Suppression of IRAK1 or IRAK4 Catalytic Activity, but Not Type 1 IFN Signaling, Prevents Lupus Nephritis in Mice Expressing a Ubiquitin Binding–Defective Mutant of ABIN1-Reference-Cited by-同舟云学术

Suppression of IRAK1 or IRAK4 Catalytic Activity, but Not Type 1 IFN Signaling, Prevents Lupus Nephritis in Mice Expressing a Ubiquitin Binding–Defective Mutant of ABIN1

Published:2016-11-02 Issue:11 Volume:197 Page:4266-4273
ISSN:0022-1767
Container-title:The Journal of Immunology
language:en
Short-container-title:J.I.

Author:

Nanda Sambit K.,Lopez-Pelaez Marta,Arthur J. Simon C.,Marchesi Francesco^ORCID,Cohen Philip

Publisher

The American Association of Immunologists

Subject

Immunology,Immunology and Allergy

Reference50 articles.

1. Polyubiquitin binding to ABIN1 is required to prevent autoimmunity

2. A20-binding inhibitor of NF- B (ABIN1) controls Toll-like receptor-mediated CCAAT/enhancer-binding protein activation and protects from inflammatory disease

3. ABIN1 Dysfunction as a Genetic Basis for Lupus Nephritis

4. Genome-wide scan reveals association of psoriasis with IL-23 and NF-κB pathways

5. A large-scale replication study identifies TNIP1, PRDM1, JAZF1, UHRF1BP1 and IL10 as risk loci for systemic lupus erythematosus

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