Multiple Mechanisms of Unfolded Protein Response–Induced Cell Death

未折叠蛋白反应 内质网 内质网相关蛋白降解 细胞生物学 蛋白质稳态 神经退行性变 生物 综合应力响应 信号转导 蛋白激酶R EIF-2激酶 蛋白激酶A 激酶 翻译(生物学) 生物化学 医学 丝裂原活化蛋白激酶激酶 疾病 病理 信使核糖核酸 基因 细胞周期蛋白依赖激酶2
作者
Naoki Hiramatsu,Wei‐Chieh Chiang,Timothy D. Kurt,Christina J. Sigurdson,Jonathan H. Lin
标识
DOI:10.1016/j.ajpath.2015.03.009
摘要

Eukaryotic cells fold and assemble membrane and secreted proteins in the endoplasmic reticulum (ER), before delivery to other cellular compartments or the extracellular environment. Correctly folded proteins are released from the ER, and poorly folded proteins are retained until they achieve stable conformations; irreparably misfolded proteins are targeted for degradation. Diverse pathological insults, such as amino acid mutations, hypoxia, or infection, can overwhelm ER protein quality control, leading to misfolded protein buildup, causing ER stress. To cope with ER stress, eukaryotic cells activate the unfolded protein response (UPR) by increasing levels of ER protein-folding enzymes and chaperones, enhancing the degradation of misfolded proteins, and reducing protein translation. In mammalian cells, three ER transmembrane proteins, inositol-requiring enzyme-1 (IRE1; official name ERN1), PKR-like ER kinase (PERK; official name EIF2AK3), and activating transcription factor-6, control the UPR. The UPR signaling triggers a set of prodeath programs when the cells fail to successfully adapt to ER stress or restore homeostasis. ER stress and UPR signaling are implicated in the pathogenesis of diverse diseases, including neurodegeneration, cancer, diabetes, and inflammation. This review discusses the current understanding in both adaptive and apoptotic responses as well as the molecular mechanisms instigating apoptosis via IRE1 and PERK signaling. We also examine how IRE1 and PERK signaling may be differentially used during neurodegeneration arising in retinitis pigmentosa and prion infection.
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
更新
大幅提高文件上传限制,最高150M (2024-4-1)

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
水怪二号完成签到,获得积分10
1秒前
Jasmine发布了新的文献求助10
1秒前
2秒前
5秒前
5秒前
白宫完成签到,获得积分10
7秒前
领导范儿应助科研的牲口采纳,获得10
7秒前
专注流沙发布了新的文献求助30
9秒前
烟花应助白小白采纳,获得10
9秒前
BJYX发布了新的文献求助10
9秒前
10秒前
研友_VZG7GZ应助yyyq0721采纳,获得10
11秒前
账号已注销完成签到,获得积分10
11秒前
沉默的谷秋完成签到,获得积分10
12秒前
12秒前
18秒前
18秒前
晴天发布了新的文献求助10
18秒前
BJYX完成签到,获得积分20
18秒前
19秒前
19秒前
20秒前
Jasmine完成签到,获得积分10
20秒前
辣辣完成签到,获得积分10
21秒前
田园发布了新的文献求助20
22秒前
Hello应助科研通管家采纳,获得10
22秒前
领导范儿应助科研通管家采纳,获得10
22秒前
不配.应助科研通管家采纳,获得10
22秒前
英姑应助BJYX采纳,获得10
22秒前
一一应助科研通管家采纳,获得10
22秒前
23秒前
23秒前
24秒前
sos38595145发布了新的文献求助10
24秒前
飞飞发布了新的文献求助10
25秒前
26秒前
专注流沙完成签到,获得积分10
27秒前
27秒前
Nuyoah发布了新的文献求助10
28秒前
kkkkai完成签到,获得积分10
29秒前
高分求助中
歯科矯正学 第7版(或第5版) 1004
SIS-ISO/IEC TS 27100:2024 Information technology — Cybersecurity — Overview and concepts (ISO/IEC TS 27100:2020, IDT)(Swedish Standard) 1000
Smart but Scattered: The Revolutionary Executive Skills Approach to Helping Kids Reach Their Potential (第二版) 1000
Semiconductor Process Reliability in Practice 720
GROUP-THEORY AND POLARIZATION ALGEBRA 500
Mesopotamian divination texts : conversing with the gods : sources from the first millennium BCE 500
Days of Transition. The Parsi Death Rituals(2011) 500
热门求助领域 (近24小时)
化学 医学 生物 材料科学 工程类 有机化学 生物化学 物理 内科学 纳米技术 计算机科学 化学工程 复合材料 基因 遗传学 催化作用 物理化学 免疫学 量子力学 细胞生物学
热门帖子
关注 科研通微信公众号,转发送积分 3233116
求助须知:如何正确求助?哪些是违规求助? 2879739
关于积分的说明 8212495
捐赠科研通 2547218
什么是DOI,文献DOI怎么找? 1376639
科研通“疑难数据库(出版商)”最低求助积分说明 647682
邀请新用户注册赠送积分活动 623073