Zobrazeno 1 - 6
of 6
pro vyhledávání: '"R. G. Boot"'
Publikováno v:
Frontiers in Cell and Developmental Biology, Vol 7 (2019)
Glycosphingolipids (GSLs), the main topic of this review, are a subclass of sphingolipids. With their glycans exposed to the extracellular space, glycosphingolipids are ubiquitous components of the plasma membrane of cells. GSLs are implicated in a v
Externí odkaz:
https://doaj.org/article/be3d45a0d4ca4b6fb093b95ead227131
Autor:
K.-Y. Li, J. Jiang, M. D. Witte, W. W. Kallemeijn, W. E. Donker-Koopman, R. G. Boot, J. M. F. G. Aerts, J. D.C. Codxe9e, G. A. van der Marel, H. S. Overkleeft
Publikováno v:
Organic and Biomolecular Chemistry.
Autor:
W. W. Kallemeijn, K.-Y. Li, M. D. Witte, A. R. A. Marques, J. Aten, S. Scheij, J.-B. Jiang, L. I. Willems, T. M. Voorn-Brouwer, C. P. A. A. van Roomen, R. Ottenhoff, R. G. Boot, H. van den Elst, M. T. C. Walvoort, B. I. Florea, J. D. C. Codxe9e, G. A. van der Marel, J. M. F. G. Aerts, H. S. Overkleeft
Publikováno v:
Angewandte Chemie - International Edition.
Publikováno v:
Acta paediatrica (Oslo, Norway : 1992). Supplement. 94(447)
The value of biomarkers in the clinical management of lysosomal storage diseases is best illustrated by the present use of plasma chitotriosidase levels in the diagnosis and monitoring of Gaucher disease. The enzyme chitotriosidase is specifically pr
Autor:
R G, Boot, G H, Renkema, M, Verhoek, A, Strijland, J, Bliek, T M, de Meulemeester, M M, Mannens, J M, Aerts
Publikováno v:
The Journal of biological chemistry. 273(40)
The human chitinase, named chitotriosidase, is a member of family 18 of glycosylhydrolases. Following the cloning of the chitotriosidase cDNA (Boot, R. G., Renkema, G. H., Strijland, A., van Zonneveld, A. J., and Aerts, J. M. F. G. (1995) J. Biol. Ch
Autor:
R G, Boot, C E, Hollak, M, Verhoek, P, Sloof, B J, Poorthuis, W J, Kleijer, R A, Wevers, M H, van Oers, M M, Mannens, J M, Aerts, S, van Weely
Publikováno v:
Human mutation. 10(5)
Gaucher disease is a recessively inherited lysosomal storage disorder that is caused by a deficiency in glucocerebrosidase activity. The clinical expression is markedly heterogeneous with respect to age of onset, progression, severity, and neurologic