XBP1 mRNA is induced by ATF6 and spliced by IRE1 in response to ER stress to produce a highly active transcription factor.

By Hiderou Yoshida, Toshie Matsui, Akira Yamamoto, T. Okada, K. Mori. Cell, 2001

4,055 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/669d322ae0fe5e1e50f019efa9fb4a79e0763c89

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In Cell Biology

1. R. Kaufman
2. G. Hotamışlıgil
3. C. Hetz
4. D. Ron
5. J. Malhotra
6. Laurie H. Glimcher
7. F. Papa
8. Peter Walter

In Molecular Biology

1. R. Kaufman
2. G. Hotamışlıgil
3. C. Hetz
4. D. Ron
5. Laurie H. Glimcher
6. J. Malhotra
7. F. Papa
8. Ann-Hwee Lee

Citations in the corpus

• Translational control in the endoplasmic reticulum stress response. (2002, background): “While non-canonical splicing of XBP-1 mRNA by activated IRE1 is an absolute requirement for expression of the encoded protein (36), transcription of this mRNA depends on both the ISR and the activation of ATF6 (36, 37).”
• The highways and byways of mRNA decay (2007, background): “Although IRE1 has not yet been shown to be directly responsible for this cleavage, it does have endonuclease activity that catalyses splicing of the XBP1 mRN”
• Endoplasmic Reticulum Stress and Oxidative Stress: A Vicious Cycle or a Double-Edged Sword? (2007, positive): “These transducers are two protein kinases IRE1 (inositol-requiring kinase 1) (129, 159), and PERK (double-stranded RNA-activated protein kinase-like ER kinase) (42), and the transcription factor ATF6 (activating transcription factor 6) (159, 160).”
• Endoplasmic reticulum stress signaling in disease. (2006, background): “frame, which introduces a new COOH-terminal transactivation domain to generate the active transcription factor (19, 99, 169, 222).”
• Mediators of endoplasmic reticulum stress‐induced apoptosis (2006, background): “The generated frameshift splice variant (sXBP1) encodes a stable, active transcription factor (Yoshida et al, 2001). sXBP1 has diverse targets, including ER chaperones and the HSP40 family member P58IPK (Lee et al, 2003; Fig 1).”
• Coupling endoplasmic reticulum stress to the cell death program (2004, background): “mRNA is a substrate for mammalian IRE1, is processed similarly to yeast Hac1p, and the resulting processed mRNA encodes a novel and potent transcriptional activator.(76,77)”
• Endoplasmic reticulum stress signalling and the pathogenesis of non-alcoholic fatty liver disease. (2018, background): “involved in protein folding and ERAD, but can also activate the transcription of XBP1u (44, 45).”
• ISMARA: automated modeling of genomic signals as a democracy of regulatory motifs (2014, background): “Indeed, it has been established that XBP1 activity is regulated post-transcriptionally through alternative splicing (Yoshida et al. 2001; Calfon et al. 2002).”
• Endoplasmic reticulum stress sensing in the unfolded protein response. (2013, background): “Once activated, Ire1’s RNase specifically cleaves its mRNA substrate, HAC1 mRNA (homolog of ATF/CREB1) in yeast or XBP1 mRNA (X-box binding protein 1) (Cox and Walter 1996; Yoshida et al. 2001) in metazoan cells to initiate an unconventional splicing reaction.”
• tRNA biology charges to the front. (2010, background): “Moreover, mammals have retained the nonconventional tRNA-like splicing of theirHAC1mRNA ortholog (XBP1) during the unfolded protein response (Yoshida et al. 2001; Calfon et al. 2002).”
• Adaptation to ER Stress Is Mediated by Differential Stabilities of Pro-Survival and Pro-Apoptotic mRNAs and Proteins (2006, background): “Although XBP1 splicing is, like eIF2a phosphorylation, a relatively rapid consequence of UPR activation, the effects of IRE1 activation on gene expression manifest somewhat later in the response, probably because basal expression of Xbp1 mRNA is low, and is itself up-regulated by UPR activation [27,”