Figure 5. Mutation of an octamer element located at the 3′ end of the BRE1 is sufficient to block BMP-induced activation of the promoter. (A) A series of specific mutations were introduced into the BRE1 by site-directed mutagenesis for potential Smad-binding sites (mutations #1–5) or for an A/T-rich sequence (mutation #6), or a putative octamer binding site (mutation #7). (B) When compared to the BMP-inducible reporter containing the intact BRE1 (−819), none of the first six mutations had a significant effect on induction. In contrast, mutation of the putative octamer binding site (mutation #7) blocked BMP-mediated induction, similar to deletion of the BRE1 (−751).
Image published in: Oren T et al. (2005)
Image downloaded from an Open Access article in PubMed Central. © The Author 2005. Published by Oxford University Press. All rights reserved
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