TY  - JOUR
AU  - Jiang, Simon H.
AU  - Mercan, Sevcan
AU  - Papa, Ilenia
AU  - Moldovan, Max
AU  - Walters, Giles D.
AU  - Koina, Mark
AU  - Fadia, Mitali
AU  - Stanley, Maurice
AU  - Lea-Henry, Tom
AU  - Cook, Amelia
AU  - Ellyard, Julia
AU  - McMorran, Brendan
AU  - Sundaram, Madhivanan
AU  - Thomson, Russell
AU  - Canete, Pablo F.
AU  - Hoy, Wendy
AU  - Hutton, Holly
AU  - Srivastava, Monika
AU  - McKeon, Kathryn
AU  - de la Rua Figueroa, Inigo
AU  - Cervera, Ricard
AU  - Faria, Raquel
AU  - D'Alfonso, Sandra
AU  - Gatto, Mariele
AU  - Athanasopoulos, Vicki
AU  - Field, Matthew
AU  - Mathews, John
AU  - Cho, Eun
AU  - Andrews, Thomas D.
AU  - Kitching, A. Richard
AU  - Cook, Matthew C.
AU  - Alarcon Riquelme, Marta
AU  - Bahlo, Melanie
AU  - Vinuesa, Carola G.
PY  - 2021
DO  - 10.1016/j.xcrm.2021.100475
SN  - 2666-3791
UR  - https://hdl.handle.net/10668/28384
T2  - Cell reports medicine
AB  - We identify an intronic deletion in VANGL1 that predisposes to renal injury in high risk populations through a kidney-intrinsic process. Half of all SLE patients develop nephritis, yet the predisposing mechanisms to kidney damage remain poorly...
LA  - en
PB  - Cell press
KW  - Systemic-lupus-erythematosus
KW  - Susceptibility loci
KW  - Renal-disease
KW  - Genome-wide
KW  - Association
KW  - Nephritis
KW  - Classification
KW  - Mutations
KW  - Gene
KW  - Glomerulonephritis
TI  - Deletions in VANGL1 are a risk factor for antibody-mediated kidney disease
TY  - research article
VL  - 2
ER  -