Polyamides Reveal a Role for Repression in Latency within Resting T Cells of HIV‐Infected Donors | Zendy

Loyda Ylisastigui | Zendy; Jason J. Coull | Zendy; Victor C. Rucker | Zendy; Christian Melander | Zendy; Ronald J. Bosch | Zendy; Scott J. Brodie | Zendy; Lawrence Corey | Zendy; Donald L. Sodora | Zendy; Peter B. Dervan | Zendy; David M. Margolis | Zendy

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Polyamides Reveal a Role for Repression in Latency within Resting T Cells of HIV‐Infected Donors

Author(s) -

Loyda Ylisastigui,

Jason J. Coull,

Victor C. Rucker,

Christian Melander,

Ronald J. Bosch,

Scott J. Brodie,

Lawrence Corey,

Donald L. Sodora,

Peter B. Dervan,

David M. Margolis

Publication year - 2004

Publication title -

the journal of infectious diseases

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.69

H-Index - 252

eISSN - 1537-6613

pISSN - 0022-1899

DOI - 10.1086/423822

Subject(s) - histone , chromatin , biology , histone deacetylase , viremia , chromatin remodeling , virology , gene silencing , long terminal repeat , hiv long terminal repeat , transcription factor , microbiology and biotechnology , human immunodeficiency virus (hiv) , dna , gene , gene expression , genetics

The persistence of human immunodeficiency virus (HIV) type 1 within resting CD4+ T cells poses a daunting therapeutic challenge. Histone deacetylase (HDAC)-1, a chromatin-remodeling enzyme that can mediate gene silencing, is recruited to the HIV-1 long terminal repeat by the host transcription factor LSF. Pyrrole-imidazole polyamides, small molecules that target specific DNA sequences, can access the nucleus of cells and specifically block transcription-factor binding.

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