AIDSWEEKLY Plus; Monday, June 21, 2004
Staff Medical Writers

"Human immunodeficiency virus type I Tat protein is one of the soluble neurotoxins. Most studies have to date focused on Tat as an extracellular molecule and its role in neuronal apoptosis, as recombinant Tat protein is often used in these studies. In this study, we expressed Tat protein in astrocytes and neurons, and examined its effects on these cells," scientists writing in the journal Neuroscience Letters report.

"We found that Tat expression resulted in growth inhibition of astrocytes, neurons, as well as non-glial cells 293T. We further showed that Tat interacted with a number of cell cycle-related proteins including cyclin A, cyclin 13, cyclin D3, Cdk2, Cdk4, Cdk1/Cdc2, cdc6, p27, p53, p63, hd1g, and PCNA," said B.Y. Zhou and coworkers.

"These data demonstrate that Tat inhibited cell proliferation when expressed intracellularly, and suggest that Tat interactions with multiple cell cycle regulators may account for this anti-proliferative effect. These results support the notion that Tat-induced neuropathogenesis is mediated by multiple mechanisms involving both intracellular and extracellular Tat protein," concluded investigators.

Zhou and colleagues published their study in Neuroscience Letters (Proliferation inhibition of astrocytes, neurons, and non-glial cells by intracellularly expressed human immunodeficiency virus type 1 (HIV-1) Tat protein. Neurosci Lett. 2004 Apr 15;359(3):155-8.

Additional information can be obtained by contacting J.J. He, Indiana University, School of Medicine, Department Microbiology & Immunology, R2 302, 950 W Walnut St., Indianapolis, IN 46202 USA.

The publisher of the journal Neuroscience Letters can be contacted at: Elsevier Science Ireland Ltd., Customer Relations Manager, Bay 15, Shannon Industrial Estate CO, Clare, Ireland.

The information in this article comes under the major subject areas of AIDS & HIV, Biotechnology, Immunology, Neuroscience and Pharmaceutical & Drug Development.

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

Reference

Zhou BY, He JJ. "Proliferation inhibition of astrocytes, neurons, and non-glial cells by intracellularly expressed human immunodeficiency virus type 1 (HIV-1) Tat protein", Neurosci Lett. 2004 Apr 15;359(3):155-8

PubMED Related articles Search

040621
AW040608

Copyright © 2004 - Charles Henderson, Publisher. All rights Reserved. Permission to reproduce granted to AEGIS by Charles W. Henderson. Authorization to reproduce for personal use granted granted by C. W. Henderson, Publisher, provided that the fee of US$4.50 per copy, per page is paid directly to the Copyright Clearance Center, 27 Congress Street, Salem, Massachusetts 01970, USA. Published by Charles Henderson, Publisher. Editorial & Publishing Office: P.O. Box 5528, Atlanta, GA 30307-0528 / Telephone: (800) 633-4931; Subscription Office: P.O. Box 830409, Birmingham, AL 35283-0409 / FAX: (205) 995-1588 http://www.newsrx.net

AEGiS is made possible through unrestricted grants from Boehringer Ingelheim, Elton John AIDS Foundation, iMetrikus, Inc., John M. Lloyd Foundation, the National Library of Medicine, and donations from users like you. Always watch for outdated information. This article first appeared in 2004. This material is designed to support, not replace, the relationship that exists between you and your doctor.

AEGiS presents published material, reprinted with permission and neither endorses nor opposes any material. All information contained on this website, including information relating to health conditions, products, and treatments, is for informational purposes only. It is often presented in summary or aggregate form. It is not meant to be a substitute for the advice provided by your own physician or other medical professionals. Always discuss treatment options with a doctor who specializes in treating HIV.

Copyright © 1980,2004. AEGiS. All materials appearing on AEGiS are protected by copyright as a collective work or compilation under U.S. copyright and other laws and are the property of AEGiS, or the party credited as the provider of the content.