期刊
FEBS LETTERS
卷 596, 期 24, 页码 3211-3231出版社
WILEY
DOI: 10.1002/1873-3468.14452
关键词
B cell; MD-1; N-glycosylation; RP105; toll-like receptor
资金
- Uehara Memorial Foundation
- JSPS KAKENHI [19 K07491, 19 K08500]
- Takeda Science Foundation
- Terumo Life Science Foundation
- Ichihara International Scholarship Foundation
- International Joint Usage/Research Center, the Institute of Medical Science, University of Tokyo [2022-3021]
- Aichi Medical University
The cell surface expression of RP105, an orphan Toll-like receptor, depends on its complex formation with MD-1. N-glycosylation of MD-1 may serve as a potential target for SLE therapy.
For its cell surface expression, radioprotective 105 (RP105) - an orphan Toll-like receptor - must form a complex with a soluble glycoprotein called myeloid differentiation 1 (MD-1). The number of RP105-negative cells is significantly increased in patients with systemic lupus erythematosus (SLE); however, to elucidate the mechanism underlying this increase, how RP105 is expressed on the cell surface depending on MD-1 should be investigated. We demonstrated that RP105 exhibits two forms depending on MD-1 and its two N-glycosylation sites, N96 and N156. Cell surface expression of RP105 decreased in the presence of mutant MD-1 (N96Q/N156Q). Nonglycosylated MD-1 decreased the de novo cell surface expression of RP105 but not pre-expressed RP105. Thus, the N-glycans of MD-1 may represent targets for SLE therapy.
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