基因MK3通过TNF/P38 MAPK通路在肉中抑制粒状细胞的细胞亡
Li Chen1,2, Jia Liu1, Ying Zhang1,2
1Institute of Animal Husbandry and Veterinary Medicine, Hubei Academy of Agricultural Sciences, Wuhan 430064, China.
Cells
|October 28, 2025
概括
基因激活蛋白激酶激活蛋白激酶3 (MK3) 促进产卵卵巢颗粒细胞的亡. WT1调节MK3,MK3通过TNF/P38 MAPK通路起作用,影响卵子的产生.
科学领域:
- 动物科学动物科学
- 分子生物学分子生物学
- 生殖生物学 生殖生物学
背景情况:
- 产卵率对于家禽的利能力至关重要.
- 基因激活蛋白激酶激活蛋白激酶3 (MK3) 与卵泡发育有关.
- 产母的卵巢中的MK3表达因光线条件而改变.
研究的目的:
- 调查MK3在调节产母毛囊颗粒细胞亡中的作用.
- 阐明MK3在卵巢功能中的调节机制.
主要方法:
- 通过RNA测序分析分析.
- 通过siRNA介导的MK3的淘汰.
- 流式细胞计,CCK-8和EDU测定.
- 双露西法酶记者测定
- 使用P38抑制剂进行治疗.
主要成果:
- 过度表达MK3诱导了颗粒细胞的亡,并抑制了细胞的增殖.
- MK3调节了与亡相关的关键基因 (FAS,Caspase3,BCL2,C-myc).
- 转录因子WT1结合并增强MK3促进体活性.
- 通过TNF/P38 MAPK通路,MK3调节了亡.
结论:
- 在产母中,MK3促进颗粒状细胞的亡.
- WT1通过转录来调节MK3.
- TNF/P38 MAPK通路调解MK3的亲亡作用.
- 了解MK3的作用可以为提高家禽蛋产量的策略提供信息.
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