NOXA contributes to the sensitivity of PERK‐deficient cells to ER stress | Zendy

Gupta Sanjeev | Zendy; Giricz Zoltan | Zendy; Natoni Alessandro | Zendy; Donnelly Neysan | Zendy; Deegan Shane | Zendy; Szegezdi Eva | Zendy; Samali Afshin | Zendy

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NOXA contributes to the sensitivity of PERK‐deficient cells to ER stress

Author(s) -

Gupta Sanjeev,

Giricz Zoltan,

Natoni Alessandro,

Donnelly Neysan,

Deegan Shane,

Szegezdi Eva,

Samali Afshin

Publication year - 2012

Publication title -

febs letters

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.593

H-Index - 257

eISSN - 1873-3468

pISSN - 0014-5793

DOI - 10.1016/j.febslet.2012.10.002

Subject(s) - unfolded protein response , gene knockdown , apoptosis , small hairpin rna , protein kinase r , microbiology and biotechnology , kinase , eif 2 kinase , chemistry , cancer research , protein kinase a , biology , mitogen activated protein kinase kinase , biochemistry , cyclin dependent kinase 2

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.

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