ArticleProceedings of the National Academy of Sciences of the United States of America2012
SEC23B is required for the maintenance of murine professional secretory tissues.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 83 citations in OpenAlex.
- Tissue-specific SEC31A alternative splicing is regulated by RBM47 and controls lipid transport.RNA (New York, N.Y.) · 2025Article
- Understanding erythroid physiology and pathology in humanized mice: A closer look.British journal of haematology · 2025Review
- SEC16A Variants Predispose to Chronic Pancreatitis by Impairing ER-to-Golgi Transport and Inducing ER Stress.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- IER3IP1-mutations cause microcephaly by selective inhibition of ER-Golgi transport.Cellular and molecular life sciences : CMLS · 2024Article
- Functional overlap between the mammalianProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Functional overlap between the mammalianbioRxiv : the preprint server for biology · 2024Article
- Basic research and opportunities for translational advancement in the field of mammalian ∼12-hour ultradian chronobiology.Frontiers in physiology · 2024Review
- The Deubiquitinase OTUD1 Suppresses Secretory Neutrophil Polarization And Ameliorates Immunopathology of Periodontitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Mammalian cargo receptors for endoplasmic reticulum-to-Golgi transport: mechanisms and interactions.Biochemical Society transactions · 2023Review
- The Sar1 GTPase is dispensable for COPII-dependent cargo export from the ER.Cell reports · 2023Article
- New Cases and Mutations inInternational journal of molecular sciences · 2023Article
- Cargo selection in endoplasmic reticulum-to-Golgi transport and relevant diseases.The Journal of clinical investigation · 2023Review
- Functional screening of congenital heart disease risk loci identifies 5 genes essential for heart development in zebrafish.Cellular and molecular life sciences : CMLS · 2022Article
- Genetic marker identification ofFrontiers in genetics · 2022Article
- SEC23A rescues SEC23B-deficient congenital dyserythropoietic anemia type II.Science advances · 2021Article
- Murine SEC24D can substitute functionally for SEC24C during embryonic development.Scientific reports · 2021Article
- Sec22b determines Weibel-Palade body length by controlling anterograde ER-Golgi transport.Haematologica · 2021Article
- Non-canonical role of wild-type SEC23B in the cellular stress response pathway.Cell death & disease · 2021Article
- ER-to-Golgi transport and SEC23-dependent COPII vesicles regulate T cell alloimmunity.The Journal of clinical investigation · 2021Article
- Mutations in the coat complex II component SEC23B promote colorectal cancer metastasis.Cell death & disease · 2020Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
In eukaryotic cells, newly synthesized secretory proteins require COPII (coat protein complex II) to exit the endoplasmic reticulum (ER). COPII contains five core components: SAR1, SEC23, SEC24, SEC13, and SEC31. SEC23 is a GTPase-activating protein that activates the SAR1 GTPase and also plays a role in cargo recognition. Missense mutations in the human COPII paralogues SEC23A and SEC23B result in craniolenticulosutural dysplasia and congenital dyserythropoietic anemia type II, respectively. We now report that mice completely deficient for SEC23B are born with no apparent anemia phenotype, but die shortly after birth, with degeneration of professional secretory tissues. In SEC23B-deficient embryonic pancreas, defects occur in exocrine and endocrine tissues shortly after differentiation. Pancreatic acini are completely devoid of zymogen granules, and the ER is severely distended. Similar ultrastructural alterations are also observed in salivary glands, but not in liver. Accumulation of proteins in the ER lumen activates the proapoptotic pathway of the unfolded protein response, suggesting a central role for apoptosis in the degeneration of these tissues in SEC23B-deficient embryos. Although maintenance of the secretory pathway should be required by all cells, our findings reveal a surprising tissue-specific dependence on SEC23B for the ER exit of highly abundant cargo, with high levels of SEC23B expression observed in professional secretory tissues. The disparate phenotypes in mouse and human could result from residual SEC23B function associated with the hypomorphic mutations observed in humans, or alternatively, might be explained by a species-specific shift in function between the closely related SEC23 paralogues.
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