A mouse model of non-Shiga toxin-associated haemolytic uraemic syndrome.

A mouse model of non-Shiga toxin-associated haemolytic uraemic syndrome.
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非志贺毒素相关溶血尿毒症综合征的小鼠模型。

DOI:
10.1093/ndt/gfm758
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发表时间:
2008
期刊:
Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association
影响因子:
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通讯作者:
Remuzzi,Giuseppe
Remuzzi,Giuseppe
中科院分区:
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文献类型:
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作者:
Caprioli,Jessica;Remuzzi,Giuseppe

文献摘要

相似文献

Impaired control of the complement system activation due to mutations in complement factor H (CFH) has been described in two apparently unrelated human diseases, membranoproliferative glomerulonephitis type II (MPGN2) and non-Shiga toxin-associated haemolytic uraemic syndrome (non-Stx-HUS). Mouse models of these diseases have been developed by Pickering et al., by knocking-out Cfh gene (MPGN2) and by subsequently transferring a mutated Cfh gene in the Cfh−/− background (non-Stx-HUS). The data obtained from the two models provided precious information to clarify the mechanisms that cause the disparate phenotypes underlying CFH genetic defect.