title: Shedding light on ADAM metalloproteinases.
abstract: 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.
authors.affiliation: Institute of Medical Technology, University of Tampere and Tampere University Hospital, Biokatu 6, FIN-33520 Tampere, Finland. ari.huovila@uta.fi
authors.forename: Ari-Pekka J
authors.initials: AP
authors.lastname: Huovila
authors.forename: Anthony J
authors.initials: AJ
authors.lastname: Turner
authors.forename: Markku
authors.initials: M
authors.lastname: Pelto-Huikko
authors.forename: Iivari
authors.initials: I
authors.lastname: Kärkkäinen
authors.forename: Rebekka M
authors.initials: RM
authors.lastname: Ortiz
mesh_terms: D016564:Amyloid beta-Protein Precursor / Q000378:metabolism; D000818:Animals; D006801:Humans; D008565:Membrane Proteins / Q000378:metabolism; D008666:Metalloendopeptidases / Q000235:genetics / Q000502:physiology; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D051880:Receptors, Notch; D015398:Signal Transduction / Q000502:physiology
chemical_list: D016564:Amyloid beta-Protein Precursor; D008565:Membrane Proteins; D051880:Receptors, Notch; D020928:Mitogen-Activated Protein Kinases; D008666:Metalloendopeptidases