Abstract

<p>(A) Genomic sequences of the functional HMG and Helper sites, with the box indicating a HMG-Helper site pair with similar orientation in each WRE. (B) Sequence logos showing the consensus of HMG and Helper sites, based on the functional sites used in this study. (C, D) Model to explain the differential requirement of HMG and Helper sites in the TCF transcriptional switch, without (C) and with (D) Wnt/ß-catenin signaling . We propose that the DNA binding properties of TCF are influenced by co-regulators, with ß-catenin stabilizing the HMG-Helper site interaction. It is suggested that POP-1 may recognize HMG sites surrounded by two Helper sites as a dimer. This model does not preclude the existence of addition DNA-binding co-factors for POP-1 in either the absence or presence of signaling.</p

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