ArticleNature communications2017
ATF3 acts as a rheostat to control JNK signalling during intestinal regeneration.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 56 citations in OpenAlex.
- Raw defines a TIR-fold cADPR hydrolase cooperating with dSarm in development and axon degeneration.Cell communication and signaling : CCS · 2026Article
- Comparative proteomic analysis indicates differential responses to fumonisin BMycotoxin research · 2025Article
- Emerging roles for integrated stress response signaling in homeostasis.The FEBS journal · 2025Review
- Age mosaic of gut epithelial cells prevents aging.Nature communications · 2025Article
- METTL3 restricts RIPK1-dependent cell death via the ATF3-cFLIP axis in the intestinal epithelium.Cell regeneration (London, England) · 2024Article
- ATF3 coordinates the survival and proliferation of cardiac macrophages and protects against ischemia-reperfusion injury.Nature cardiovascular research · 2024Article
- Slik maintains tissue homeostasis by preventing JNK-mediated apoptosis.Cell division · 2023Article
- Atf3 defines a population of pulmonary endothelial cells essential for lung regeneration.eLife · 2023Article
- Activating transcription factor 3, glucolipid metabolism, and metabolic diseases.Journal of molecular cell biology · 2023Article
- Opposing roles of Fos, Raw, and SARM1 in the regulation of axonal degeneration and synaptic structure.Frontiers in cellular neuroscience · 2023Article
- Review
- Transcriptome Profile Analysis of Intestinal Upper Villus Epithelial Cells and Crypt Epithelial Cells of Suckling Piglets.Animals : an open access journal from MDPI · 2022Article
- Single-cell profiling of environmental enteropathy reveals signatures of epithelial remodeling and immune activation.Science translational medicine · 2022Article
- Injury-induced MAPK activation triggers body axis formation inProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Screening for modulators of the cellular composition of gut epithelia via organoid models of intestinal stem cell differentiation.Nature biomedical engineering · 2022Article
- SUMOylation of Jun fine-tunes the Drosophila gut immune response.PLoS pathogens · 2022Article
- Activating Transcription Factor 3 Protects against Restraint Stress-Induced Gastrointestinal Injury in Mice.Cells · 2021Article
- ATF3 induces RAB7 to govern autodegradation in paligenosis, a conserved cell plasticity program.EMBO reports · 2021Article
- Functional conservation in genes and pathways linking ageing and immunity.Immunity & ageing : I & A · 2021Review
- Transcriptional factor ATF3 promotes liver fibrosis via activating hepatic stellate cells.Cell death & disease · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial barrier function is maintained by coordination of cell proliferation and cell loss, whereas barrier dysfunction can lead to disease and organismal death. JNK signalling is a conserved stress signalling pathway activated by bacterial infection and tissue damage, often leading to apoptotic cell death and compensatory cell proliferation. Here we show that the stress inducible transcription factor ATF3 restricts JNK activity in the Drosophila midgut. ATF3 regulates JNK-dependent apoptosis and regeneration through the transcriptional regulation of the JNK antagonist, Raw. Enterocyte-specific ATF3 inactivation increases JNK activity and sensitivity to infection, a phenotype that can be rescued by Raw overexpression or JNK suppression. ATF3 depletion enhances intestinal regeneration triggered by infection, but does not compensate for the loss of enterocytes and ATF3-depleted flies succumb to infection due to intestinal barrier dysfunction. In sum, we provide a mechanism to explain how an ATF3-Raw module controls JNK signalling to maintain normal intestinal barrier function during acute infection.
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Registered trials
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