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• W3118032135 startingPage "e0224953" @default.
• W3118032135 abstract "The spliceosome assembles on pre-mRNA in a stepwise manner through five successive pre-spliceosome complexes. The spliceosome functions to remove introns from pre-mRNAs to generate mature mRNAs that encode functional proteins. Many small molecule inhibitors of the spliceosome have been identified and they are cytotoxic. However, little is known about genetic determinants of cell sensitivity. Activating transcription factor 3 (ATF3) is a transcription factor that can stimulate apoptotic cell death in response to a variety of cellular stresses. Here, we used a genetic approach to determine if ATF3 was important in determining the sensitivity of mouse embryonic fibroblasts (MEFs) to two splicing inhibitors: pladienolide B (PB) and isoginkgetin (IGG), that target different pre-spliceosome complexes. Both compounds led to increased ATF3 expression and apoptosis in control MEFs while ATF3 null cells were significantly protected from the cytotoxic effects of these drugs. Similarly, ATF3 was induced in response to IGG and PB in the two human tumour cell lines tested while knockdown of ATF3 protected cells from both drugs. Taken together, ATF3 appears to contribute to the cytotoxicity elicited by these spliceosome inhibitors in both murine and human cells." @default.
• W3118032135 created "2021-01-05" @default.
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• W3118032135 date "2020-12-28" @default.
• W3118032135 modified "2023-10-01" @default.
• W3118032135 title "The spliceosome inhibitors isoginkgetin and pladienolide B induce ATF3-dependent cell death" @default.
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• W3118032135 doi "https://doi.org/10.1371/journal.pone.0224953" @default.
• W3118032135 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7769279" @default.
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