网膜食受体FAM134C抑制了BMP受体的信号传递
Shuchen Gu1,2,3, Hanchenxi Zhang4, Jin Cao4,5,6
1MOE Key Laboratory of Biosystems Homeostasis & Protection and Zhejiang Key Laboratory of Molecular Cancer Biology, Innovation Center for Cell Signaling Network, Life Sciences Institute, Zhejiang University, Hangzhou, Zhejiang, 310058, China. fenglab@zju.edu.cn.
The EMBO journal
|October 20, 2025
概括
RETREG3/FAM134C充当了自受体,降低了BMP型I受体 (BMPRIA),以控制BMP信号传输. 这一功能独立于其在ER-phagy中的已知作用,并影响肠道再生.
科学领域:
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
- 自学研究 自学研究
背景情况:
- 已知FAM134/RETREG蛋白质是细胞平衡至关重要的内细胞网膜 (ER) 受体.
- FAM134蛋白的非ER-phagy功能在很大程度上尚未被探索.
- 了解自受体的不同作用对于细胞调节至关重要.
研究的目的:
- 为了研究FAM134蛋白质的潜在非ER-phagy功能.
- 为了确定RETREG3/FAM134C是否与其他细胞组件相互作用并调节.
- 阐明FAM134C在BMP信号通路中的作用.
主要方法:
- 研究了RETREG3/FAM134C作为I型BMP受体 (BMPRIA/ALK3) 的自受体.
- 利用化学自抑制和自调节器 (ATG5,Beclin-1) 的淘汰.
- 干扰了FAM134C中的LC3相互作用区域 (LIR) 动机,并分析了FAM134C缺乏的小鼠中的BMPR1A降解.
主要成果:
- 通过RETREG3/FAM134C选择性地将BMPRIA招募到自细胞中,通过自细胞分解.
- 由FAM134C介导的BMPRIA降解降低了BMP的信号强度.
- 自抑制或LIR动机干扰可以防止BMPRIA降解;FAM134C缺乏可以增强小鼠肠道中的BMP反应.
结论:
- FAM134C作为BMPRIA的特定自受体,控制BMP信号,独立于ER-phagy.
- 这种新的机制突显了FAM134C在调节超越ER周转的蜂信号通路中的作用.
- 由FAM134C介导的BMP信号调节影响肠道密室再生.
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