Mammalian tolloid proteinases: role in growth factor signalling.

Autor: Troilo H; Wellcome Trust Centre for Cell-Matrix Research, Faculty of Life Sciences, University of Manchester, UK., Bayley CP; Wellcome Trust Centre for Cell-Matrix Research, Faculty of Life Sciences, University of Manchester, UK., Barrett AL; Wellcome Trust Centre for Cell-Matrix Research, Faculty of Life Sciences, University of Manchester, UK., Lockhart-Cairns MP; Wellcome Trust Centre for Cell-Matrix Research, Faculty of Life Sciences, University of Manchester, UK.; Beamline B21, Diamond Light Source, Harwell Science & Innovation Campus, Didcot, Oxfordshire, UK., Jowitt TA; Wellcome Trust Centre for Cell-Matrix Research, Faculty of Life Sciences, University of Manchester, UK., Baldock C; Wellcome Trust Centre for Cell-Matrix Research, Faculty of Life Sciences, University of Manchester, UK.
Jazyk: angličtina
Zdroj: FEBS letters [FEBS Lett] 2016 Aug; Vol. 590 (15), pp. 2398-407. Date of Electronic Publication: 2016 Jul 22.
DOI: 10.1002/1873-3468.12287
Abstrakt: Tolloid proteinases are essential for tissue patterning and extracellular matrix assembly. The members of the family differ in their substrate specificity and activity, despite sharing similar domain organization. The mechanisms underlying substrate specificity and activity are complex, with variation between family members, and depend on both multimerization and substrate interaction. In addition, enhancers, such as Twisted gastrulation (Tsg), promote cleavage of tolloid substrate, chordin, to regulate growth factor signalling. Although Tsg and mammalian tolloid (mTLD) are involved in chordin cleavage, no interaction has been detected between them, suggesting Tsg induces a change in chordin to increase susceptibility to cleavage. All members of the tolloid family bind the N terminus of latent TGFβ-binding protein-1, providing support for their role in TGFβ signalling.
(© 2016 The Authors. FEBS Letters published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies.)
Databáze: MEDLINE
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