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. 2021 Aug 10;26(3):309–320. doi: 10.1007/s10911-021-09496-1

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© The Author(s) 2021

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — Canonical Notch signaling cascades in mammals. Notch ligands bind to the extracellular domain (NECD) of their receptor proteins, inducing receptor transactivation to expose the receptor transmembrane domain for ADAM/TACE metalloenzyme-mediated hydrolysis. NECD is pulled from the intracellular domain (NICD), and the NICD is cleaved by γ-secretase at an intracellular position to produce the free NICD fragment. The NICD is translocated from the cytoplasm to the nucleus, where it binds with CSL (CBF1/RBP-J/Su(H)/Lag-1) transcription factors to recruit a coactivator (MAML) and form a transcription complex that can activate the transcription of downstream genes (HEY, HES, HERP, CyclinD1, c-Myc, and others)