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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

TitleRole of ERO1-α-mediated stimulation of inositol 1,4,5-triphosphate receptor activity in endoplasmic reticulum stress-induced apoptosis
Authors
Issue Date2009
Citation
Journal of Cell Biology, 2009, v. 186, n. 6, p. 783-792 How to Cite?
AbstractEndoplasmic 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 Identifierhttp://hdl.handle.net/10722/205727
ISSN
2015 Impact Factor: 8.717
2015 SCImago Journal Rankings: 7.923
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLi-, Gang-
dc.contributor.authorMongillo, Marco-
dc.contributor.authorChin, Kingtung-
dc.contributor.authorHarding, Heather P.-
dc.contributor.authorRon, David-
dc.contributor.authorMarks, Andrew R.-
dc.contributor.authorTabas, Ira A.-
dc.date.accessioned2014-10-06T08:02:16Z-
dc.date.available2014-10-06T08:02:16Z-
dc.date.issued2009-
dc.identifier.citationJournal of Cell Biology, 2009, v. 186, n. 6, p. 783-792-
dc.identifier.issn0021-9525-
dc.identifier.urihttp://hdl.handle.net/10722/205727-
dc.description.abstractEndoplasmic 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.languageeng-
dc.relation.ispartofJournal of Cell Biology-
dc.titleRole of ERO1-α-mediated stimulation of inositol 1,4,5-triphosphate receptor activity in endoplasmic reticulum stress-induced apoptosis-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1083/jcb.200904060-
dc.identifier.pmid19752026-
dc.identifier.scopuseid_2-s2.0-70349905357-
dc.identifier.volume186-
dc.identifier.issue6-
dc.identifier.spage783-
dc.identifier.epage792-
dc.identifier.eissn0021-9525-
dc.identifier.isiWOS:000269960800004-

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