BI-1 regulates an apoptosis pathway linked to endoplasmic reticulum stress

Han Jung Chae; Hyung Ryong Kim; Chunyan Xu; Beatrice Bailly-Maitre; Maryla Krajewska; Stan Krajewski; Steven Banares; Janice Cui; Murat Digicaylioglu; Ning Ke; Shinichi Kitada; Edward Monosov; Michael Thomas; Christina L. Kress; Jeremy R. Babendure; Roger Y. Tsien; Stuart A. Lipton; John C. Reed

doi:10.1016/j.molcel.2004.06.038

BI-1 regulates an apoptosis pathway linked to endoplasmic reticulum stress

Han Jung Chae, Hyung Ryong Kim, Chunyan Xu, Beatrice Bailly-Maitre, Maryla Krajewska, Stan Krajewski, Steven Banares, Janice Cui, Murat Digicaylioglu, Ning Ke, Shinichi Kitada, Edward Monosov, Michael Thomas, Christina L. Kress, Jeremy R. Babendure, Roger Y. Tsien, Stuart A. Lipton, John C. Reed

Research output: Contribution to journal › Article › peer-review

266 Scopus citations

Abstract

Bax inhibitor-1 (BI-1) is an evolutionarily conserved endoplasmic reticulum (ER) protein that suppresses cell death in both animal and plant cells. We characterized mice in which the bi-1 gene was ablated. Cells from BI-1-deficient mice, including fibroblasts, hepatocytes, and neurons, display selective hypersensitivity to apoptosis induced by ER stress agents (thapsigargin, tunicamycin, brefeldin A), but not to stimulators of mitochondrial or TNF/Fas-death receptor apoptosis pathways. Conversely, BI-1 overexpression protects against apoptosis induced by ER stress. BI-1-mediated protection from apoptosis induced by ER stress correlated with inhibition of Bax activation and translocation to mitochondria, preservation of mitochondrial membrane potential, and suppression of caspase activation. BI-1 overexpression also reduces releasable Ca²⁺ from the ER. In vivo, bi-1^-/- mice exhibit increased sensitivity to tissue damage induced by stimuli that trigger ER stress, including stroke and tunicamycin injection. Thus, BI-1 regulates a cell death pathway important for cytopreservation during ER stress.

Original language	English (US)
Pages (from-to)	355-366
Number of pages	12
Journal	Molecular Cell
Volume	15
Issue number	3
DOIs	https://doi.org/10.1016/j.molcel.2004.06.038
State	Published - Aug 13 2004
Externally published	Yes

ASJC Scopus subject areas

Molecular Biology
Cell Biology

Access to Document

10.1016/j.molcel.2004.06.038

Cite this

Chae, H. J., Kim, H. R., Xu, C., Bailly-Maitre, B., Krajewska, M., Krajewski, S., Banares, S., Cui, J., Digicaylioglu, M., Ke, N., Kitada, S., Monosov, E., Thomas, M., Kress, C. L., Babendure, J. R., Tsien, R. Y., Lipton, S. A., & Reed, J. C. (2004). BI-1 regulates an apoptosis pathway linked to endoplasmic reticulum stress. Molecular Cell, 15(3), 355-366. https://doi.org/10.1016/j.molcel.2004.06.038

Chae, HJ, Kim, HR, Xu, C, Bailly-Maitre, B, Krajewska, M, Krajewski, S, Banares, S, Cui, J, Digicaylioglu, M, Ke, N, Kitada, S, Monosov, E, Thomas, M, Kress, CL, Babendure, JR, Tsien, RY, Lipton, SA & Reed, JC 2004, 'BI-1 regulates an apoptosis pathway linked to endoplasmic reticulum stress', Molecular Cell, vol. 15, no. 3, pp. 355-366. https://doi.org/10.1016/j.molcel.2004.06.038

@article{f552c196bde3408281acac83b9eb86e8,

title = "BI-1 regulates an apoptosis pathway linked to endoplasmic reticulum stress",

abstract = "Bax inhibitor-1 (BI-1) is an evolutionarily conserved endoplasmic reticulum (ER) protein that suppresses cell death in both animal and plant cells. We characterized mice in which the bi-1 gene was ablated. Cells from BI-1-deficient mice, including fibroblasts, hepatocytes, and neurons, display selective hypersensitivity to apoptosis induced by ER stress agents (thapsigargin, tunicamycin, brefeldin A), but not to stimulators of mitochondrial or TNF/Fas-death receptor apoptosis pathways. Conversely, BI-1 overexpression protects against apoptosis induced by ER stress. BI-1-mediated protection from apoptosis induced by ER stress correlated with inhibition of Bax activation and translocation to mitochondria, preservation of mitochondrial membrane potential, and suppression of caspase activation. BI-1 overexpression also reduces releasable Ca2+ from the ER. In vivo, bi-1-/- mice exhibit increased sensitivity to tissue damage induced by stimuli that trigger ER stress, including stroke and tunicamycin injection. Thus, BI-1 regulates a cell death pathway important for cytopreservation during ER stress.",

author = "Chae, {Han Jung} and Kim, {Hyung Ryong} and Chunyan Xu and Beatrice Bailly-Maitre and Maryla Krajewska and Stan Krajewski and Steven Banares and Janice Cui and Murat Digicaylioglu and Ning Ke and Shinichi Kitada and Edward Monosov and Michael Thomas and Kress, {Christina L.} and Babendure, {Jeremy R.} and Tsien, {Roger Y.} and Lipton, {Stuart A.} and Reed, {John C.}",

note = "Funding Information: We thank J. Yuan and D. Bredesen for reagents; R. Cornell, M. Lamie, and J. Valois for manuscript preparation; and the National Institutes of Health (AG15393; NS36821; HD29587; EY05477; NS27177; NS47855) and Foundation pour la Recherche Medicale for support.",

year = "2004",

month = aug,

day = "13",

doi = "10.1016/j.molcel.2004.06.038",

language = "English (US)",

volume = "15",

pages = "355--366",

journal = "Molecular Cell",

issn = "1097-2765",

publisher = "Cell Press",

number = "3",

}

TY - JOUR

T1 - BI-1 regulates an apoptosis pathway linked to endoplasmic reticulum stress

AU - Chae, Han Jung

AU - Kim, Hyung Ryong

AU - Xu, Chunyan

AU - Bailly-Maitre, Beatrice

AU - Krajewska, Maryla

AU - Krajewski, Stan

AU - Banares, Steven

AU - Cui, Janice

AU - Digicaylioglu, Murat

AU - Ke, Ning

AU - Kitada, Shinichi

AU - Monosov, Edward

AU - Thomas, Michael

AU - Kress, Christina L.

AU - Babendure, Jeremy R.

AU - Tsien, Roger Y.

AU - Lipton, Stuart A.

AU - Reed, John C.

N1 - Funding Information: We thank J. Yuan and D. Bredesen for reagents; R. Cornell, M. Lamie, and J. Valois for manuscript preparation; and the National Institutes of Health (AG15393; NS36821; HD29587; EY05477; NS27177; NS47855) and Foundation pour la Recherche Medicale for support.

PY - 2004/8/13

Y1 - 2004/8/13

N2 - Bax inhibitor-1 (BI-1) is an evolutionarily conserved endoplasmic reticulum (ER) protein that suppresses cell death in both animal and plant cells. We characterized mice in which the bi-1 gene was ablated. Cells from BI-1-deficient mice, including fibroblasts, hepatocytes, and neurons, display selective hypersensitivity to apoptosis induced by ER stress agents (thapsigargin, tunicamycin, brefeldin A), but not to stimulators of mitochondrial or TNF/Fas-death receptor apoptosis pathways. Conversely, BI-1 overexpression protects against apoptosis induced by ER stress. BI-1-mediated protection from apoptosis induced by ER stress correlated with inhibition of Bax activation and translocation to mitochondria, preservation of mitochondrial membrane potential, and suppression of caspase activation. BI-1 overexpression also reduces releasable Ca2+ from the ER. In vivo, bi-1-/- mice exhibit increased sensitivity to tissue damage induced by stimuli that trigger ER stress, including stroke and tunicamycin injection. Thus, BI-1 regulates a cell death pathway important for cytopreservation during ER stress.

AB - Bax inhibitor-1 (BI-1) is an evolutionarily conserved endoplasmic reticulum (ER) protein that suppresses cell death in both animal and plant cells. We characterized mice in which the bi-1 gene was ablated. Cells from BI-1-deficient mice, including fibroblasts, hepatocytes, and neurons, display selective hypersensitivity to apoptosis induced by ER stress agents (thapsigargin, tunicamycin, brefeldin A), but not to stimulators of mitochondrial or TNF/Fas-death receptor apoptosis pathways. Conversely, BI-1 overexpression protects against apoptosis induced by ER stress. BI-1-mediated protection from apoptosis induced by ER stress correlated with inhibition of Bax activation and translocation to mitochondria, preservation of mitochondrial membrane potential, and suppression of caspase activation. BI-1 overexpression also reduces releasable Ca2+ from the ER. In vivo, bi-1-/- mice exhibit increased sensitivity to tissue damage induced by stimuli that trigger ER stress, including stroke and tunicamycin injection. Thus, BI-1 regulates a cell death pathway important for cytopreservation during ER stress.

UR - http://www.scopus.com/inward/record.url?scp=4143087106&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=4143087106&partnerID=8YFLogxK

U2 - 10.1016/j.molcel.2004.06.038

DO - 10.1016/j.molcel.2004.06.038

M3 - Article

C2 - 15304216

AN - SCOPUS:4143087106

SN - 1097-2765

VL - 15

SP - 355

EP - 366

JO - Molecular Cell

JF - Molecular Cell

IS - 3

ER -

BI-1 regulates an apoptosis pathway linked to endoplasmic reticulum stress

Abstract

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this