已入深夜,您辛苦了!由于当前在线用户较少,发布求助请尽量完整的填写文献信息,科研通机器人24小时在线,伴您度过漫漫科研夜!祝你早点完成任务,早点休息,好梦!

Proteotoxicity and endoplasmic reticulum stress-mediated cell death

蛋白质毒性 未折叠蛋白反应 内质网 内质网相关蛋白降解 细胞生物学 自噬 ATF6 神经退行性变 蛋白质折叠 蛋白质稳态 好斗的 蛋白质聚集 平衡 程序性细胞死亡 生物 细胞 医学 生物化学 内科学 细胞凋亡 疾病
作者
Mengxiong Wang,Mary E. Law,Brian K. Law
出处
期刊:Elsevier eBooks [Elsevier]
卷期号:: 119-174 被引量:2
标识
DOI:10.1016/b978-0-12-814208-0.00006-3
摘要

Proteotoxicity is defined as irreparable damage to the cell that is caused by an accumulation of impaired and misfolded proteins. Uncontrolled or severe proteotoxicity will ultimately result in cell death. The endoplasmic reticulum (ER), which controls the synthesis, folding, sorting, and transportation of over one-third of cellular proteins, is an essential organelle for regulating proteotoxicity. Either the increase of the damaged/misfolded protein load or the reduction of ER folding capacity could disrupt ER homeostasis and induce ER stress. Cells utilize a series of protective actions to restore ER homeostasis, including the induction of a coordinated adaptive program termed the Unfolded Protein Response (UPR). UPR helps to relieve ER stress by increasing the protein folding capacity of the ER and by promoting the ER-Associated Degradation (ERAD) of damaged/misfolded protein. Proteins that are not cleared by ERAD are transferred to quality control autophagy. It is well documented that ER stress is involved in the initiation and progression of various types of health problems, including neurodegeneration, cancer, muscle degeneration, cardiovascular disease, and autoimmune disorders. It is important to characterize the underlying mechanisms of ER stress that contribute to these diseases and to identify potential targets for their prevention and treatment. This chapter will introduce the signaling elements in ER stress pathways and crucial factors that regulate ER homeostasis, followed by a discussion of the mechanisms by which these factors or processes induce ER stress-mediated cell death. Subsequently, ER stress-related diseases and the potential targets for their treatment will be discussed, as well as the drugs that have been developed to target these disorders. Finally, this chapter will pose suggestions for future research directions.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
彭于晏应助唐军采纳,获得10
1秒前
禁止通行发布了新的文献求助10
1秒前
所所应助蓝桉采纳,获得10
2秒前
冻凉之材关注了科研通微信公众号
4秒前
tian发布了新的文献求助10
5秒前
6秒前
毛豆应助LIn采纳,获得10
6秒前
8秒前
9秒前
9秒前
情怀应助含糊的皮卡丘采纳,获得10
9秒前
9秒前
Biu完成签到,获得积分20
10秒前
Jasper应助梦里格斗家采纳,获得10
11秒前
FULAWEN完成签到,获得积分10
12秒前
佳远发布了新的文献求助10
12秒前
14秒前
ccc完成签到 ,获得积分10
16秒前
16秒前
17秒前
所所应助年轻的冰海采纳,获得10
19秒前
19秒前
20秒前
赘婿应助欢呼的冰蝶采纳,获得10
20秒前
21秒前
23秒前
FULAWEN发布了新的文献求助10
23秒前
24秒前
25秒前
冻凉之材发布了新的文献求助10
25秒前
Jasper应助梦里格斗家采纳,获得10
27秒前
香蕉觅云应助普通人001采纳,获得30
28秒前
科研通AI40应助犹豫书瑶采纳,获得10
28秒前
迅速的雅彤完成签到,获得积分10
29秒前
今后应助布吉岛采纳,获得10
29秒前
糖歌吃瘦发布了新的文献求助10
30秒前
31秒前
Biu发布了新的文献求助50
32秒前
34秒前
冬瓜君完成签到,获得积分10
34秒前
高分求助中
Genetics: From Genes to Genomes 3000
Production Logging: Theoretical and Interpretive Elements 2500
Continuum thermodynamics and material modelling 2000
Healthcare Finance: Modern Financial Analysis for Accelerating Biomedical Innovation 2000
Applications of Emerging Nanomaterials and Nanotechnology 1111
Les Mantodea de Guyane Insecta, Polyneoptera 1000
Diabetes: miniguías Asklepios 800
热门求助领域 (近24小时)
化学 医学 材料科学 生物 工程类 有机化学 生物化学 纳米技术 内科学 物理 化学工程 计算机科学 复合材料 基因 遗传学 物理化学 催化作用 细胞生物学 免疫学 电极
热门帖子
关注 科研通微信公众号,转发送积分 3471228
求助须知:如何正确求助?哪些是违规求助? 3064103
关于积分的说明 9087449
捐赠科研通 2754912
什么是DOI,文献DOI怎么找? 1511625
邀请新用户注册赠送积分活动 698541
科研通“疑难数据库(出版商)”最低求助积分说明 698404