Skip to main content
Fig. 1 | Molecular Medicine

Fig. 1

From: Transcription Factor-Based Drug Design in Anticancer Drug Development

Fig. 1

Multiple interactions between the transactivation domains of DNA-bound transcription factors and RNA polymerase II (Pol II)/basal transcription factors facilitate gene transcription

In the model depicted here a number of potential mechanisms are illustrated whereby DNA, gene-specific transcription factors (TF1-5) and Pol II/basal transcription factors (TFIIB, TFIID-TBP-TAFs, TFIIE, and TFIIH are the only ones shown here) are brought together to form an active transcription complex. TF1 binds close to the transcription initiation site and is able to communicate directly with components of the basal transcriptional machinery. TF2 and TF3 bind DNA as a heterodimer to a sequence distant from the transcriptional start, thus making indirect (via protein-protein interactions with TF1, for example) contacts with Pol II and associated basal transcription factors. Heterodimerization and/or the transactivation potential of TF2 are subject to regulation by inducible phosphorylations. TF4 interacts with the basal transcriptional machinery via a second, phosphorylation-modulated protein, TF5, that does not itself bind to DNA. The intervening DNA loops out to accommodate the interaction. CTD, Pol II carboxy-terminal domain; TBP, TATA box-binding protein; TAFs, TBP-associated factors; P, phosphoryl group.

Back to article page