ArticleDevelopment (Cambridge, England)2016
Delineation of proteolytic and non-proteolytic functions of the membrane-anchored serine protease prostasin.
Article in Development (Cambridge, England), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
25 citing papers in PubMed, 39 citations in OpenAlex.
- Membrane-Anchored Serine Protease Inhibitors: Physiological Functions, Mechanisms, and Roles in Cancer.International journal of molecular sciences · 2026Review
- GPI-anchored serine proteases: essential roles in development, homeostasis, and disease.Biological chemistry · 2025Review
- Early-onset tufting enteropathy in HAI-2-deficient mice is independent of matriptase-mediated cleavage of EpCAM.Development (Cambridge, England) · 2023Article
- Type II Transmembrane Serine Proteases as Modulators in Adipose Tissue Phenotype and Function.Biomedicines · 2023Review
- EPCAM and TROP2 share a role in claudin stabilization and development of intestinal and extraintestinal epithelia in mice.Biology open · 2022Article
- ENaC activation by proteases.Acta physiologica (Oxford, England) · 2022Review
- Circulating SPINT1 Is Reduced in a Preeclamptic Cohort with Co-Existing Fetal Growth Restriction.Journal of clinical medicine · 2022Article
- Widespread discrepancy ineLife · 2022Article
- Elevated Circulating and Placental SPINT2 Is Associated with Placental Dysfunction.International journal of molecular sciences · 2021Article
- Recombinant Soluble Corin Improves Cardiac Function in Mouse Models of Heart Failure.Journal of the American Heart Association · 2021Article
- Intracellular autoactivation of TMPRSS11A, an airway epithelial transmembrane serine protease.The Journal of biological chemistry · 2020Article
- Article
- Large-scale discovery of male reproductive tract-specific genes through analysis of RNA-seq datasets.BMC biology · 2020Article
- Transcriptome profiling and protease inhibition experiments identify proteases that activate H3N2 influenza A and influenza B viruses in murine airways.The Journal of biological chemistry · 2020Article
- Review
- Matriptase drives early-onset intestinal failure in a mouse model of congenital tufting enteropathy.Development (Cambridge, England) · 2019Article
- The catalytic, stem, and transmembrane portions of matriptase-2 are required for suppressing the expression of the iron-regulatory hormone hepcidin.The Journal of biological chemistry · 2019Article
- Promoter Hypomethylation Is Responsible for Upregulated Expression of HAI-1 in Hepatocellular Carcinoma.Disease markers · 2019Article
- Congenital sodium diarrhea and chorioretinal coloboma with optic disc coloboma in a patient with biallelic SPINT2 mutations, including p.(Tyr163Cys).American journal of medical genetics. Part A · 2018Article
- Hepatocyte growth factor activator inhibitor type-2 (HAI-2)/Oncotarget · 2018Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The membrane-anchored serine proteases prostasin (PRSS8) and matriptase (ST14) initiate a cell surface proteolytic pathway essential for epithelial function. Mice expressing only catalytically inactive prostasin are viable, unlike prostasin null mice, indicating that at least some prostasin functions are non-proteolytic. Here we used knock-in mice expressing catalytically inactive prostasin (Prss8(Ki/Ki)) to show that the physiological and pathological functions of prostasin vary in their dependence on its catalytic activity. Whereas prostasin null mice exhibited partial embryonic and complete perinatal lethality, Prss8(Ki/Ki) mice displayed normal prenatal and postnatal survival. Unexpectedly, catalytically inactive prostasin caused embryonic lethality in mice lacking its cognate inhibitors HAI-1 (SPINT1) or HAI-2 (SPINT2). Proteolytically inactive prostasin, unlike the wild-type protease, was unable to activate matriptase during placentation. Surprisingly, all essential functions of prostasin in embryonic and postnatal development were compensated for by loss of HAI-1, indicating that prostasin is only required for mouse development and overall viability in the presence of this inhibitor. This study expands our knowledge of non-proteolytic functions of membrane-anchored serine proteases and provides unexpected new data on the mechanistic interactions between matriptase and prostasin in the context of epithelial development.
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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.