Increased outer arm and core fucose residues on the N-glycans of mutated alpha-1 antitrypsin protein from alpha-1 antitrypsin deficient individuals.

Abstract

Alpha-1 antitrypsin (AAT) is the major physiological inhibitor of a range of serine proteases, and in the lung, it maintains a protease-antiprotease balance. AAT deficiency (AATD) is an autosomal co-dominant condition with the Z mutation being the most common cause. Individuals homozygous for Z (PiZZ) have low levels of circulating mutant Z-AAT protein… (More)
DOI: 10.1021/pr400752t

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Cite this paper

@article{McCarthy2014IncreasedOA, title={Increased outer arm and core fucose residues on the N-glycans of mutated alpha-1 antitrypsin protein from alpha-1 antitrypsin deficient individuals.}, author={Cormac McCarthy and Radka Saldova and Mary R O'Brien and David A. Bergin and Tom{\'a}s P. Carroll and Joanne Keenan and Paula Meleady and Michael Henry and Martin Clynes and Pauline M. Rudd and Emer P Reeves and N Gerald McElvaney}, journal={Journal of proteome research}, year={2014}, volume={13 2}, pages={596-605} }