C
Celia J. Fang
Researcher at Washington University in St. Louis
Publications - 8
Citations - 1103
Celia J. Fang is an academic researcher from Washington University in St. Louis. The author has contributed to research in topics: CD46 & Atypical hemolytic uremic syndrome. The author has an hindex of 6, co-authored 8 publications receiving 1037 citations. Previous affiliations of Celia J. Fang include University of California, San Francisco.
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Journal ArticleDOI
Genetics of HUS: the impact of MCP, CFH, and IF mutations on clinical presentation, response to treatment, and outcome.
Jessica Caprioli,Marina Noris,Simona Brioschi,Gaia Pianetti,Federica Castelletti,Paola Bettinaglio,Caterina Mele,Elena Bresin,Linda Cassis,Sara Gamba,Francesca Porrati,Sara Bucchioni,Giuseppe Monteferrante,Celia J. Fang,M K Liszewski,David J. Kavanagh,John P. Atkinson,Giuseppe Remuzzi +17 more
TL;DR: The presentation, the response to therapy, and the outcome of the disease are influenced by the genotype, which will translate into improved management and therapy of patients and will provide the way to design tailored treatments.
Journal ArticleDOI
Membrane cofactor protein mutations in atypical hemolytic uremic syndrome (aHUS), fatal Stx-HUS, C3 glomerulonephritis, and the HELLP syndrome
Celia J. Fang,Véronique Frémeaux-Bacchi,M. Kathryn Liszewski,Gaia Pianetti,Marina Noris,Timothy H.J. Goodship,John P. Atkinson +6 more
TL;DR: Both the R69W and A304V MCP mutations were deficient in their ability to control the alternative pathway of complement activation on a cell surface, illustrating the importance of modeling transmembrane proteins in situ.
Journal ArticleDOI
Implications of the initial mutations in membrane cofactor protein (MCP; CD46) leading to atypical hemolytic uremic syndrome.
Anna Richards,M. Kathryn Liszewski,David J. Kavanagh,Celia J. Fang,Elizabeth A. Moulton,Véronique Frémeaux-Bacchi,Giuseppe Remuzzi,Marina Noris,Timothy H.J. Goodship,John P. Atkinson +9 more
TL;DR: MCP mutants as a cause of aHUS have a favorable clinical outcome in comparison to patients with factor H (CFH) or factor I (IF) mutations, but demonstrate incomplete penetrance, indicating that additional genetic and environmental factors are required to manifest disease.
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Advances in understanding of pathogenesis of aHUS and HELLP.
TL;DR: The pathogeneses of both diseases are reviewed focusing on the role of the complement system and how its dysfunction could result in a thrombotic microangiopathy in the kidney in the case of aHUS and in the liver in the cases of the HELLP syndrome.
Journal ArticleDOI
Smallpox Inhibitor of Complement Enzymes (SPICE): Dissecting Functional Sites and Abrogating Activity
M. Kathryn Liszewski,Marilyn K. Leung,Richard E. Hauhart,Celia J. Fang,Paula Bertram,John P. Atkinson +5 more
TL;DR: The major goals of the present study were to further characterize the complement regulatory and heparin binding sites of SPICE and to evaluate a mAb that abrogates its function and identify and characterized a mB that inhibits the complement Regulatory activity of SPice, MOPICE, and VCP.