期刊
AUTOIMMUNITY
卷 43, 期 2, 页码 111-120出版社
TAYLOR & FRANCIS LTD
DOI: 10.3109/08916930903214033
关键词
-
类别
资金
- Instituto de Salud Carlos III [PI050047, REDINREN RD06/0016]
- Spanish Ministry of Education and Science [SAF2005-07930-CO2-01]
Multiple evidences support the notion that cell-cycle deregulation or apoptosis alterations can lead to autoimmune syndrome (AIS). Inactivation of the cell-cycle regulator E2F2 or over-expression of the anti-apoptotic Bcl-2 protein induces spontaneously an AIS in certain mouse strains. In the present study, we have examined the contribution of the genetic background on the development of autoimmunity after E2F2 gene inactivation, and the effect that a simultaneous inactivation of the E2F2 gene and over-expression of the Bcl-2 gene in B cells has on lymphoid homeostasis and autoimmunity. We show that E2F2
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据