Suppr超能文献

一种新型的小 EDRK 丰富因子 2(Serf2)敲除小鼠,表现出发育和其他缺陷。

A novel knockout mouse for the small EDRK-rich factor 2 (Serf2) showing developmental and other deficits.

机构信息

Department of Neuromuscular Diseases, Queen Square Institute of Neurology, London, UK.

The UK Dementia Research Institute, University College London, Queen Square, London, WC1N 3BG, UK.

出版信息

Mamm Genome. 2021 Apr;32(2):94-103. doi: 10.1007/s00335-021-09864-6. Epub 2021 Mar 13.

Abstract

The small EDRK-rich factor 2 (SERF2) is a highly conserved protein that modifies amyloid fibre assembly in vitro and promotes protein misfolding. However, the role of SERF2 in regulating age-related proteotoxicity remains largely unexplored due to a lack of in vivo models. Here, we report the generation of Serf2 knockout mice using an ES cell targeting approach, with Serf2 knockout alleles being bred onto different defined genetic backgrounds. We highlight phenotyping data from heterozygous Serf2 mice, including unexpected male-specific phenotypes in startle response and pre-pulse inhibition. We report embryonic lethality in Serf2 null animals when bred onto a C57BL/6 N background. However, homozygous null animals were viable on a mixed genetic background and, remarkably, developed without obvious abnormalities. The Serf2 knockout mice provide a powerful tool to further investigate the role of SERF2 protein in previously unexplored pathophysiological pathways in the context of a whole organism.

摘要

富含小 EDRK 因子 2(SERF2)是一种高度保守的蛋白质,可在体外修饰淀粉样纤维的组装并促进蛋白质错误折叠。然而,由于缺乏体内模型,SERF2 在调节与年龄相关的蛋白毒性中的作用在很大程度上仍未得到探索。在这里,我们使用 ES 细胞靶向方法报告了 Serf2 敲除小鼠的产生,Serf2 敲除等位基因被繁殖到不同的定义遗传背景上。我们强调了杂合 Serf2 小鼠的表型数据,包括在惊跳反应和前脉冲抑制中出现的意外雄性特异性表型。我们报告了当 Serf2 缺失动物繁殖到 C57BL/6N 背景时会发生胚胎致死。然而,纯合子缺失动物在混合遗传背景上是可行的,而且非常引人注目,它们在没有明显异常的情况下发育。Serf2 敲除小鼠为进一步研究 SERF2 蛋白在整个生物体背景下以前未探索的病理生理途径中的作用提供了有力工具。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5647/8012326/bcf8d8472053/335_2021_9864_Fig1_HTML.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验