期刊
BLOOD
卷 137, 期 25, 页码 3462-3463出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood.2021011364
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- NCI NIH HHS [R01 CA177909, R01 CA231141] Funding Source: Medline
This study identified the mechanism of excessive complement activation caused by recurrent mutations in FHR-1 in patients with aHUS, providing a better understanding of complement regulation in rare mutations in a rare disease.
In this issue of Blood, Martin Merinero et al identified the mechanism of excessive complement activation caused by recurrent mutations in factor H-related protein-1 (FHR-1) in a few patients with atypical hemolytic uremic syndrome (aHUS). These are rare mutations in a rare disease, but the results provide a better understanding of complement regulation.(1)
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