ArticlePloS one2014
Ire1 mediated mRNA splicing in a C-terminus deletion mutant of Drosophila Xbp1.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Fbxo42 promotes the degradation of Ataxin-2 granules to trigger terminal Xbp1 signaling.Nature communications · 2025Article
- Pumilio protects Xbp1 mRNA from regulated Ire1-dependent decay.Nature communications · 2022Article
- Drosophila Unfolded Protein Response (UPR) Assays In Vitro and In Vivo.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Deletion of the Actin-Associated TropomyosinCells · 2021Article
- The Structure, Activation and Signaling of IRE1 and Its Role in Determining Cell Fate.Biomedicines · 2021Review
- Inositol-Requiring Enzyme 1 Facilitates Diabetic Wound Healing Through Modulating MicroRNAs.Diabetes · 2017Article
- Apoptosis, autophagy and unfolded protein response pathways in Arbovirus replication and pathogenesis.Expert reviews in molecular medicine · 2016Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Unfolded Protein Response is a homeostatic mechanism that permits eukaryotic cells to cope with Endoplasmic Reticulum (ER) stress caused by excessive accumulation of misfolded proteins in the ER lumen. The more conserved branch of the UPR relies on an ER transmembrane enzyme, Ire1, which, upon ER stress, promotes the unconventional splicing of a small intron from the mRNA encoding the transcription factor Xbp1. In mammals, two specific regions (the hydrophobic region 2--HR2--and the C-terminal translational pausing site) present in the Xbp1unspliced protein mediate the recruitment of the Xbp1 mRNA-ribosome-nascent chain complex to the ER membrane, so that Xbp1 mRNA can be spliced by Ire1. Here, we generated a Drosophila Xbp1 deletion mutant (Excision101) lacking both HR2 and C-terminal region, but not the Ire1 splicing site. We show that Ire1-dependent splicing of Xbp1 mRNA is reduced, but not abolished in Excision101. Our results suggest the existence of additional mechanisms for ER membrane targeting of Xbp1 mRNA that are independent of the C-terminal domain of Drosophila Xbp1unspliced.
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