TOKYO UNIVERSITY OF SCIENCE TAKAHASHI TSUJI'S LABORATORY

Involvement of PI3-kinase cascade in the period of infection

The mechanisms of ATLL onset have been studying from the aspect of HTLV-I infection and pathogenesis after the long incubation. To reveal the common mechanisms of tumorigenesis in the period of HTLV-I infection and pathogenesis of ATLL, we focused on the involvement of HTLV-I activated Tax in the PI3-kinase cascade.

We studied in detail and found that transcription factor NF-kB, activated by Tax, bound to the cofactor p300, which was involved in the transcription of PTEN and SHIP-1, and suppressed these genes expression. These suppressions leaded to the over-activation of PI3-kinase, phosphorylation of Akt and abnormal cellular proliferation.