If the plug-in named ChemScape Chime is properly installed on your computer, you should see a rotating 3D HIV-Tat molecule. The molecule can be moved by clicking it with the left button of your mouse and its characteristics, including automatic rotation, can be modified by clicking it with the right button.
To download the plug-in: 
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We examined whether two sulfonated distamycin A derivatives, PNU145156E and PNU153529, inhibit the trans-activating and angiogenic effects of HIV-1 Tat protein.
The study was carried out by analyzing the activity of the two drugs on: (1) extracellular and intracellular Tat protein, introduced into HL3T1 cells containing an integrated HIV-1 LTR/CAT plasmid; (2) binding of Tat to 3H-labeled heparin and to 14C-labeled PNU145156E; and (3) the angiogenic response induced in vivo by culture medium conditioned by T53c14 cells, which release extracellular Tat.
PNU145156E and PNU153429 interacted with extracellular
Tat in the culture medium and physically bound the Tat protein, most likely
sequestering it in the extracellular space. As a consequence, the two drugs
inhibited trans-activation of the HIV-1 LTR on addition of the free Tat
protein to HL3T1 cells. However, the two compounds inhibited the activity
of intracellular Tat when they were introduced into the cells by
lipofection.
In vivo experiments showed that the two drugs blocked the neoangiogenesis induced by Tat released in the conditioned medium of T53c14 cells.
Owing to the critical role of intracellular and
extracellular Tat in HIV-1 replication, these drugs show promise as a means
to control the progression of HIV-1 infection as well as the neoplastic
and angiogenic effects induced by Tat in the course of AIDS.
AIDS Res Hum Retroviruses 1998 Nov 20;14(17):1561-71
