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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of mouse embryonic fibroblasts (MEF) from wild type vs CHOP-/- genotypes treated with tunicamycin reveals CHOP induces death by promoting protein synthesis and oxidation in the stressed endoplasmic reticulum

ABSTRACT: Primary mouse embryonic fibroblasts (pass 3 to 4) were treated with tunicamycin (2 micrograms/ml) for specified times - genotypes were WILDTYPE and CHOP-/-. Each time point n=4. C/EBP homologous protein CHOP is activated by ER stress, and CHOP deletion protects against its lethal consequences.

ORGANISM(S): Mus musculus

SUBMITTER: Stefan Marciniak

PROVIDER: E-GEOD-2082 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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CHOP induces death by promoting protein synthesis and oxidation in the stressed endoplasmic reticulum.

Marciniak Stefan J SJ Yun Chi Y CY Oyadomari Seiichi S Novoa Isabel I Zhang Yuhong Y Jungreis Rivka R Nagata Kazuhiro K Harding Heather P HP Ron David D

Genes & development 20041201 24

Unfolded and malfolded client proteins impose a stress on the endoplasmic reticulum (ER), which contributes to cell death in pathophysiological conditions. The transcription factor C/EBP homologous protein (CHOP) is activated by ER stress, and CHOP deletion protects against its lethal consequences. We find that CHOP directly activates GADD34, which promotes ER client protein biosynthesis by dephosphorylating phospho-Ser 51 of the alpha-subunit of translation initiation factor 2 (eIF2alpha) in st ...[more]

PMID: 15601821

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