Open AccessHuman GLI-2 Is a Tat Activation Response Element-Independent Tat Cofactor
Author(s) -
Catherine M. Browning,
Michael J. Smith,
Nina M. Clark,
Brian R. Lane,
Camilo A. Parada,
Monty Montano,
Vineet N. KewalRamani,
Dan R. Littman,
Max Essex,
Robert G. Roeder,
David M. Markovitz
Publication year - 2001
Publication title -
journal of virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.617
H-Index - 292
eISSN - 1070-6321
pISSN - 0022-538X
DOI - 10.1128/jvi.75.5.2314-2323.2001
Subject(s) - biology , xenopus , dna replication , microbiology and biotechnology , caenorhabditis elegans , gene isoform , zinc finger , dna binding protein , dna , transcription factor , genetics , gene
Zinc finger-containing GLI proteins are involved in the development of Caenorhabditis elegans, Xenopus, Drosophila, zebrafish, mice, and humans. In this study, we show that an isoform of human GLI-2 strongly synergizes with the Tat transactivating proteins of human immunodeficiency virus types 1 and 2 (HIV-1 and -2) and markedly stimulates viral replication. GLI-2 also synergizes with the previously described Tat cofactor cyclin T1 to stimulate Tat function. Surprisingly, GLI-2/Tat synergy is not dependent on either a typical GLI DNA binding site or an intact Tat activation response element but does require an intact TATA box. Thus, GLI-2/Tat synergy results from a mechanism of action which is novel both for a GLI protein and for a Tat cofactor. These findings link the GLI family of transcriptional and developmental regulatory proteins to Tat function and HIV replication.