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Binding of HTLV-1 tax oncoprotein to the precursor of interleukin-16, a T cell PDZ domain-containing protein. | LitMetric

AI Article Synopsis

  • HTLV-1 Tax oncoprotein interacts with cellular proteins, particularly pro-IL-16, influencing T cell malignancies and the cell cycle.
  • Pro-IL-16, which contains three PDZ domains, can induce G(0)/G(1) cell cycle arrest when expressed in certain cells.
  • Tax binds to the first PDZ domain of pro-IL-16, promoting cell cycle progression when over-expressed, while negating the arrest induced by pro-IL-16, indicating a potential mechanism for growth deregulation in HTLV-1 infected T cells.

Article Abstract

HTLV-1 Tax oncoprotein interacts with various cellular factors and modulates transcription and the cell cycle. In that role it is sufficient to create T cell malignancies in the absence of HTLV-1 infection. HTLV-1 Tax protein has been reported to bind to cellular proteins containing PDZ domains in vitro. The precursor of human interleukin 16, pro-IL-16, is an abundant cellular protein present in human peripheral blood T cells. Pro-IL-16 contains three PDZ domains. It has been shown that expression of pro-IL-16 in pro-IL-16 negative cells induces a G(0)/G(1) arrest in the cell cycle. The current studies demonstrate that Tax binds to pro-IL-16 in HTLV-1 infected human T cells. We mapped the Tax binding site to the first PDZ domain of pro-IL-16. Over-expression of Tax in COS cells resulted in fewer cells in G(0)/G(1) consistent with its activity to induce G(1)- to S-phase progression in lymphocytes, while over-expression of pro-IL-16 in COS cells resulted in G(0)/G(1) arrest. Co-expression of wild type Tax with pro-IL-16 in COS cells negated the effects of pro-IL-16, an effect not observed with Tax mutated at its PDZ binding C-terminus. These results suggest that one of the effects of Tax on growth deregulation in HTLV-1 infected T cells might be mediated by its binding to pro-IL-16.

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Source
http://dx.doi.org/10.1016/s0042-6822(02)00056-9DOI Listing

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