ArticleThe Journal of biological chemistry2017
Function of inhibitor of Bruton's tyrosine kinase isoform α (IBTKα) in nonalcoholic steatohepatitis links autophagy and the unfolded protein response.
Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Curcumin's dual effect on pyroptosis and autophagy in metabolic- associated fatty liver disease: a potential therapeutic strategy.Scientific reports · 2025Article
- Therapeutic Potential of Quercetin, Silibinin, and Crocetin in a High-Fat Diet-Induced Mouse Model of MASLD: The Role of CD36 and PLIN3.Life (Basel, Switzerland) · 2025Article
- Broad rim lesions are a new pathological and imaging biomarker for rapid disease progression in multiple sclerosis.Nature medicine · 2025Article
- The Effect of Quercetin on Non-Alcoholic Fatty Liver Disease (NAFLD) and the Role of Beclin1, P62, and LC3: An Experimental Study.Nutrients · 2024Article
- Quercetin's Potential in MASLD: Investigating the Role of Autophagy and Key Molecular Pathways in Liver Steatosis and Inflammation.Nutrients · 2024Review
- Article
- Autophagy and hepatic lipid metabolism: mechanistic insight and therapeutic potential for MASLD.npj metabolic health and disease · 2024Review
- Surviving and Adapting to Stress: Translational Control and the Integrated Stress Response.Antioxidants & redox signaling · 2023Review
- An RNA stem-loop functions in conjunction with an upstream open reading frame to direct preferential translation in the integrated stress response.The Journal of biological chemistry · 2023Article
- Sitagliptin Is More Effective Than Gliclazide in Preventing Pro-Fibrotic and Pro-Inflammatory Changes in a Rodent Model of Diet-Induced Non-Alcoholic Fatty Liver Disease.Molecules (Basel, Switzerland) · 2022Article
- Emerging Roles of Impaired Autophagy in Fatty Liver Disease and Hepatocellular Carcinoma.International journal of hepatology · 2021Review
- RINT1 Bi-allelic Variations Cause Infantile-Onset Recurrent Acute Liver Failure and Skeletal Abnormalities.American journal of human genetics · 2019Article
- Autophagy in non-alcoholic fatty liver disease and alcoholic liver disease.Liver research (Beijing, China) · 2018Article
- To die or not to die: death signaling in nonalcoholic fatty liver disease.Journal of gastroenterology · 2018Review
- Role of eIF2α Kinases in Translational Control and Adaptation to Cellular Stress.Cold Spring Harbor perspectives in biology · 2018Review
- Mutations in Vps15 perturb neuronal migration in mice and are associated with neurodevelopmental disease in humans.Nature neuroscience · 2018Article
- Review
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Authors and funding
7 authors.
Funding
Abstract
Nonalcoholic fatty liver disease (steatosis) is the most prevalent liver disease in the Western world. One of the advanced pathologies is nonalcoholic steatohepatitis (NASH), which is associated with induction of the unfolded protein response (UPR) and disruption of autophagic flux. However, the mechanisms by which these processes contribute to the pathogenesis of human diseases are unclear. Herein, we identify the α isoform of the inhibitor of Bruton's tyrosine kinase (IBTKα) as a member of the UPR, whose expression is preferentially translated during endoplasmic reticulum (ER) stress. We found that IBTKα is located in the ER and associates with proteins LC3b, SEC16A, and SEC31A and plays a previously unrecognized role in phagophore initiation from ER exit sites. Depletion of IBTKα helps prevent accumulation of autophagosome intermediates stemming from exposure to saturated free fatty acids and rescues hepatocytes from death. Of note, induction of IBTKα and the UPR, along with inhibition of autophagic flux, was associated with progression from steatosis to NASH in liver biopsies. These results indicate a function for IBTKα in NASH that links autophagy with activation of the UPR.
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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.