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活性氧介导的植入前胚胎中的未折叠蛋白反应途径

Reactive oxygen species-mediated unfolded protein response pathways in preimplantation embryos.

作者信息

Ali Ihsan, Shah Syed Zahid Ali, Jin Yi, Li Zhong-Shu, Ullah Obaid, Fang Nan-Zhu

机构信息

Laboratory of Animal Genetic Breeding and Reproduction, Agriculture College of Yanbian University, Yanji 133002, China.

National Animal Transmissible Spongiform Encephalopathy Laboratory, Key Laboratory of Animal Epidemiology and Zoonosis of Ministry of Agriculture, College of Veterinary Medicine and State Key Laboratory of Agro Biotechnology, China Agricultural University, Beijing 100193, China.

出版信息

J Vet Sci. 2017 Mar 30;18(1):1-9. doi: 10.4142/jvs.2017.18.1.1.

Abstract

Excessive production of reactive oxygen species (ROS) and endoplasmic reticulum (ER) stress-mediated responses are critical to embryonic development in the challenging environment. ROS production increases during early embryonic development with the increase in protein requirements for cell survival and growth. The ER is a multifunctional cellular organelle responsible for protein folding, modification, and cellular homeostasis. ER stress is activated by a variety of factors including ROS. Such stress leads to activation of the adaptive unfolded protein response (UPR), which restores homeostasis. However, chronic stress can exceed the toleration level of the ER, resulting in cellular apoptosis. In this review, we briefly describe the generation and impact of ROS in preimplantation embryo development, the ROS-mediated activation mechanism of the UPR via the ER, and the subsequent activation of signaling pathways following ER stress in preimplantation embryos.

摘要

活性氧(ROS)的过度产生以及内质网(ER)应激介导的反应对于在具有挑战性的环境中的胚胎发育至关重要。在早期胚胎发育过程中,随着细胞存活和生长对蛋白质需求的增加,ROS的产生也会增加。内质网是一种多功能细胞器,负责蛋白质折叠、修饰和细胞内稳态。内质网应激可由多种因素激活,包括ROS。这种应激会导致适应性未折叠蛋白反应(UPR)的激活,从而恢复内稳态。然而,慢性应激可能会超过内质网的耐受水平,导致细胞凋亡。在本综述中,我们简要描述了ROS在植入前胚胎发育中的产生及其影响、ROS通过内质网介导的UPR激活机制,以及植入前胚胎内质网应激后信号通路的后续激活。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd69/5366292/26e239d6df40/jvs-18-1-g001.jpg

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