An essential role for ectodomain shedding in mammalian development.
By J. Peschon, J. Slack, P. Reddy, K. Stocking, S. Sunnarborg, David C. Lee, W. Russell, B. Castner, Richard S. Johnson, J. Fitzner and 9 more. 1998
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Citations in the corpus
- A Disintegrin and Metalloproteinase (ADAM) and ADAM with Thrombospondin Motifs (ADAMTS) Family in Vascular Biology and Disease (2019, background): “Because of its wide involvement in development, ADAM-17−/− embryos die perinatally [85], supporting its essential role in embryonic development [86].”
- How matrix metalloproteinases regulate cell behavior. (2001, background): “TACE also probably contributes to the shedding of several other cell surface molecules and appears to be an essential activator of TGF-α in vivo (Peschon et al. 1998).”
- Helicobacter pylori: gastric cancer and beyond (2010, background): “Furthermore, the processing and availability of at least three EGFR ligands, HBEGF, transforming growth factor-α ( TGFα ) and amphiregulin ( AREG ), requires ADAM17 expressio”
- Metalloproteinases: role in breast carcinogenesis, invasion and metastasis (2000, background): “For example, a member of the ADAM family, known as TACE, has been shown to cause cell-shedding of transforming growth factor-α, tumour necrosis factor-α and other growth factors [29].”
- Neuregulins: functions, forms, and signaling strategies. (2003, background): “TACE) has demonstrated that this metalloprotease is essential for the processing of TGF and likely one or more other ligands of the EGFR [103,116].”
- 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 Lack of ADAM17 Activity during Embryonic Development Causes Hemorrhage and Impairs Vessel Formation (2010, unknown): “In addition, ADAM17 activity appears to be important during embryonic development since mice lacking ADAM17 activity die during the late gestational stages or soon after birth [5].”
- The discovery of receptor tyrosine kinases: targets for cancer therapy (2004, result): “results in a similar phenotype to that found in Egfr -null mice — it is characterized by multiple epithelial defect”
- Adam10 is essential for early embryonic cardiovascular development (2010, background): “7D), suggesting that no compensating roles exist between Adam10 and Adam17.”