ArticleProceedings of the National Academy of Sciences of the United States of America1997
Defective prohormone processing and altered pancreatic islet morphology in mice lacking active SPC2.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers.
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Who cites it
139 citing papers in PubMed, 428 citations in OpenAlex.
- A pangenome framework uncovers the role of deletions in repeated evolution of cave-derived traits.Genome research · 2026Article
- A domain-swapped proPC1/3 structure reveals a conformational checkpoint for ER export.bioRxiv : the preprint server for biology · 2026Article
- SEL1L-HRD1 ER-associated degradation facilitates prohormone convertase 2 maturation and glucagon production in islet α cells.Nature communications · 2026Article
- Single-cell virtual knockout network perturbation prioritizes candidate regulators of beta-cell functional failure in type 2 diabetes.Frontiers in endocrinology · 2026Article
- α cells use both PC1/3 and PC2 to process proglucagon peptides and control insulin secretion.Science advances · 2025Article
- Insulin receptor isoform B is required for efficient proinsulin processing in pancreatic β cells.iScience · 2024Article
- Advances in basic research on glucagon and alpha cells.Diabetology international · 2024Review
- Blockade of glucagon increases muscle mass and alters fiber type composition in mice deficient in proglucagon-derived peptides.Journal of diabetes investigation · 2023Article
- Glucagon and Its Receptors in the Mammalian Heart.International journal of molecular sciences · 2023Review
- Models in Pancreatic Neuroendocrine Neoplasms: Current Perspectives and Future Directions.Cancers · 2023Review
- Cell-specific secretory granule sorting mechanisms: the role of MAGEL2 and retromer in hypothalamic regulated secretion.Frontiers in cell and developmental biology · 2023Review
- GLP-1 and GLP-2 Orchestrate Intestine Integrity, Gut Microbiota, and Immune System Crosstalk.Microorganisms · 2022Review
- Prohormone convertase 1/3 deficiency causes obesity due to impaired proinsulin processing.Nature communications · 2022Article
- Proteolysis in Reproduction: Lessons From Gene-Modified Organism Studies.Frontiers in endocrinology · 2022Review
- Domestication of farmed fishFrontiers in endocrinology · 2022Review
- Obesity, POMC, and POMC-processing Enzymes: Surprising Results From Animal Models.Endocrinology · 2021Review
- Article
- Mouse Models of Human Proprotein Convertase Insufficiency.Endocrine reviews · 2021Review
- Mice lacking PC1/3 expression in POMC-expressing cells do not develop obesity.Endocrinology · 2021Article
- In vivo studies of glucagon secretion by human islets transplanted in mice.Nature metabolism · 2020Article
79 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
Abstract
The prohormone convertase SPC2 (PC2) participates in the processing of proinsulin, proglucagon, and a variety of other neuroendocrine precursors, acting either alone or in conjunction with the structurally related dense-core granule convertase SPC3 (PC3/PC1). We have generated a strain of mice lacking active SPC2 by introducing the neomycin resistance gene (Neor) into the third exon of the mSPC2 gene. This gene insertion results in the synthesis of an exon 3-deleted form of SPC2 that does not undergo autoactivation and is not secreted. The homozygous mutant mice appear to be normal at birth. However, they exhibit a small decrease in rate of growth. They also have chronic fasting hypoglycemia and a reduced rise in blood glucose levels during an intraperitoneal glucose tolerance test, which is consistent with a deficiency of circulating glucagon. The processing of proglucagon, prosomatostatin, and proinsulin in the alpha, delta, and beta cells, respectively, of the pancreatic islets is severely impaired. The islets in mutant mice at 3 months of age show marked hyperplasia of alpha and delta cells and a relative diminution of beta cells. SPC2-defective mice offer many possibilities for further delineating neuroendocrine precursor processing mechanisms and for exploring more fully the physiological roles of many neuropeptides and peptide hormones.
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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.