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The HIV‐1 Tat Transactivator Protein: a Therapeutic Target?
Author(s) -
Fulcher Alex J.,
Jans David A.
Publication year - 2003
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1080/15216540310001643440
Subject(s) - transactivation , nuclear transport , importin , nuclear export signal , human immunodeficiency virus (hiv) , ran , viral life cycle , virology , nuclear localization sequence , mechanism (biology) , biology , nuclear protein , cytoplasm , microbiology and biotechnology , chromosomal translocation , cell nucleus , virus , viral replication , gene , genetics , transcription factor , physics , quantum mechanics
The human immunodeficiency virus‐1 (HIV‐1), the causative agent of autoimmune deficiency syndrome (AIDS) is a major health problem world‐wide. Central to HIV infection is the transactivator protein Tat, that plays a critical role in the nucleus during the HIV infectious cycle, by binding the transactivation‐responsive region (TAR) and thereby enhancing transcriptional elongation. Tat appears to gain nuclear entry through a novel mechanism, independent of the normal cellular importin/Ran‐dependent pathways, and regulated by a cytoplasmic retention mechanism. Since blocking Tat nuclear import is likely to prevent HIV infection, detailed delineation of Tat's nuclear import pathway is critical to assessing its viability as a therapeutic target. Other feasible anti‐HIV therapies include approaches to inhibit Tat‐TAR interaction. IUBMB Life, 55: 669‐680, 2003