模仿脏流量剪切有效地诱导LECT2的聚合,LECT2是一种参与脏粉样化症的蛋白质
Jeung-Hoi Ha1, Yikang Xu2, Harsimranjit Sekhon1
1Department of Biochemistry and Molecular Biology, State University of New York Upstate Medical University, Syracuse, NY 13210.
bioRxiv : the preprint server for biology
|July 28, 2023
概括
像脏这样的微通道中的液体流动,而不是动,有效地驱动白细胞细胞衍生的化学毒素2 (LECT2) 聚合. I40V突变加快了这一过程,揭示了对粉样粉症机制的新见解.
科学领域:
- 生物化学 生物化学
- 生物物理学的生物物理.
- 医学 医学 医学 医学 医学
背景情况:
- 系统性氨基粉症,如ALECT2,是由白细胞细胞衍生的化学毒素2 (LECT2) 聚合引起的,主要影响脏和肝脏.
- I40V LECT2突变与疾病的发病有关,尽管它本身是不够的.
- 之前的研究表明,LECT2纤维化加速与离子损失和机械动,如震动,但这些方法缺乏生理相关性.
结论:
- 与损失和I40V突变相结合的样流量剪切是LECT2氨基代发生的关键触发因素.
- 开发的微流体装置为研究血流动力学如何导致蛋白质错折和全身性粉样性病的研究提供了宝贵的工具.
- 这项研究提供了一个更具生理相关性的模型,以了解与LECT2相关的粉样化症背后的机制.
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