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Fueling clonal dominance through TRAFficking of NF-κB signaling.
Nature Immunology ( IF 27.7 ) Pub Date : 2020-05-01 , DOI: 10.1038/s41590-020-0662-0
Koki Ueda 1, 2 , Rajni Kumari 1, 2 , Ulrich Steidl 1, 2, 3, 4
Affiliation  

Activation of TLR–TRAF6 signaling by chronic inflammation in myelodysplastic syndromes increases the competitive advantage of HSPCs harboring MDS mutations through the upregulation of the ubiquitin-modifying enzyme A20 and a switch from canonical to non-canonical NF-κB signaling.

中文翻译:

通过TRAFfickingNF-κB信号增强克隆优势。

骨髓增生异常综合症中慢性炎症激活TLR–TRAF6信号通过增加泛素修饰酶A20的上调以及从经典的NF-κB信号转换为非经典的NF-κB信号,增加了具有MDS突变的HSPC的竞争优势。
更新日期:2020-04-24
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