UGA BCMB 8020 - N-Glycan-Paper2 (6 pages)

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N-Glycan-Paper2



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N-Glycan-Paper2

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Pages:
6
School:
University of Georgia
Course:
Bcmb 8020 - Adv Biochem Ii
Adv Biochem Ii Documents

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Genetic remodeling of protein glycosylation in vivo induces autoimmune disease Daniel Chui Gayathri Sellakumar Ryan S Green Mark Sutton Smith Tammie McQuistan Kurt W Marek Howard R Morris Anne Dell and Jamey D Marth Glycobiology Research and Training Center Howard Hughes Medical Institute Department of Cellular and Molecular Medicine University of California at San Diego La Jolla CA 92093 and Department of Biochemistry Imperial College of Science Technology and Medicine London SW7 2AY England Edited by Stuart A Kornfeld Washington University School of Medicine St Louis MO and approved December 1 2000 received for review August 9 2000 Autoimmune diseases are among the most prevalent of afflictions yet the genetic factors responsible are largely undefined Protein glycosylation in the Golgi apparatus produces structural variation at the cell surface and contributes to immune self recognition Altered protein glycosylation and antibodies that recognize endogenous glycans have been associated with various autoimmune syndromes with the possibility that such abnormalities may reflect genetic defects in glycan formation We show that mutation of a single gene encoding mannosidase II which regulates the hybrid to complex branching pattern of extracellular asparagine N linked oligosaccharide chains N glycans results in a systemic autoimmune disease similar to human systemic lupus erythematosus Mannosidase IIdeficient autoimmune disease is due to an incomplete overlap of two conjoined pathways in complex type N glycan production Lymphocyte development abundance and activation parameters are normal however serum immunoglobulins are increased and kidney function progressively falters as a disorder consistent with lupus nephritis develops Autoantibody reactivity and circulating immune complexes are induced and anti nuclear antibodies exhibit reactivity toward histone Sm antigen and DNA These findings reveal a genetic cause of autoimmune disease provoked by a defect in the pathway



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