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The Journal of Immunology, 1998, 161: 776-781.
Copyright © 1998 by The American Association of Immunologists

HIV-Tat Protein Activates c-Jun N-Terminal Kinase and Activator Protein-11

Ashok Kumar*, Sunil K. Manna*, Subhash Dhawan{dagger} and Bharat B. Aggarwal2,*

* Cytokine Research Section, Department of Molecular Oncology, University of Texas M. D. Anderson Cancer Center, Houston, TX 77030; and {dagger} Laboratory of Immunochemistry, Division of Transfusion Transmitted Diseases, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, MD 20892

Human immunodeficiency virus-1 tat (HIV-tat) protein, like other proinflammatory cytokines (such as TNF), activates a wide variety of cellular responses, some of which play a critical role in progression of HIV infection. Whether HIV-tat, like TNF, also activates c-Jun N-terminal kinase (JNK) and the transcription factor activator protein (AP)-1 is not known. We show that treatment of human histiocytic lymphoma U937 cells with the HIV-tat protein causes activation of JNK and AP-1 in a time- and dose-dependent manner. Transfection of a T cell line, H9 cells with the HIV-tat gene also resulted in an activation of JNK that was not further increased by treatment of cells with exogenous HIV-tat protein. Neutralizing Ab against HIV-tat inhibited the HIV-tat-mediated JNK activation. The activation of JNK by HIV-tat appears to be mediated through generation of free radical species, since pretreatment of cells with N-acetylcysteine (NAC) abolished the effect. Overall our results demonstrate that HIV-tat activates JNK and AP-1, which may contribute to the pathogenesis of AIDS.




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