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SEPS1 protects RAW264.7 cells from pharmacological ER stress agent-induced apoptosis
journal contributionposted on 2007-03-02, 00:00 authored by K H Kim, Yuan Gao, Ken WalderKen Walder, Gregory Collier, J Skelton, A Kissebah
Selenoprotein S (SEPS1) is a novel endoplasmic reticulum (ER) resident protein and it is known to play an important role in production of inflammatory cytokines. Here, we show evidence that SEPS1 is stimulated by pharmacological ER stress agents in RAW264.7 macrophages as well as other cell types. Overexpression studies reveal a protective action of SEPS1 in macrophages against ER stress-induced cytotoxicity and apoptosis, resulting in promoting cell survival during ER stress. The protective action of SEPS1 is largely dependent on ER stress-mediated cell death signal with less effect on non-ER stress component cell death signals. Conversely, suppression of SEPS1 in macrophages results in sensitization of cells to ER stress-induced cell death. These findings suggest that SEPS1 could be a new ER stress-dependent survival factor that protects macrophage against ER stress-induced cellular dysfunction.
JournalBiochemical and biophysical research communications
Pagination127 - 132
NotesAvailable online 2 January 2007.
Publication classificationC1 Refereed article in a scholarly journal; C Journal article
Copyright notice2006, Elsevier
CategoriesNo categories selected
selenoprotein StanisVIMPendoplasmic reticulum stressmacrophagesapoptosistunicamycinthapsigarginScience & TechnologyLife Sciences & BiomedicineBiochemistry & Molecular BiologyBiophysicsENDOPLASMIC-RETICULUM STRESSINFLAMMATORY RESPONSEACTIVATIONCASPASE-12MEMBRANEDEATHCYTOTOXICITYEXPRESSIONPROTEINSGROWTH