Peer-Reviewed Journal Details
Mandatory Fields
Gupta, S,Giricz, Z,Natoni, A,Donnelly, N,Deegan, S,Szegezdi, E,Samali, A
2012
November
Febs Letters
NOXA contributes to the sensitivity of PERK-deficient cells to ER stress
Published
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Optional Fields
PERK NOXA Apoptosis ER stress Unfolded protein response UNFOLDED PROTEIN RESPONSE ENDOPLASMIC-RETICULUM STRESS INDUCED APOPTOSIS OXIDATIVE STRESS UP-REGULATION SURVIVAL EIF2-ALPHA PATHWAY KINASE
586
4023
4030
PKR-like ER kinase (PERK) deficient mouse embryonic fibroblasts (MEFs) are hypersensitive to ER stress-induced apoptosis. However, the molecular determinants of increased sensitivity of PERK-/- MEFs are not clearly understood. Here we show that induction of several Unfolded Protein Response (UPR) target genes is attenuated in PERK-/- MEFs. We also report elevated expression of the BH3-only protein, NOXA in PERK-/- MEFs. Further, shRNA-mediated knockdown of NOXA rescued the hypersensitivity of PERK-/- MEFs to ER stress-induced apoptosis. Taken together our results suggest that compromised induction of UPR and increased NOXA expression contributes to hypersensitivity of PERK-/- MEFs to ER stress-induced apoptosis. (c) 2012 Published by Elsevier B.V. on behalf of the Federation of European Biochemical Societies.
10.1016/j.febslet.2012.10.002
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