Abstract
This chapter brings to light a very short signaling pathway where the intracellular segment of the receptor is cleaved and then acts as a transcription factor. This mechanism is employed by the Notch receptor, upon binding of its ligands Delta-like or Jagged. Ligand binding causes a set of cleavages, first in the LNR-HD region, S2-site cleaved by ADAM, followed by an intracellular cleavage (S3) by the γ-secretase complex. We then show how the intracellular segment forms a transcription complex with RBPJ and drives expression of HES and HEY proteins which play a role in cell fate decisions. We place the action of Notch in the context of Drosophila sensory organ precursor cell differentiation, in maintaining undifferentiated stem cells in the intestine and in arresting cell migration. Mutations in the LNR-HD regions are associated with leukemia.
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