A novel proteolytic cleavage involved in Notch signaling: the role of the disintegrin-metalloprotease TACE.

By C. Brou, F. Logeat, N. Gupta, C. Bessia, O. Lebail, J. Doedens, A. Cumano, P. Roux, R. Black, A. Israël. Molecules and Cells, 2000

1,203 citations recorded by the source corpus.

Subfields: Molecular Biology, Neurology

View Paper: https://www.semanticscholar.org/paper/7f5ca95acce11d7516edaf35038a9d3148109d34

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Citations in the corpus

A ligand-induced extracellular cleavage regulates gamma-secretase-like proteolytic activation of Notch1. (2000, methodology): “Thewith the observation that TACE, a metalloprotease, can cleave Notch at Ala-1710 in vitro (Brou et al., 2000). cells used in our cotransfection assay (HEK 293T; Figure 6A) could allow either form of interaction to take place because they maintain an epithelial morphology withDo Kuzbanian or…”
Notch signaling: simplicity in design, versatility in function (2011, background): “Interestingly, different ADAMs have been implicated in this cleavage event (Brou et al., 2000; Canault et al., 2010; Tian et al., 2008; Tousseyn et al., 2009; van Tetering et al., 2009), and a recent report indicates that specific ADAM proteases may cleave Notch specifically in a liganddependent or…”
The Cysteine-Rich Domain of Human Adam 12 Supports Cell Adhesion through Syndecans and Triggers Signaling Events That Lead to β1 Integrin–Dependent Cell Spreading (2000, background): “A well-studied example is ADAM 17 (TACE), which functions in cell surface shedding of a number of growth factors, including tumor necrosis factor- a (TNF a ), transforming growth factora (TGF a ), and Notch (Black et al., 1997; Moss et al., 1997; Peschon et al., 1998; Brou et al., 2000).”
The ADAM metalloproteinases (2008, background): “Controversially, ADAM-17 was also reported to participate in Notch cleavage in vitro and in cultured mammalian cells (Brou et al., 2000).”
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).”
SHARP is a novel component of the Notch/RBP‐Jκ signalling pathway (2002, background): “After ligand binding, an extracellular cleavage step mediated by TACE, an ADAM family protease, occurs (Brou et al., 2000) followed by a cleavage step near the transmembrane region of the C-terminal protein fragment.”
iNOS promotes CD24+CD133+ liver cancer stem cell phenotype through a TACE/ADAM17-dependent Notch signaling pathway (2018, background): “TACE/ADAM17 (TNF-α converting enzyme) has previously been shown to cleave/activate Notch (35).”
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).”
Nicastrin Is Required for γ-Secretase Cleavage of the Drosophila Notch Receptor (2002, background): “A third 120 companied by removal of the extracellular domain by TNF -converting enzyme (TACE)-mediated proteolysis kDa C-terminal fragment (DNIC-3) that migrates slightly faster than DNIC-2 is unaltered in the Nic mutants relaat an extracellular site located just beyond the transmembrane domain (Mum”
A Disintegrin and Metalloprotease (ADAM): Historical Overview of Their Functions (2016, background): “ADAM-10 and -17 can cleave the extracellular domain of Notch when it is bound to ligands like Delta or Jagged, and from this follows subsequent intramembrane processing of Notch by γ-secretase activity [62,63].”