS. Chronic persistent infection is an important reason for the presence of “latent cell populations” even after Anti-Retroviral Therapy (ART). We have analyzed the effect of ATP analogs in inhibiting cdk9/T1 complex in infected cells. A third generation drug named CR8#13 is an effective inhibitor of Tat activated transcription. Following drug treatment, we observed a decreased loading of cdk9 onto the HIV-1 DNA. We found multiple novel cdk9/T1 complexes present in infected and uninfected cells with one complex being unique to infected cells. This complex is sensitive to CR8#13 in kinase assays. Treatment of PBMC with CR8#13 does not kill infected cells as compared to Flavopiridol. Interestingly, there is a difference in sensitivity of various clades to these analogs. Collectively, these results point to targeting novel complexes for inhibition of cellular proteins that are unique to infected cells.
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Details
- Title
- Use of ATP analogs to inhibit HIV-1 transcription
- Creators
- Aarthi Narayanan - George Mason UniversityGavin Sampey - George Mason UniversityRachel Van Duyne - George Mason UniversityIrene Guendel - George Mason UniversityKylene Kehn-Hall - George Mason UniversityJessica Roman - George Mason UniversityRobert Currer - George Mason UniversityHervé Galons - Centre National de la Recherche ScientifiqueNassima Oumata - Laboratoire de Chimie OrganiqueBenoît Joseph - Institut de Chimie et Biochimie Moléculaires et SupramoléculairesLaurent Meijer - C.N.R.S. USR3151, ‘Protein Phosphorylation & Human Disease’ Group, Station Biologique, Bretagne, FranceMassimo Caputi - Florida Atlantic UniversitySergei Nekhai - Howard UniversityFatah Kashanchi - George Mason University
- Publication Details
- Virology (New York, N.Y.), v 432(1), pp 219-231
- Publisher
- Elsevier
- Number of pages
- 13
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- Pharmacology and Physiology
- Web of Science ID
- WOS:000307027100024
- Scopus ID
- 2-s2.0-84864023093
- Other Identifier
- 991021903117604721
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- Collaboration types
- Domestic collaboration
- International collaboration
- Web of Science research areas
- Virology