Title : Disturbed sialic acid recognition on endothelial cells and platelets in complement attack causes atypical hemolytic uremic syndrome.

Pub. Date : 2016 Jun 2

PMID : 27006390






2 Functional Relationships(s)
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1 In this article, we show that, instead of disturbed heparin interactions, the impaired ability of C-terminal mutant FH molecules to recognize sialic acid in the context of surface-bound C3b explains their pathogenicity. N-Acetylneuraminic Acid complement C3 Homo sapiens
2 Proper formation of FH-sialic acid-C3b complexes on surfaces exposed to plasma is essential for preventing cell damage and thrombogenesis characteristic of aHUS. N-Acetylneuraminic Acid complement C3 Homo sapiens