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神经 IL-17 控制了通过 CEP-1/p53 的发育隔膜
Abhishiktha Godthi1,2, Sehee Min1,2, Srijit Das2
1Department of Cell Stress Biology, Roswell Park Comprehensive Cancer Center, Buffalo, NY 14263.
概括
通过神经细胞因子ILC-17.1发出的营养可用性信号,控制了Caenorhabditis elegans的发展. 这种信号抑制CEP-1/p53以促进生长,或在缺席时允许永久停留.
科学领域:
- 发育生物学 发展生物学
- 神经免疫学 神经免疫学
- 代谢过程中的代谢.
背景情况:
- 细胞分裂和新陈代谢与发育过程中的营养物质可用性的协调还不太清楚.
- 神经元信号传递在将营养状况与发育命运联系起来的作用正在出现.
研究的目的:
- 为了研究营养的可用性如何调节在Caenorhabditis elegans的发展过渡.
- 阐明连接神经元信号,新陈代谢和细胞周期控制的分子机制.
主要方法:
- 使用Caenorhabditis elegans作为一个模型生物.
- 研究了神经元细胞因子ILC-17.1及其下游效应器CEP-1/p53.1的作用.
- 分析了基因表达 (果酸酶,细胞染色体C) 和发育结果 (生长,持续性停止).
主要成果:
- 由ILC-17.1发出信号的营养素可用性,促进葡萄糖利用,抑制CEP-1/p53活动,促进生长.
- 缺少ILC-17.1激活CEP-1/p53,导致细胞循环的抑制和幼虫的停止.
- 在无脊椎动物的发育过程中确定了CEP-1/p53的新型DNA损伤独立功能.
结论:
- 通过CEP-1/p53.1,ILC-17.1信号将营养物质的可用性和能量代谢与细胞循环的进展联系起来.
- 揭示了在发育过程中IL-17和p53家族蛋白质的祖先功能.
- 发现了一种新的C. elegans传染途径和神经免疫机制,这与癌症研究有关.
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