权益分类	功能权益	普通用户	{{item.name}}会员
{{category.name}}	{{benefitItem.name}}

Roles of Foxc transcription factors in podocyte injury.

Foxc 转录因子在足细胞损伤中的作用。

基本信息

批准号：
22590899
负责人：
MOTOJIMA Masaru
金额：
$ 2.83万
依托单位：
Tokai University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2010
资助国家：
日本
起止时间：
2010 至 2012
项目状态：
已结题

项目摘要

This project is aimed to clarify roles of Foxc1 and Foxc2 in the kidney development and the development of glomerular sclerosis. Mice carrying null mutated Foxc1 gene frequently develop anomalous double collecting system due to ectopic budding. However, ectopic budding per se does not contribute to kidney dysplasia. It is intriguing that Foxc1 expression does not affect the fate of metanephric mesenchyme where it is expressed but controls the site of bud formation by the Wolffian duct. We are analyzing kidney tissues from Foxc2 null mice, podocyte specific Foxc1 knockoutmice. We also generated Foxc2 loxP mice that enable us to generate kidney specific Foxc2 conditional knockout mice.

本研究旨在阐明Foxc1和FOXC2在肾脏发育和肾小球硬化发生发展中的作用。携带Foxc1基因缺失突变的小鼠，由于异位萌发，经常发生异常的双收集系统。然而，异位萌发本身并不会导致肾脏发育不良。耐人寻味的是，Foxc1的表达并不影响表达它的后肾间充质的命运，但控制着Wolffian管形成芽的位置。我们正在分析FOXC2基因缺失小鼠的肾脏组织，足细胞特异的Foxc1基因敲除小鼠。我们还培育了FOXC2 loxP小鼠，这使我们能够产生肾脏特异的FOXC2条件性基因敲除小鼠。