Author Correction: Genome-wide association study identifies Sjögren’s risk loci with functional implications in immune and glandular cells.
Genome-wide association study identifies Sjögren’s risk loci with functional implications in immune and glandular cells.
And Yet It Moves: Oxidation of the Nuclear Autoantigen La/SS-B Is the Driving Force for Nucleo-Cytoplasmic Shuttling.
Defective Efferocytosis in a Murine Model of Sjögren’s Syndrome Is Mediated by Dysfunctional Mer Tyrosine Kinase Receptor.
Two Be or Not Two Be: The Nuclear Autoantigen La/SS-B Is Able to Form Dimers and Oligomers in a Redox Dependent Manner.
