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对于EGF受体在自开始过程中的酶独立作用
Xiaojun Tan1, Narendra Thapa1, Yue Sun1
1Program in Molecular and Cellular Pharmacology, University of Wisconsin-Madison School of Medicine and Public Health, 1300 University Avenue, Madison, WI 53706, USA.
Cell
|January 17, 2015
概括
不活跃的表皮生长因子受体 (EGFR) 通过与LAPTM4B和Sec5.5的相互作用启动自. 这条通路调节瘤细胞代谢和压力期间的生存.
科学领域:
- 细胞生物学 细胞生物学
- 癌症研究 癌症研究
- 分子瘤学分子瘤学
背景情况:
- 皮表皮生长因子受体 (EGFR) 在人类癌症中经常被上调.
- 抑制EGFR信号传递可以触发瘤细胞的自.
研究的目的:
- 研究非活性EGFR在自开始中的作用.
- 阐明将非活性EGFR与自连接的分子机制.
主要方法:
- 同免疫沉试验用于研究蛋白质相互作用.
- 西方斑点测试用于评估蛋白质水平和自标志物.
- 免疫光显微镜可视化蛋白质定位.
主要成果:
- 不活跃的EGFR与coprotein LAPTM4B相互作用,这对于血清饥饿期间的EGFR内体积累至关重要.
- 不活跃的EGFR,LAPTM4B和Sec5亚复合体对于基底和饥饿诱导的自都至关重要.
- LAPTM4B和Sec5促进EGFR与Rubicon的结合,导致Beclin 1的释放和自的启动.
结论:
- 蛋白LAPTM4B调解了非活性EGFR在启动自过程中的作用.
- 这种新发现的途径涉及不活跃的EGFR,LAPTM4B和Sec5,调节瘤细胞代谢和在代谢压力下生存.
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