The disintegrin/metalloprotease ADAM 10 is essential for Notch signalling but not for alpha-secretase activity in fibroblasts.

By D. Hartmann, B. de Strooper, L. Serneels, K. Craessaerts, A. Herreman, W. Annaert, L. Umans, T. Lübke, Anna Lena Illert, K. von Figura and 1 more. 2002

732 citations recorded by the source corpus.

Subfields: Immunology and Allergy, Molecular Biology, Oncology

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology and Allergy

1. C. Blobel

In Molecular Biology

1. C. Blobel
2. D. Edwards
3. S. Eguchi
4. H. Ohtsu
5. P. Dempsey
6. M. Handsley
7. C. Pennington
8. R. Baron

In Oncology

1. C. Blobel
2. D. Edwards
3. S. Eguchi
4. H. Ohtsu
5. P. Dempsey
6. M. Handsley
7. C. Pennington

Citations in the corpus

• Potential Role for ADAM15 in Pathological Neovascularization in Mice (2003, background): “ADAM10/ KUZ has a critical role in Notch signaling and is required for early development in Drosophila melanogaster and mice (19, 24 , 59, 68).”
• Distinct roles for ADAM10 and ADAM17 in ectodomain shedding of six EGFR ligands (2004, unknown): “5 embryos have been described previously (Hartmann et al., 2002).”
• The disintegrin/metalloproteinase ADAM10 is essential for the establishment of the brain cortex (2010, background): “It also controls the proteolytic processing of the Notch receptor (Pan and Rubin, 1997; Wen et al., 1997; Hartmann et al., 2002; Lieber et al., 2002), which mediates lateral inhibition during neurogenesis.”
• ADAM10 is the physiologically relevant, constitutive α‐secretase of the amyloid precursor protein in primary neurons (2010, background): “In contrast, knockout cells deficient in ADAM9, 10 or 17 showed no change in APP shedding (Buxbaum et al, 1998; Hartmann et al, 2002; Weskamp et al, 2002).”
• Deficits in spatial learning and motor coordination in ADAM11-deficient mice (2006, background): “For example, ADAM10, ADAM17 and ADAM19 are critical for normal development by providing growth signals at the correct times and places [3-6].”
• A Disintegrin and Metalloprotease (ADAM): Historical Overview of Their Functions (2016, background): “5 of embryogenesis due to multiple defects of the developing central nervous system, somites, cardiovascular system, and missing Notch signaling thus providing a key evidence for the functional role of ADAM-10 in Notch processing in vivo [82].”