分析未折叠蛋白反应（UPR）通路元件的小鼠基因敲除模型。

Analyze Mouse Knockout Models of UPR Pathway Elements.

作者信息

Zheng Chao, Wang Cheng, Jie Qiang, Yang Liu

机构信息

Institute of Orthopedic Surgery, Xijing Hospital, Fourth Military Medical University, Xi'an, China.

School of Biomedical Sciences, University of Hong Kong, Pok Fu Lam, Hong Kong, China.

出版信息

Methods Mol Biol. 2022;2378:205-219. doi: 10.1007/978-1-0716-1732-8_13.

DOI:10.1007/978-1-0716-1732-8_13

PMID:34985702

Abstract

Evidence from genetic studies in human and mice indicates that defective skeletal development is one of the major phenotypic outcomes for aberrant UPR signaling. Visualization of morphological alterations in whole-mount skeleton and protein secretion and UPR activation on tissue sections is the very first step to investigate skeletal phenotypes of UPR-related mouse models. In this chapter, we introduce the major techniques that have been frequently used in our laboratory to study UPR-induced skeletal disorders with genetically modified mice and provide descriptive directions of mouse genotyping, bone tissue grossing, whole-mount skeletal staining, immunostaining assays of matrix secretion, and UPR activation.

摘要

来自人类和小鼠基因研究的证据表明，骨骼发育缺陷是异常未折叠蛋白反应（UPR）信号传导的主要表型结果之一。对整体骨骼形态改变以及组织切片上蛋白质分泌和UPR激活进行可视化，是研究UPR相关小鼠模型骨骼表型的第一步。在本章中，我们介绍了在我们实验室中经常用于研究转基因小鼠UPR诱导的骨骼疾病的主要技术，并提供了小鼠基因分型、骨组织取材、整体骨骼染色、基质分泌免疫染色测定以及UPR激活的描述性指导。