Nature Medicine (06/99) Vol. 5, No. 6, P. 635
A study of Sam68 (Src-associated protein in mitosis) and a
mutant Rev protein, RevM10, indicate potential methods for
viral gene therapy. Investigators found that Sam68
specifically interacts with the Rev response element (RRE) and
can partially replace and synergize with Rev in RRE-mediated
gene expression and virus replication. According to the data,
c-terminally deleted mutants of Sam68 blocked the
transactivation of RRE-mediated expression by wild-type Sam68
and Rev. The mutants, which hampered the nuclear localization
of Rev in co-expressed cells, stopped wild-type HIV-1
replication as well as the RevM10 mutant. The researchers
suggest they may be useful in anti-AIDS treatments.