William Wong

Uromodulin mutations causing familial juvenile hyperuricaemic nephropathy lead to protein maturation defects and retention in the endoplasmic reticulum.

P. Rorsman, C. Antignac, P. Williams, 2009, Human molecular genetics.

Mutations in complement C3 predispose to development of atypical hemolytic uremic syndrome.

W. Fridman, N. Moghal, J. Atkinson, 2008, Blood.

hemolytic uremic syndrome Mutations in complement C3 predispose to development of atypical

W. Fridman, N. Moghal, J. Atkinson, 2013 .

Novel pathogenic mutations identified in the first Chinese pedigree of complete C6 deficiency

C. Lau, E. Au, P. Li, 2020, Clinical & translational immunology.

Molecular, biochemical and functional characterizations of C1q/TNF family members: adipose-tissue-selective expression patterns, regulation by PPAR-gamma agonist, cysteine-mediated oligomerizations, combinatorial associations and metabolic functions.

H. Lodish, R. Gimeno, G. W. Wong, 2008, The Biochemical journal.

Genome-wide study of familial juvenile hyperuricaemic (gouty) nephropathy (FJHN) indicates a new locus, FJHN3, linked to chromosome 2p22.1-p21

M. Brown, K. Dahan, P. Danoy, 2010, Human Genetics.