摘要
Ankyrin repeat domain 17 (Ankrd17) encodes an ubiquitously expressed protein with two clusters of ankyrin repeats. We have used gene targeting strategy to ablate the Ankrd17 gene in mouse. The Ankrd17-deficient mice died between embryonic day (E) 10.5 and E11.5 due to cardiovascular defects. Serious hemorrhages were detected and the vascular smooth muscle cells (vSMCs) surrounding the vessels were drastically reduced in the Ankrd17-deficient embryos, suggesting that the vascular maturation was not completed. Interestingly, vSMC differentiation marker genes were up-regulated in the mutant embryos. Our data have demonstrated the indispensability of Ankrd17 functioning for vascular maturation during early development. The Ankrd17-deficient mice also provide a new animal model for the analysis of the regulatory pathways of the differentiation of vSMC precursor cells.
原文 | 英語 |
---|---|
頁(從 - 到) | 2765-2771 |
頁數 | 7 |
期刊 | FEBS Letters |
卷 | 583 |
發行號 | 17 |
DOIs | |
出版狀態 | 已發佈 - 9月 3 2009 |
對外發佈 | 是 |
ASJC Scopus subject areas
- 生物物理學
- 結構生物學
- 生物化學
- 分子生物學
- 遺傳學
- 細胞生物學