The HTLV-I Tax oncoprotein: hyper-tasking at the molecular level.
HTLV-I is a complex retrovirus that encodes a transcriptional activator, Tax, which regulates expression of the viral promoter. Tax has been shown to be both necessary and sufficient to effect immortalization and transformation of cells in culture and tumorigenesis in animal models. Tax exerts its influence through protein-protein interactions with a variety of molecular targets, including transcription factors and cofactors, histone modifying enzymes and post-translational modifying enzymes. Through these interactions, Tax disrupts cellular regulatory cascades and checkpoints designed to control a variety of systems. The result is untimely activation or repression of gene expression, inappropriate protein modifications, incorrect cell cycling, loss of adequate DNA repair capacity, and potential release of the cell from tumor suppression. Whereas for the virus these functions of Tax provide a means for successful completion of its life cycle, for the cell, they result at best in anarchy, and at worst in death of both the cell and the organism of which that cell is a part.
Wycuff
Diane R
DR
Dept. Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX 77030, USA.
Marriott
Susan J
SJ
D000782:Aneuploidy; D000818:Animals; D017362:Cyclic AMP Response Element-Binding Protein / Q000378:metabolism; D004260:DNA Repair; D004195:Disease Models, Animal; D016356:Gene Products, tax / Q000378:metabolism / Q000502:physiology*; D016679:Genome, Viral; D015368:Human T-lymphotropic virus 1 / Q000378:metabolism*; D006801:Humans; D016328:NF-kappa B / Q000378:metabolism; D014158:Transcription, Genetic; D015533:Transcriptional Activation
D017362:Cyclic AMP Response Element-Binding Protein; D016356:Gene Products, tax; D016328:NF-kappa B