Plasma Membrane-associated Sialidase as a Crucial Regulator of Transmembrane Signalling

Mammalian sialidases, glycosidases responsible for the removal of sialic acids from glycoproteins and glycolipids, has been implicated to participate in many biological processes as well as in lysosomal catabolism. Among those forms identified to date, plasma membrane-associated sialidase, Neu3, is...

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Bibliographic Details
Published in:Journal of biochemistry (Tokyo) 2008-09, Vol.144 (3), p.279-285
Main Authors: Miyagi, Taeko, Wada, Tadashi, Yamaguchi, Kazunori, Hata, Keiko, Shiozaki, Kazuhiro
Format: Article
Language:English
Subjects:
Animals
Apoptosis
cancer
Cell Line, Tumor
Cell Membrane - enzymology
Cell Membrane - metabolism
diabetes
gangliosides
Gene Expression Regulation, Enzymologic
Humans
Mice
Mice, Transgenic
Models, Biological
Neoplasms - metabolism
Neuraminidase - biosynthesis
Neuraminidase - chemistry
Neuraminidase - metabolism
Neuraminidase - physiology
Neurites - metabolism
sialidase
Signal Transduction
transmembrane signalling
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Summary:Mammalian sialidases, glycosidases responsible for the removal of sialic acids from glycoproteins and glycolipids, has been implicated to participate in many biological processes as well as in lysosomal catabolism. Among those forms identified to date, plasma membrane-associated sialidase, Neu3, is a key enzyme in degradation of gangliosides, for which it exhibits a special substrate preference. This sialidase has been shown to control transmembrane signalling for many cellular processes, including cell differentiation, cell growth and apoptosis, and human orthologue NEU3 is markedly up-regulated in various cancers. It is known to suppress apoptosis in cancer cells. Furthermore, its overexpression causes impaired glucose tolerance and hyper-insulinaemia together with overproduction of insulin in enlarged islets in the transgenic mice. The present review primarily summarizes our recent results, focusing on Neu3 as a regulator of transmembrane signalling.
ISSN:0021-924X
1756-2651
DOI:10.1093/jb/mvn089