(Downloading may take up to 30 seconds.
If the slide opens in your browser, select File -> Save As to save it.)
Click on image to view larger version.

Fig. 4. KEN selectively regulates STAT92E targets depending on the binding sites
present. (A) In vitro selection experiments have defined the
optimal DNA-binding sites of KEN and STAT92E. The `core' positions essential
for binding are shown in red (for KEN) or green (for STAT92E). There is
overlap in the sequences recognised. (B) Reporters differing only in
their STAT92E-binding sites respond differently to the activity of STAT92E and
KEN. In reporters to which only STAT92E can bind (green; top row), activation
by STAT92E cannot be modulated by KEN. When both STAT92E and KEN are able to
bind to a reporter (green and red; lower row), activation by STAT92E can be
countered by the co-expression of KEN. Neither reporter is active in the
absence of STAT92E. Green tick represents activation of reporter
transcription, red cross implies repression.