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. 2016 Dec 27;8(1):61–66. doi: 10.1080/21541264.2016.1265702

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© 2017 The Author(s). Published with license by Taylor & Francis

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License (http://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited, and is not altered, transformed, or built upon in any way.

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Figure 1. — Model for the regulation of Notch target genes. Activation of the Notch pathway via binding of ligands to Notch receptor, leads to the release of the NICD which interacts with the transcription factor RBPJ. The RBPJ/NICD complex activates gene expression via recruiting MAM, the histone acetyltransferase (HAT) p300 and additional coactivators (CoA; active state, right). Upon termination of the signal, SHARP is recruited to RBPJ-bound enhancer sites where it keeps genes in a responsive state (responsive state, middle) via interaction with KMT2D or with phospho-NCoR. Furthermore, repression of Notch target genes can be enforced via interaction of RBPJ with corepressors (CoR; repressed state, left).