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- Publisher Website: 10.1083/jcb.200904060
- Scopus: eid_2-s2.0-70349905357
- PMID: 19752026
- WOS: WOS:000269960800004
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Article: Role of ERO1-α-mediated stimulation of inositol 1,4,5-triphosphate receptor activity in endoplasmic reticulum stress-induced apoptosis
Title | Role of ERO1-α-mediated stimulation of inositol 1,4,5-triphosphate receptor activity in endoplasmic reticulum stress-induced apoptosis |
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Authors | |
Issue Date | 2009 |
Citation | Journal of Cell Biology, 2009, v. 186, n. 6, p. 783-792 How to Cite? |
Abstract | Endoplasmic reticulum (ER) stress-induced apoptosis is involved in many diseases, but the mechanisms linking ER stress to apoptosis are incompletely understood. Based on roles for C/EPB homologous protein (CHOP) and ER calcium release in apoptosis, we hypothesized that apoptosis involves the activation of inositol 1,4,5-triphosphate (IP3) receptor (IP3R) via CHOP-induced ERO1-α (ER oxidase 1 α). In ER-stressed cells, ERO1-α is induced by CHOP, and small interfering RNA (siRNA) knockdown of ERO1-α suppresses apoptosis. IP3-induced calcium release (IICR) is increased during ER stress, and this response is blocked by siRNA-mediated silencing of ERO1-α or IP3R1 and by loss-of-function mutations in Ero1a or Chop. Reconstitution of ERO1-α in Chop-/- macrophages restores ER stress-induced IICR and apoptosis. In vivo, macrophages from wild-type mice but not Chop-/- mice have elevated IICR when the animals are challenged with the ER stressor tunicamycin. Macrophages from insulin-resistant ob/ob mice, another model of ER stress, also have elevated IICR. These data shed new light on how the CHOP pathway of apoptosis triggers calciumdependent apoptosis through an ERO1-α-IP3R pathway. © 2009 Li et al. |
Persistent Identifier | http://hdl.handle.net/10722/205727 |
ISSN | 2021 Impact Factor: 8.077 2020 SCImago Journal Rankings: 5.414 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Li-, Gang | - |
dc.contributor.author | Mongillo, Marco | - |
dc.contributor.author | Chin, Kingtung | - |
dc.contributor.author | Harding, Heather P. | - |
dc.contributor.author | Ron, David | - |
dc.contributor.author | Marks, Andrew R. | - |
dc.contributor.author | Tabas, Ira A. | - |
dc.date.accessioned | 2014-10-06T08:02:16Z | - |
dc.date.available | 2014-10-06T08:02:16Z | - |
dc.date.issued | 2009 | - |
dc.identifier.citation | Journal of Cell Biology, 2009, v. 186, n. 6, p. 783-792 | - |
dc.identifier.issn | 0021-9525 | - |
dc.identifier.uri | http://hdl.handle.net/10722/205727 | - |
dc.description.abstract | Endoplasmic reticulum (ER) stress-induced apoptosis is involved in many diseases, but the mechanisms linking ER stress to apoptosis are incompletely understood. Based on roles for C/EPB homologous protein (CHOP) and ER calcium release in apoptosis, we hypothesized that apoptosis involves the activation of inositol 1,4,5-triphosphate (IP3) receptor (IP3R) via CHOP-induced ERO1-α (ER oxidase 1 α). In ER-stressed cells, ERO1-α is induced by CHOP, and small interfering RNA (siRNA) knockdown of ERO1-α suppresses apoptosis. IP3-induced calcium release (IICR) is increased during ER stress, and this response is blocked by siRNA-mediated silencing of ERO1-α or IP3R1 and by loss-of-function mutations in Ero1a or Chop. Reconstitution of ERO1-α in Chop-/- macrophages restores ER stress-induced IICR and apoptosis. In vivo, macrophages from wild-type mice but not Chop-/- mice have elevated IICR when the animals are challenged with the ER stressor tunicamycin. Macrophages from insulin-resistant ob/ob mice, another model of ER stress, also have elevated IICR. These data shed new light on how the CHOP pathway of apoptosis triggers calciumdependent apoptosis through an ERO1-α-IP3R pathway. © 2009 Li et al. | - |
dc.language | eng | - |
dc.relation.ispartof | Journal of Cell Biology | - |
dc.title | Role of ERO1-α-mediated stimulation of inositol 1,4,5-triphosphate receptor activity in endoplasmic reticulum stress-induced apoptosis | - |
dc.type | Article | - |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1083/jcb.200904060 | - |
dc.identifier.pmid | 19752026 | - |
dc.identifier.scopus | eid_2-s2.0-70349905357 | - |
dc.identifier.volume | 186 | - |
dc.identifier.issue | 6 | - |
dc.identifier.spage | 783 | - |
dc.identifier.epage | 792 | - |
dc.identifier.eissn | 0021-9525 | - |
dc.identifier.isi | WOS:000269960800004 | - |
dc.identifier.issnl | 0021-9525 | - |