A ligand-induced extracellular cleavage regulates gamma-secretase-like proteolytic activation of Notch1.

By J. Mumm, E. Schroeter, M. Saxena, A. Griesemer, X. Tian, D. Pan, W. Ray, Raphael Kopan. Molecules and Cells, 2000

921 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/b25780d5deefdfc6a3ac701bc59bf97bba0d1531

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Citations in the corpus

The Canonical Notch Signaling Pathway: Unfolding the Activation Mechanism (2009, background): “transduction is ligand-induced and ADAM metalloproteasemediated Notch receptor cleavage to release the ectodomain (Brou et al., 2000; Mumm et al., 2000).”
The disintegrin/metalloprotease ADAM 10 is essential for Notch signalling but not for alpha-secretase activity in fibroblasts. (2002, background): “ADAM 10 (40,41), whereas the ADAM 17-deficient mouse shows no indication of a ‘Notch phenotype’ (43).”
The disintegrin/metalloproteinase ADAM10 is essential for the establishment of the brain cortex (2010, background): “Whereas in Drosophila, the ADAM10 ortholog Kuzbanian has been amply demonstrated to act as Notch sheddase, in the mammalian system, cell-based assays have in contrast implicated mainly ADAM17 in the S2 Notch-1 cleavage (Brou et al., 2000; Mumm et al., 2000).”
Notch signaling: from the outside in. (2000, background): “…secondary 151 o 1 M t d m g i ( h g 1 t in an fate pathways (reviewed in Beatus and Lendahl, 1998; Greenwald and Rubin, 1992; Kopan and Turner, 1996; Lewis, 1998; Muskavitch, 1994; Rooke and Xu, 1998; Sawamoto and Okano, 1996; Schlosser and Northcutt, 2000; Simpson, 1990; Tiedemann et al., 1998).”
Notch signaling: the core pathway and its posttranslational regulation. (2009, background): “…cells, led to the idea that the dynamic forces of membrane invagination during endocytosis of Notch and its ligands might facilitate ligand-induced ectodomain removal and exposure of the ADAM10/TACE/Kuz/SUP-17 cleavage site (Brou et al., 2000; Mumm et al., 2000; Parks et al., 2000; Figure 4).”
Mitochondrial rhomboid PARL regulates cytochrome c release during apoptosis via OPA1-dependent cristae remodeling. (2006, background): “In other examples of intramembrane proteolysis, like Notch signaling (Mumm et al., 2000), the substrate is cleaved after a conformational switch induced by binding to a ligand and/or cleavage by a second protease.”
Furin at the cutting edge: From protein traffic to embryogenesis and disease (2002, background): “This intracellular domain then binds to the transcriptional regulator CSL (for 'C promoter binding factor/Suppressor of Hairless/Lag-1'), which activates genes required for cell–cell communication during developmen”
Engineering T cells with Customized Therapeutic Response Programs Using Synthetic Notch Receptors (2016, neutral): “SynNotch Receptors Can Drive Antigen-Induced Transcription in CD4 and CD8 Human Primary T Lymphocytes The native Notch receptor has three critical components: (1) the ligand-binding epidermal growth factor (EGF) repeats, (2) the core regulatory region that controls cleavage of the receptor during ac”