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Updated: May 23, 2026

A Chromatin Immunoprecipitation Assay to Identify Novel NFAT2 Target Genes in Chronic Lymphocytic Leukemia
Published on: December 4, 2018
The multifaceted oncoprotein Tax: subcellular localization, posttranslational modifications, and NF-κB activation
Youmna Kfoury1, Rihab Nasr, Chloé Journo
1Department of Internal Medicine, Faculty of Medicine, American University of Beirut, Beirut, Lebanon.
Abstract:
The human T-cell lymphotropic virus type-I (HTLV-I) is the etiologic agent of adult T-cell leukemia/lymphoma (ATL) and of tropical spastic paraparesis/HTLV-I-associated myelopathy. Constitutive NF-κB activation by the viral oncoprotein Tax plays a crucial role in the induction and maintenance of cellular proliferation, transformation, and inhibition of apoptosis. In an attempt to provide a general view of the molecular mechanisms of constitutive Tax-induced NF-κB activation, we summarize in this review the recent body of literature that supports a major role for Tax posttranslational modifications, chiefly ubiquitination, and SUMOylation, in the NF-κB activity of Tax. These modifications indeed participate in the control of Tax subcellular localization and modulate its protein-protein interaction potential. Tax posttranslational modifications, which highlight the ability of HTLV-I to optimize its limited viral genome size, might represent an attractive target for the design of new therapies for ATL.
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