Abstract
The HTLV-1 Tax protein both activates viral replication and is involved in HTLV-1-mediated transformation of T lymphocytes. The transforming properties of Tax include altering the expression of select cellular genes via activation of cellular pathways and perturbation of both cell cycle control mechanisms and apoptotic signals. The recent discovery that Tax undergoes a hierarchical sequence of posttranslational modifications that control its intracellular localization provides provocative insights into the mechanisms regulating Tax transcriptional and transforming activities.
Highlights
The multipotent HTLV-1 Tax oncoprotein acts on a plethora of viral and cellular processes by interfering with cellular activation pathways and cell cycle controls
Do the HTLV-1 provirus and specific cellular genes contact the surface of the Tax nuclear bodies (Tax NBs) in the course of viral and cellular transcription?
What is the role of IKK /NEMO in the Tax NBs?
Summary
The multipotent HTLV-1 Tax oncoprotein acts on a plethora of viral and cellular processes by interfering with cellular activation pathways and cell cycle controls. HTLV-1 genes by interacting with members of the ATF/CREB AMP Response Element Binding protein) family of transcription factors This interaction increases the dimerization and affinity of binding of ATF/CREB proteins to the Tax-responsive elements (TRE). Tax perturbs cell cycle progression by acting on cellular regulatory effectors involved in the passage through cell cycle checkpoints [17,18,19,20]. Tax activates the expression of specific cellular genes involved in proliferation and differentiation of T lymphocytes via activation of the NF- B pathway. Tax physically interacts with IKK /NEMO, the regulatory subunit of the I B kinase (IKK) complex, resulting in activation of the IKKα and IKKβ catalytic subunits of the complex, followed by phosphorylation, polyubiquitination and degradation of the NF- B inhibitors (I B). NF- B heterodimers p50/RelA ( designated as p65) are released from cytoplasmic sequestration by the I B inhibitors and the active form of p50/RelA accumulates in the nucleus for activation of NF- B controlled promoters [22,23,24,25,26,27,28]
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