Title : Regulation of endoplasmic reticulum stress-induced cell death by ATF4 in neuroectodermal tumor cells.

Pub. Date : 2010 Feb 26

PMID : 20022965






4 Functional Relationships(s)
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1 The aim of this study was to test the hypothesis that the early events of ER stress signaling and response pathways induced by fenretinide and bortezomib are mediated by the eukaryotic initiation factor 2alpha (eIF2alpha)-ATF4 signaling pathway. Fenretinide eukaryotic translation initiation factor 2A Homo sapiens
2 Treatment of neuroblastoma and melanoma cell lines with fenretinide, bortezomib, or thapsigargin resulted in induction of eIF2alpha signaling, characterized by increased expression of phosphorylated eIF2alpha, ATF4, ATF3, and GADD34. Fenretinide eukaryotic translation initiation factor 2A Homo sapiens
3 Treatment of neuroblastoma and melanoma cell lines with fenretinide, bortezomib, or thapsigargin resulted in induction of eIF2alpha signaling, characterized by increased expression of phosphorylated eIF2alpha, ATF4, ATF3, and GADD34. Fenretinide eukaryotic translation initiation factor 2A Homo sapiens
4 Although PERK-dependent phosphorylation of eIF2alpha enhanced ATF4 protein levels during ER stress, cell death in response to fenretinide, bortezomib, or thapsigargin was not abrogated by inhibition of eIF2alpha phosphorylation through PERK knockdown or overexpression of wild-type eIF2alpha. Fenretinide eukaryotic translation initiation factor 2A Homo sapiens