ArticleThe Journal of clinical investigation2013
The Xbp1s/GalE axis links ER stress to postprandial hepatic metabolism.
Article in The Journal of clinical investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
91 citing papers in PubMed, 133 citations in OpenAlex.
- mTOR signaling contributes to system-driven rhythmic gene expression in mouse liver.Science advances · 2026Article
- Discovery of cell-active small molecule inhibitors of UDP-galactose 4'-epimerase.bioRxiv : the preprint server for biology · 2026Article
- Proteomic Mechanisms of Hepatic- and Cardio-Protection of a Food-Hoarding Hibernator, Tamias sibiricus.Integrative zoology · 2026Article
- Transcriptome and DNA methylation responses in the liver of Megalobrama amblycephala under hypoxia and heat stress.Fish physiology and biochemistry · 2026Article
- An Autonomous Clock that Controls Genetic Information Flow and Cellular Proteostasis.Advances in experimental medicine and biology · 2026Review
- Identification of a Selective Pharmacologic IRE1/XBP1s Activator with Enhanced Tissue Exposure.ACS chemical biology · 2025Article
- Roles of X-box binding protein 1 in liver pathogenesis.Clinical and molecular hepatology · 2025Review
- Upregulation of Xbp1 in NPY/AgRP neurons reverses diet-induced obesity and ameliorates leptin and insulin resistance.Neuropeptides · 2024Article
- Article
- Article
- Endoplasmic reticulum unfolded protein response transcriptional targets of XBP-1s mediate rescue from tauopathy.Communications biology · 2024Article
- Evidence for ~12-h ultradian gene programs in humans.Npj biological timing and sleep · 2024Article
- Tisp40 prevents cardiac ischemia/reperfusion injury through the hexosamine biosynthetic pathway in male mice.Nature communications · 2023Article
- Inherited Thrombocytopenia Caused by Variants in Crucial Genes for Glycosylation.International journal of molecular sciences · 2023Review
- Modulation of Unfolded Protein Response Restores Survival and Function of β-Cells Exposed to the Endocrine Disruptor Bisphenol A.International journal of molecular sciences · 2023Article
- Molecular Mechanism Underlying Role of the XBP1s in Cardiovascular Diseases.Journal of cardiovascular development and disease · 2022Review
- Protective Role of Hepassocin against Hepatic Endoplasmic Reticulum Stress in Mice.International journal of molecular sciences · 2022Article
- Metabolic Adaptation in Lactation: Insulin-dependent and -independent Glycemic Control.Journal of translational internal medicine · 2022Article
- Review
- Pharmacologic IRE1/XBP1s activation promotes systemic adaptive remodeling in obesity.Nature communications · 2022Article
31 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 4 institutions in 3 countries.
Funding
Abstract
Postprandially, the liver experiences an extensive metabolic reprogramming that is required for the switch from glucose production to glucose assimilation. Upon refeeding, the unfolded protein response (UPR) is rapidly, though only transiently, activated. Activation of the UPR results in a cessation of protein translation, increased chaperone expression, and increased ER-mediated protein degradation, but it is not clear how the UPR is involved in the postprandial switch to alternate fuel sources. Activation of the inositol-requiring enzyme 1 (IRE1) branch of the UPR signaling pathway triggers expression of the transcription factor Xbp1s. Using a mouse model with liver-specific inducible Xbp1s expression, we demonstrate that Xbp1s is sufficient to provoke a metabolic switch characteristic of the postprandial state, even in the absence of caloric influx. Mechanistically, we identified UDP-galactose-4-epimerase (GalE) as a direct transcriptional target of Xbp1s and as the key mediator of this effect. Our results provide evidence that the Xbp1s/GalE pathway functions as a novel regulatory nexus connecting the UPR to the characteristic postprandial metabolic changes in hepatocytes.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.