Does tBP binding to the TATA box induce a specific downstream unwinding site that is targeted by pluramycin?
We propose that the TBP-DNA-pluramycin ternary complex is a 'specific' binding mode in which TBP and pluramycin make compensatory alterations in DNA, accounting for the improved stability of the ternary complex. We also propose a model of the ternary complex that explains the observed asymmetric effect of TBP binding to the TATA box.
EDIL3-mediated activation of TGF-β and ERK signaling could provide therapeutic implications for HCC.