AIDSWEEKLY Plus; Monday, August 8, 2005
Staff Medical Writers

According to a study from South Korea, "Tat activates transcription by interacting with Sp1, NF-kappa B, positive transcription elongation factor b, and trans-activator-responsive element (TAR). Tat and Sp1 play major roles in transcription by protein-protein interactions at human immunodeficiency virus, type 1 (HIV-1) long terminal repeat."

"Sp1 activates transcription by interacting with cyclin T1 in the absence of Tat. To disrupt the transcription activation by Tat and Sp1, we fused Sp1-inhibiting polypeptides, zinc finger polypeptide, and the TAR-binding mutant Tat (TatdMt) together.

"A designed or natural zinc finger and Tat mutant fusion was used to target the fusion to the key regulatory sites (GC box and TAR) on the long terminal repeat and nascent short transcripts to disrupt the molecular interaction that normally result in robust transcription," investigators wrote

"The designed zinc finger and TatdMt fusions were targeted to the TAR, and they potently repressed both transcription and replication of HIV-1. The Sp1-yinhibiting POZ domain, TatdMt, and zinc fingers are key functional domains important in repression of transcription and replication," said Y.S. Kim and colleagues at Yonsei University in Seoul.

The authors concluded, "The designed artificial zinc fingers were targeted to the high affinity Sp1-binding site, and by being fused with TatdMt and POZ domain, they strongly block both Sp1-cyclin T1-dependent transcription and Tat-dependent transcription, even in the presence of excess expressed Tat."

Kim and colleagues published the results of their research in the Journal of Biological Chemistry (Artificial zinc finger fusions targeting Sp1-binding sites and the trans-activator-responsive element potently repress transcription and replication of HIV-1. J Biol Chem. 2005 Jun 3;280(22):21545-52.

For additional information, contact M.W. Hur, Yonsei University, School of Medicine, Institute Genetics Science, Dept. Biochemistry & Molecular Biology, 134 ShinChonDong, Seoul 120752, South Korea.

The publisher of the Journal of Biological Chemistry can be contacted at: American Society Biochemistry Molecular Biology Inc., 9650 Rockville Pike, Bethesda, MD 20814-3996, USA.

Keywords: Seoul, South Korea, HIV/AIDS, Zinc Finger, Sp1-Binding Sites, HIV-1 Transcription, Viral Replication.

This article was prepared by AIDS Weekly editors from staff and other reports.

Reference

Kim YS, Kim JM, Jung DL, et al. Artificial zinc finger fusions targeting Sp1-binding sites and the trans-activator-responsive element potently repress transcription and replication of HIV-1., J Biol Chem. 2005 Jun 3;280(22):21545-52.

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