New directions in ER stress-induced cell death

New directions in ER stress-induced cell death Endoplasmic reticulum (ER) stress has been implicated in the pathophysiology of many diseases including heart disease, cancer and neurodegenerative diseases such as Alzheimer’s and Huntington’s. Prolonged or excessive ER stress results in the initiation of signaling pathways resulting in cell death. Over the past decade much research investigating the onset and progression of ER stress-induced cell death has been carried out. Owing to this we now have a better understanding of the signaling pathways leading to ER stress-mediated cell death and have begun to appreciate the importance of ER localized stress sensors, IRE1α, ATF6 and PERK in this process. In this article we provide an overview of the current thinking and concepts concerning the various stages of ER stress-induced cell death, focusing on the role of ER localized proteins in sensing and triggering ER stress-induced death signals with particular emphasis on the contribution of calcium signaling and Bcl-2 family members to the execution phase of this process. We also highlight new and emerging directions in ER stress-induced cell death research particularly the role of microRNAs, ER-mitochondria cross talk and the prospect of mitochondria-independent death signals in ER stress-induced cell death. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Apoptosis Springer Journals

New directions in ER stress-induced cell death

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Publisher
Springer Journals
Copyright
Copyright © 2013 by Springer Science+Business Media New York
Subject
Biomedicine; Cancer Research; Cell Biology; Oncology; Biochemistry, general; Virology
ISSN
1360-8185
eISSN
1573-675X
D.O.I.
10.1007/s10495-013-0818-6
Publisher site
See Article on Publisher Site

Abstract

Endoplasmic reticulum (ER) stress has been implicated in the pathophysiology of many diseases including heart disease, cancer and neurodegenerative diseases such as Alzheimer’s and Huntington’s. Prolonged or excessive ER stress results in the initiation of signaling pathways resulting in cell death. Over the past decade much research investigating the onset and progression of ER stress-induced cell death has been carried out. Owing to this we now have a better understanding of the signaling pathways leading to ER stress-mediated cell death and have begun to appreciate the importance of ER localized stress sensors, IRE1α, ATF6 and PERK in this process. In this article we provide an overview of the current thinking and concepts concerning the various stages of ER stress-induced cell death, focusing on the role of ER localized proteins in sensing and triggering ER stress-induced death signals with particular emphasis on the contribution of calcium signaling and Bcl-2 family members to the execution phase of this process. We also highlight new and emerging directions in ER stress-induced cell death research particularly the role of microRNAs, ER-mitochondria cross talk and the prospect of mitochondria-independent death signals in ER stress-induced cell death.

Journal

ApoptosisSpringer Journals

Published: Feb 21, 2013

References

  • Cloning of mammalian Ire1 reveals diversity in the ER stress responses
    Wang, XZ; Harding, HP; Zhang, Y; Jolicoeur, EM; Kuroda, M; Ron, D
  • Tumour necrosis factor receptor 1 mediates endoplasmic reticulum stress-induced activation of the MAP kinase JNK
    Yang, Q; Kim, YS; Lin, Y; Lewis, J; Neckers, L; Liu, ZG
  • Translation reinitiation at alternative open reading frames regulates gene expression in an integrated stress response
    Lu, PD; Harding, HP; Ron, D
  • CHOP and AP-1 cooperatively mediate PUMA expression during lipoapoptosis
    Cazanave, SC; Elmi, NA; Akazawa, Y; Bronk, SF; Mott, JL; Gores, GJ
  • TRB3, a novel ER stress-inducible gene, is induced via ATF4-CHOP pathway and is involved in cell death
    Ohoka, N; Yoshii, S; Hattori, T; Onozaki, K; Hayashi, H
  • Bcl-2 family on guard at the ER
    Szegezdi, E; MacDonald, DC; Chonghaile, TN; Gupta, S; Samali, A
  • Bcl-2 functionally interacts with inositol 1,4,5-trisphosphate receptors to regulate calcium release from the ER in response to inositol 1,4,5-trisphosphate
    Chen, R; Valencia, I; Zhong, F; McColl, KS; Roderick, HL; Bootman, MD; Berridge, MJ; Conway, SJ; Holmes, AB; Mignery, GA; Velez, P; Distelhorst, CW
  • Bax and Bak can localize to the endoplasmic reticulum to initiate apoptosis
    Zong, WX; Li, C; Hatzivassiliou, G; Lindsten, T; Yu, QC; Yuan, J; Thompson, CB
  • Reduced loading of intracellular Ca2 + stores and downregulation of capacitative Ca2 + influx in Bcl-2-overexpressing cells
    Pinton, P; Ferrari, D; Magalhaes, P; Schulze-Osthoff, K; Virgilio, F; Pozzan, T; Rizzuto, R
  • The ER-mitochondria interface: the social network of cell death
    Grimm, S
  • Chaperone-mediated coupling of endoplasmic reticulum and mitochondrial Ca2 + channels
    Szabadkai, G; Bianchi, K; Várnai, P; Stefani, D; Wieckowski, MR; Cavagna, D; Nagy, AI; Balla, T; Rizzuto, R
  • MiR-221/222 suppression protects against endoplasmic reticulum stress-induced apoptosis via p27 Kip1- and MEK/ERK-mediated cell cycle regulation
    Dai, R; Li, J; Liu, Y; Yan, D; Chen, S; Duan, C; Liu, X; He, T; Li, H
  • MicroRNA-30c-2* limits expression of proadaptive factor XBP1 in the unfolded protein response
    Byrd, AE; Aragon, IV; Brewer, JW

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