Article
ABIN1 dysfunction as a genetic basis for lupus nephritis.
Journal of the American Society of Nephrology : JASN - 1 Nov 2013
Caster Dawn J, Korte Erik A, Nanda Sambit K, McLeish Kenneth R, Oliver Rebecca K, G'sell Rachel T, Sheehan Ryan M, Freeman Darrell W, Coventry Susan C, Kelly Jennifer A, Guthridge Joel M, James Judith A, Sivils Kathy L, Alarcon-Riquelme Marta E, Scofield R Hal, Adrianto Indra, Gaffney Patrick M, Stevens Anne M, Freedman Barry I, Langefeld Carl D, Tsao Betty P, Pons-Estel Bernardo A, Jacob Chaim O, Kamen Diane L, Gilkeson Gary S, Brown Elizabeth E, Alarcon Graciela S, Edberg Jeffrey C, Kimberly Robert P, Martin Javier, Merrill Joan T, Harley John B, Kaufman Kenneth M, Reveille John D, Anaya Juan-Manuel, Criswell Lindsey A, Vila Luis M, Petri Michelle, Ramsey-Goldman Rosalind, Bae Sang-Cheol, Boackle Susan A, Vyse Timothy J, Niewold Timothy B, Cohen Philip, Powell David W
Abstract excerpt
The genetic factors underlying the pathogenesis of lupus nephritis associated with systemic lupus erythematosus are largely unknown, although animal studies indicate that nuclear factor (NF)-κB is involved. We reported previously that a knockin mouse expressing an inactive form of ABIN1 (ABIN1[D485N]) develops lupus-like autoimmune disease and demonstrates enhanced activation of NF-κB and mitogen-activated...
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