Nucleotide sugar

From Wikipedia, the free encyclopedia
Jump to: navigation, search

Nucleotide sugars are the activated forms of monosaccharides. Nucleotide sugars act as glycosyl donors in glycosylation reactions. Those reactions are catalyzed by a group of enzymes called glycosyltransferases.

History[edit]

The anabolism of oligosaccharides - and, hence, the role of nucleotide sugars - was not clear until the 1950s when Leloir and his coworkers found that the key enzymes in this process are the glycosyltransferases. These enzymes transfer a glycosyl group from a sugar nucleotide to an acceptor.[1]

Biological Importance[edit]

To act as glycosyl donors, those monosaccharides should exist in a highly energetic form. This occurs as a result of a reaction between nucleoside triphosphate (NTP) and glycosyl monophosphate (phosphate at anomeric carbon).

Activation of Monosaccharides

Types[edit]

There are nine sugar nucleotides in complex animals which act as glycosyl donors and they can be classified depending on the type of the nucleoside forming them:[2]

In other forms of life many other sugars are used and various donors are utilized for them. All five of the common nucleosides are used as a base for a nucleotide sugar donor somewhere in nature. As examples, CDP-glucose and TDP-glucose give rise to various other forms of CDP and TDP-sugar donor nucleotides.[3][4]

Structures[edit]

listed below are the structures of some nucleotide sugars (example from each type).

UDP-Gal CMP-NeuNAc GDP-Man
UDP-Gal CMP-NeuNAc GDP-Man

Relationship between glycosylation pathways and different diseases[edit]

Normal metabolism of nucleotide sugars is very important. Any malfunction in any contributing enzyme will lead to a certain disease [5] for example:

  1. Inclusion body myopathy: is a congenital disease resulted from altered function of UDP-GlcNAc epimerase .
  2. Macular corneal dystrophy: is a congenital disease resulted from malfunction of GlcNAc-6-sulfotransferase.
  3. Congenital disorder in α-1,3 mannosyl transferase will result in a variety of clinical symptoms, e.g. hypotonia, psychomotor retardation, liver fibrosis and various feeding problems.

See also[edit]

References[edit]

  1. ^ Derek Horton (2008). "The Development of Carbohydrate Chemistry and Biology". Carbohydrate Chemistry, Biology and Medical Applications: 1–28. doi:10.1016/B978-0-08-054816-6.00001-X. ISBN 978-0-08-054816-6. 
  2. ^ Cold Spring Harbor Laboratory Press Essentials of Glycobiology, Second Edition
  3. ^ Samuel G, Reeves P (2003). "Biosynthesis of O-antigens: genes and pathways involved in nucleotide sugar precursor synthesis and O-antigen assembly". Carbohydr. Res. 338 (23): 2503–19. doi:10.1016/j.carres.2003.07.009. PMID 14670712. 
  4. ^ Xue M. He and Hung-wen Liu (2002). "Formation of unusual sugars: Mechanistic studies and biosynthetic applications". Annu Rev Biochem 71: 701–754. doi:10.1146/annurev.biochem.71.110601.135339. PMID 12045109. 
  5. ^ Encyclopedia of Biological Chemistry, Volume 2. 2004, Elsevier Inc. Hudson H. Freeze 302-307.

External links[edit]