排序方式: 共有4条查询结果,搜索用时 15 毫秒
1
1.
Dishevelled 2 is essential for cardiac outflow tract development,somite segmentation and neural tube closure 总被引:14,自引:0,他引:14
Hamblet NS Lijam N Ruiz-Lozano P Wang J Yang Y Luo Z Mei L Chien KR Sussman DJ Wynshaw-Boris A 《Development (Cambridge, England)》2002,129(24):5827-5838
The murine dishevelled 2 (Dvl2) gene is an ortholog of the Drosophila segment polarity gene Dishevelled, a member of the highly conserved Wingless/Wnt developmental pathway. Dvl2-deficient mice were produced to determine the role of Dvl2 in mammalian development. Mice containing null mutations in Dvl2 present with 50% lethality in both inbred 129S6 and in a hybrid 129S6-NIH Black Swiss background because of severe cardiovascular outflow tract defects, including double outlet right ventricle, transposition of the great arteries and persistent truncus arteriosis. The majority of the surviving Dvl2(-/-) mice were female, suggesting that penetrance was influenced by sex. Expression of Pitx2 and plexin A2 was attenuated in Dvl2 null mutants, suggesting a defect in cardiac neural crest development during outflow tract formation. In addition, approximately 90% of Dvl2(-/-) mice have vertebral and rib malformations that affect the proximal as well as the distal parts of the ribs. These skeletal abnormalities were more pronounced in mice deficient for both Dvl1 and Dvl2. Somite differentiation markers used to analyze Dvl2(-/-) and Dvl1(-/-);Dvl2(-/-) mutant embryos revealed mildly aberrant expression of Uncx4.1, delta 1 and myogenin, suggesting defects in somite segmentation. Finally, 2-3% of Dvl2(-/-) embryos displayed thoracic spina bifida, while virtually all Dvl1/2 double mutant embryos displayed craniorachishisis, a completely open neural tube from the midbrain to the tail. Thus, Dvl2 is essential for normal cardiac morphogenesis, somite segmentation and neural tube closure, and there is functional redundancy between Dvl1 and Dvl2 in some phenotypes. 相似文献
2.
Luo Zhenge Wang Qiang Dobbins G. Clement Levy Shoshanah Xiong Wen C. Mei Lin 《Brain Cell Biology》2003,32(5-8):697-708
The receptor tyrosine kinase MuSK is activated by agrin, an extracellular matrix protein believed to be utilized by motoneurons to regulate the formation or maintenance of the neuromuscular junction (NMJ). Recent studies have shed light on intracellular signaling mechanisms downstream of MuSK. Agrin enhances the activity of Rho GTPases and PAK, which is required for AChR clustering. Activation of these enzymes requires not only the kinase activity of MuSK, but also its interaction with proteins such as Dishevelled. These results suggest that MuSK may function as a scaffold tyrosine kinase that forms a multi-molecule complex for AChR clustering. 相似文献
3.
用PCR法扩增出编码人FAS分子胞外区的cDNA片段,直接克隆到pGEM-T载体上,经DNA序列测定后,再插入到谷胱甘肽转硫酶(GST)融合蛋白表达载体pGEX-KG的EcoRⅠ和SalⅠ位点之间,构成重组质粒pKG-hFAS,将此质粒导入大肠杆菌,经IPTG诱导后获得GST-hFAS重组融合蛋白的表达,用谷胱甘肽偶联的Sepharose4B经亲合层析获得纯化的GST-hFAS蛋白,经凝血酶酶切和二次亲合层析去除GST部分,得到纯化的FAS蛋白.用纯化的FAS抗原免疫家兔制备了抗FAS抗体,经检测发现抗FAS抗体能诱导U937细胞发生细胞凋亡 相似文献
4.
Chennian Xu Jian Wang Zhenge Fan Shuang Zhang Rui Qiao Yu Liu Jian Yang Lifang Yang Huishan Wang 《Journal of cellular and molecular medicine》2021,25(13):6455-6459
Although reperfusion is the most effective therapy for patients with acute myocardial infarction, reperfusion injury limits the therapeutic effects of early reperfusion. Oxidative stress plays a crucial role in myocardial ischaemia/reperfusion (I/R) injury. Melatonin, a circulating hormone, is well-known as an antioxidant in cardiovascular diseases. In this short communication, we show that melatonin significantly improves post-ischaemic cardiac function, reduces infarct size and decreases oxidative stress. Furthermore, melatonin markedly increases AMPK activation and Nrf2 nuclear translocation. Nevertheless, these melatonin-induced changes are abrogated by compound C. In addition, ML-385, an Nrf2 inhibitor, also withdraws the antioxidative effects of melatonin but has little effect on AMPK activation. In conclusion, our results demonstrate that melatonin alleviates myocardial I/R injury by inhibiting oxidative stress via the AMPK/Nrf2 signalling pathway. 相似文献
1