NDLI: Rheumatoid arthritis as a hyper-endoplasmic reticulum-associated degradation disease

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Rheumatoid arthritis as a hyper-endoplasmic reticulum-associated degradation disease

Content Provider	Semantic Scholar
Author	Yamasaki, Satoshi Yagishita, Naoko Tsuchimochi, Kaneyuki Nishioka, Kusuki Nakajima, Toshihiro
Copyright Year	2005
Abstract	We introduce Synoviolin as a novel pathogenic factor in rheumatoid arthritis (RA). Experimental studies indicate that this endoplasmic reticulum (ER)-resident E3 ubiquitin ligase has important functions in the ER-associated degradation (ERAD) system, an essential system for ER homeostasis. Overexpression of Synoviolin in mice causes arthropathy with synovial hyperplasia, whereas heterozygous knockdown results in increased apoptosis of synovial cells and resistance to collagen-induced arthritis in mice. On the basis of these experimental data, we propose that excess elimination of unfolded proteins (that is, 'hyper-ERAD') by overexpression of Synoviolin triggers synovial cell overgrowth and hence a worsening of RA. Further analysis of the hyper-ERAD system may permit the complex pathomechanisms of RA to be uncovered.
Starting Page	181
Ending Page	186
Page Count	6
File Format	PDF HTM / HTML
PubMed reference number	16207344
Volume Number	7
Journal	Arthritis research & therapy
Alternate Webpage(s)	http://arthritis-research.biomedcentral.com/track/pdf/10.1186/ar1808?site=arthritis-research.biomedcentral.com
Alternate Webpage(s)	http://www.biomedcentral.com/content/pdf/ar1808.pdf
Language	English
Access Restriction	Open
Subject Keyword	Arthropathy Endoplasmic Reticulum Excretory function Hyperactive behavior Precipitating Factors Rheumatoid Arthritis SYVN1 gene Synovial Fluid Synoviocytes ubiquitin-protein ligase
Content Type	Text
Resource Type	Article

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