ArticleScientific reports2016
Pancreatic SEC23B deficiency is sufficient to explain the perinatal lethality of germline SEC23B deficiency in mice.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- LSD1 inhibition ameliorates congenital dyserythropoietic anemia type II.Science translational medicine · 2026Article
- p27Kip1 regulates γ-globin production.Blood · 2026Article
- LMAN1 serves as a cargo receptor for thrombopoietin.JCI insight · 2024Article
- SEC16A Variants Predispose to Chronic Pancreatitis by Impairing ER-to-Golgi Transport and Inducing ER Stress.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- 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
- ER-to-Golgi transport and SEC23-dependent COPII vesicles regulate T cell alloimmunity.The Journal of clinical investigation · 2021Article
- Altered phenotype in LMAN1-deficient mice with low levels of residual LMAN1 expression.Blood advances · 2020Article
- The Endoplasmic Reticulum Cargo Receptor SURF4 Facilitates Efficient Erythropoietin Secretion.Molecular and cellular biology · 2020Article
- Mutations in the coat complex II component SEC23B promote colorectal cancer metastasis.Cell death & disease · 2020Article
- Murine Surf4 is essential for early embryonic development.PloS one · 2020Article
- The Functional Role of SEC23 in Vesicle Transportation, Autophagy and Cancer.International journal of biological sciences · 2019Review
- Molecular Regulatory Mechanism of Exocytosis in the Salivary Glands.International journal of molecular sciences · 2018Review
- Functions of the COPII gene paralogs SEC23A and SEC23B are interchangeable in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Article
- SEC23B is required for pancreatic acinar cell function in adult mice.Molecular biology of the cell · 2017Article
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12 authors at 2 institutions in 1 country.
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Abstract
In humans, loss of function mutations in SEC23B result in Congenital Dyserythropoietic Anemia type II (CDAII), a disease limited to defective erythroid development. Patients with two nonsense SEC23B mutations have not been reported, suggesting that complete SEC23B deficiency might be lethal. We previously reported that SEC23B-deficient mice die perinatally, exhibiting massive pancreatic degeneration and that mice with hematopoietic SEC23B deficiency do not exhibit CDAII. We now show that SEC23B deficiency restricted to the pancreas is sufficient to explain the lethality observed in mice with global SEC23B-deficiency. Immunohistochemical stains demonstrate an acinar cell defect but normal islet cells. Mammalian genomes contain two Sec23 paralogs, Sec23A and Sec23B. The encoded proteins share ~85% amino acid sequence identity. We generate mice with pancreatic SEC23A deficiency and demonstrate that these mice survive normally, exhibiting normal pancreatic weights and histology. Taken together, these data demonstrate that SEC23B but not SEC23A is essential for murine pancreatic development. We also demonstrate that two BAC transgenes spanning Sec23b rescue the lethality of mice homozygous for a Sec23b gene trap allele, excluding a passenger gene mutation as the cause of the pancreatic lethality, and indicating that the regulatory elements critical for Sec23b pancreatic function reside within the BAC transgenes.
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