ArticleThe Journal of biological chemistry2014
Endocytosis of secreted carboxyl ester lipase in a syndrome of diabetes and pancreatic exocrine dysfunction.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.
- Pooled it
- Early-onset diabetes with low utilization of lipid as an energy source carrying a rare missense mutation in the CEL gene.Endocrinology, diabetes & metabolism case reports · 2025Article
- Identification of biomarkers and potential drug targets for esophageal cancer: a Mendelian randomization study.Scientific reports · 2025Article
- Common single-base insertions in the VNTR of the carboxyl ester lipase (CEL) gene are benign and also likely to arise somatically in the exocrine pancreas.Human molecular genetics · 2024Article
- Deceived by Elevated A1C: Cases of Misdiagnosed Diabetes.Clinical diabetes : a publication of the American Diabetes Association · 2024Article
- Current views on etiology, diagnosis, epidemiology and gene therapy of maturity onset diabetes in the young.Frontiers in endocrinology · 2024Review
- From glucose sensing to exocytosis: takes from maturity onset diabetes of the young.Frontiers in endocrinology · 2023Review
- Identification and characterization of novel carboxyl ester lipase gene variants in patients with different subtypes of diabetes.BMJ open diabetes research & care · 2023Article
- The genetic risk factor CEL-HYB1 causes proteotoxicity and chronic pancreatitis in mice.Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2022Article
- Maturity-Onset Diabetes of the Young: Mutations, Physiological Consequences, and Treatment Options.Journal of personalized medicine · 2022Review
- Two New Mutations in the CEL Gene Causing Diabetes and Hereditary Pancreatitis: How to Correctly Identify MODY8 Cases.The Journal of clinical endocrinology and metabolism · 2022Article
- Abnormal exocrine-endocrine cell cross-talk promotes β-cell dysfunction and loss in MODY8.Nature metabolism · 2022Article
- Integrated bioinformatics analysis reveals novel key biomarkers in diabetic nephropathy.SAGE open medicine · 2022Article
- Detecting cell-type-specific allelic expression imbalance by integrative analysis of bulk and single-cell RNA sequencing data.PLoS genetics · 2021Article
- Single nucleotide polymorphisms in CEL-HYB1 increase risk for chronic pancreatitis through proteotoxic misfolding.Human mutation · 2020Article
- Pathogenic Carboxyl Ester Lipase (CEL) Variants Interact with the Normal CEL Protein in Pancreatic Cells.Cells · 2020Article
- Molecular Genetic Study in a Cohort of Iranian Families Suspected to Maturity-Onset Diabetes of the Young, Reveals a Recurrent Mutation and a High-Risk Variant in theAdvanced biomedical research · 2020Article
- The mucinous domain of pancreatic carboxyl-ester lipase (CEL) contains core 1/core 2The Journal of biological chemistry · 2018Article
- Loss of complex O-glycosylation impairs exocrine pancreatic function and induces MODY8-like diabetes in mice.Experimental & molecular medicine · 2018Article
- Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Maturity-onset diabetes of the young, type 8 (MODY8) is characterized by a syndrome of autosomal dominantly inherited diabetes and exocrine pancreatic dysfunction. It is caused by deletion mutations in the last exon of the carboxyl ester lipase (CEL) gene, resulting in a CEL protein with increased tendency to aggregate. In this study we investigated the intracellular distribution of the wild type (WT) and mutant (MUT) CEL proteins in cellular models. We found that both CEL-WT and CEL-MUT were secreted via the endoplasmic reticulum and Golgi compartments. However, their subcellular distributions differed, as only CEL-MUT was observed as an aggregate at the cell surface and inside large cytoplasmic vacuoles. Many of the vacuoles were identified as components of the endosomal system, and after its secretion, the mutant CEL protein was re-internalized, transported to the lysosomes, and degraded. Internalization of CEL-MUT also led to reduced viability of pancreatic acinar and beta cells. These findings may have implications for the understanding of how the acinar-specific CEL-MUT protein causes both exocrine and endocrine pancreatic disease.
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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.