A2 Vertaisarvioitu katsausartikkeli tieteellisessä lehdessä
Shedding light on ADAM metalloproteinases
Tekijät: Huovila AP, Turner AJ, Pelto-Huikko M, Kärkkäinen I, Ortiz RM
Julkaisuvuosi: 2005
Journal: Trends in Biochemical Sciences
Tietokannassa oleva lehden nimi: Trends in biochemical sciences
Lehden akronyymi: Trends Biochem Sci
Vuosikerta: 30
Numero: 7
Aloitussivu: 413
Lopetussivu: 22
ISSN: 0968-0004
DOI: https://doi.org/10.1016/j.tibs.2005.05.006
Tiivistelmä
ADAM metalloproteinase disintegrins have emerged as the major proteinase family that mediates ectodomain shedding, the proteolytic release of extracellular domains from their membrane-bound precursors. Recent gene-manipulation studies have established the role of ADAM-mediated shedding in mammalian physiology and, in addition, raised the issue of functional redundancy among ADAM sheddases. ADAM sheddases activate, for example, growth factors and cytokines, thus regulating signalling pathways that are important in development and pathological processes such as cancer. The recent studies have also begun to elucidate the substrate specificity and the mechanisms that control ADAM-mediated shedding events that regulate, for example, growth-factor and Notch signalling, and the processing of the amyloid precursor protein.
ADAM metalloproteinase disintegrins have emerged as the major proteinase family that mediates ectodomain shedding, the proteolytic release of extracellular domains from their membrane-bound precursors. Recent gene-manipulation studies have established the role of ADAM-mediated shedding in mammalian physiology and, in addition, raised the issue of functional redundancy among ADAM sheddases. ADAM sheddases activate, for example, growth factors and cytokines, thus regulating signalling pathways that are important in development and pathological processes such as cancer. The recent studies have also begun to elucidate the substrate specificity and the mechanisms that control ADAM-mediated shedding events that regulate, for example, growth-factor and Notch signalling, and the processing of the amyloid precursor protein.
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