RGC-32 and diseases: the first 20 years |
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Authors: | Vlaicu Sonia I Tatomir Alexandru Anselmo Freidrich Boodhoo Dallas Chira Romeo Rus Violeta Rus Horea |
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Institution: | 1.Department of Internal Medicine, “Iuliu Hatieganu” University of Medicine and Pharmacy, Cluj-Napoca, Romania ;2.Department of Neurology, University of Maryland, School of Medicine, 655 W Baltimore St., BRB 12-033, Baltimore, MD, 21201, USA ;3.Department of Neurosciences, “Iuliu Hatieganu” University of Medicine and Pharmacy, Cluj-Napoca, Romania ;4.Department of Medicine, Division of Rheumatology and Immunology, University of Maryland, School of Medicine, Baltimore, MD, USA ;5.Research Service, Veterans Administration Maryland Health Care System, Baltimore, MD, USA ; |
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Abstract: | The response gene to complement (RGC)-32 acts as a cell cycle regulator and mediator of TGF-β effects. However, recent studies have revealed other functions for RGC-32 in diverse processes such as cellular migration, differentiation, and fibrosis. In addition to its induction by complement activation and the C5b-9 terminal complement complex, RGC-32 expression is also stimulated by growth factors, hormones, and cytokines. RGC-32 is induced by TGF-β through Smad3 and RhoA signaling and plays an important role in cell differentiation. In particular, RGC-32 is essential for the differentiation of Th17 cells. RGC-32−/− mice display an attenuated experimental autoimmune encephalomyelitis phenotype that is accompanied by decreased central nervous system inflammation and reductions in IL-17- and GM-CSF-producing CD4+ T cells. Accumulating evidence has drawn attention to the deregulated expression of RGC-32 in human cancers, atherogenesis, metabolic disorders, and autoimmune disease. Furthermore, RGC-32 is a potential therapeutic target in multiple sclerosis and other Th17-mediated autoimmune diseases. A better understanding of the mechanism(s) by which RGC-32 contributes to the pathogenesis of all these diseases will provide new insights into its therapeutic potential. |
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