ArticlePloS one2014
Increased susceptibility to dextran sulfate sodium-induced colitis in the endoplasmic reticulum stress transducer OASIS deficient mice.
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 27 papers.
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Who cites it
27 citing papers in PubMed, 38 citations in OpenAlex.
- Autophagy prevents ER stress-induced Tight Junction barrier disruption via claudin-2 homeostasis.bioRxiv : the preprint server for biology · 2026Article
- Tauroursodeoxycholic Acid (TUDCA) Reduces ER Stress and Lessens Disease Activity in Ulcerative Colitis.medRxiv : the preprint server for health sciences · 2025Article
- Guts for Self-Eating: Role of Autophagy in Gastrointestinal Health and Disease.Gastro hep advances · 2025Review
- The Regulatory Network of CREB3L1 and Its Roles in Physiological and Pathological Conditions.International journal of medical sciences · 2024Review
- Investigating Causality and Shared Genetic Architecture between Neurodegenerative Disorders and Inflammatory Bowel Disease.Aging and disease · 2023Article
- Upregulation of OASIS/CREB3L1 in podocytes contributes to the disturbance of kidney homeostasis.Communications biology · 2022Article
- Endoplasmic Reticulum Stress of Gut Enterocyte and Intestinal Diseases.Frontiers in molecular biosciences · 2022Review
- Targeted deletion of Atg5 in intestinal epithelial cells promotes dextran sodium sulfate-induced colitis.Journal of clinical biochemistry and nutrition · 2021Article
- Transcription factor old astrocyte specifically induced substance is a novel regulator of kidney fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Idebenone Protects against Spontaneous Chronic Murine Colitis by Alleviating Endoplasmic Reticulum Stress and Inflammatory Response.Biomedicines · 2020Article
- Dextran Sodium Sulfate-Induced Impairment of Protein Trafficking and Alterations in Membrane Composition in Intestinal Caco-2 Cell Line.International journal of molecular sciences · 2020Article
- Endoplasmic Reticulum Stress and Intestinal Inflammation: A Perilous Union.Frontiers in immunology · 2020Review
- [Kirenol relieves dextran sulfate sodium-induced ulcerative colitis in mice by inhibiting inflammatory cytokines and inducing CD4Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2019Article
- Inflammatory bowel disease-associated ubiquitin ligase RNF183 promotes lysosomal degradation of DR5 and TRAIL-induced caspase activation.Scientific reports · 2019Article
- ER Stress and the UPR in Shaping Intestinal Tissue Homeostasis and Immunity.Frontiers in immunology · 2019Review
- The Role of Mammalian Creb3-Like Transcription Factors in Response to Nutrients.Frontiers in genetics · 2019Review
- Calcium/calmodulin-dependent protein kinase IV (CaMKIV) activation contributes to the pathogenesis of experimental colitis via inhibition of intestinal epithelial cell proliferation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Endoplasmic Reticulum Stress and Oxidative Stress: A Vicious Nexus Implicated in Bowel Disease Pathophysiology.International journal of molecular sciences · 2017Review
- Intestinal Epithelial Cell Endoplasmic Reticulum Stress and Inflammatory Bowel Disease Pathogenesis: An Update Review.Frontiers in immunology · 2017Review
- The unfolded protein response in immunity and inflammation.Nature reviews. Immunology · 2016Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
OASIS is a basic leucine zipper (bZIP) transmembrane transcription factor that is activated in response to endoplasmic reticulum (ER) stress. Previously, we showed that OASIS regulates final maturation of goblet cells in the large intestine. In the present study, to elucidate the roles of OASIS under pathophysiological conditions, we examined the stress response and inflammatory responses in Oasis deficient (Oasis⁻/⁻) mice exposed to dextran sulfate sodium (DSS) to induce colitis. A significant loss of body weight and an increase of mortality were observed in Oasis⁻/⁻ mice with DSS-induced colitis compared with those in WT mice. The mucosa of the large intestine in Oasis⁻/⁻ mice exhibited severe damage involving inflammatory cell infiltration. The expression levels of ER stress and apoptosis markers in intestinal epithelial cells were upregulated in Oasis⁻/⁻ mice. These abnormalities were improved by treatment with tauroursodeoxycholic acid, a chemical chaperone that facilitates protein folding. Taken together, our findings demonstrate that OASIS plays important roles in protection of the large intestinal mucosa in DSS-induced colitis through attenuation of ER stress and inflammation.
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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.