ArticlePloS one2013
The channel-activating protease CAP1/Prss8 is required for placental labyrinth maturation.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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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.
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Who cites it
21 citing papers in PubMed, 31 citations in OpenAlex.
- Article
- Autologous Paracrine Prostasin-Matriptase Serine Protease Interaction in Lymphoid Cancer Cells.Cells · 2025Article
- GPI-anchored serine proteases: essential roles in development, homeostasis, and disease.Biological chemistry · 2025Review
- Emerging connections between GPI-anchored proteins and their extracellular carriers in colorectal cancer.Extracellular vesicles and circulating nucleic acids · 2023Article
- Cap-independent translation of GPLD1 enhances markers of brain health in long-lived mutant and drug-treated mice.Aging cell · 2022Article
- Kidney-Specific CAP1/Prss8-Deficient Mice Maintain ENaC-Mediated Sodium Balance through an Aldosterone Independent Pathway.International journal of molecular sciences · 2022Article
- Sodium retention in nephrotic syndrome is independent of the activation of the membrane-anchored serine protease prostasin (CAP1/PRSS8) and its enzymatic activity.Pflugers Archiv : European journal of physiology · 2022Article
- ENaC activation by proteases.Acta physiologica (Oxford, England) · 2022Review
- Decreased prostasin expression is associated with aggressiveness of oral squamous cell carcinoma.Human cell · 2021Article
- Zymogen-locked mutant prostasin (Prss8) leads to incomplete proteolytic activation of the epithelial sodium channel (ENaC) and severely compromises triamterene tolerance in mice.Acta physiologica (Oxford, England) · 2021Article
- Association between preeclampsia and prostasin polymorphism in Pakistani females.Saudi medical journal · 2020Article
- Membrane-anchored serine proteases as regulators of epithelial function.Biochemical Society transactions · 2020Review
- Article
- Delineation of proteolytic and non-proteolytic functions of the membrane-anchored serine protease prostasin.Development (Cambridge, England) · 2016Article
- GPI-AP release in cellular, developmental, and reproductive biology.Journal of lipid research · 2016Review
- Distinct Developmental Functions of Prostasin (CAP1/PRSS8) Zymogen and Activated Prostasin.The Journal of biological chemistry · 2016Article
- Ibuprofen regulates the expression and function of membrane-associated serine proteases prostasin and matriptase.BMC cancer · 2015Article
- Epithelial Sodium Channel-Mediated Sodium Transport Is Not Dependent on the Membrane-Bound Serine Protease CAP2/Tmprss4.PloS one · 2015Article
- TMPRSS13 deficiency impairs stratum corneum formation and epidermal barrier acquisition.The Biochemical journal · 2014Article
- Colon-specific deletion of epithelial sodium channel causes sodium loss and aldosterone resistance.Journal of the American Society of Nephrology : JASN · 2014Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The serine protease CAP1/Prss8 is crucial for skin barrier function, lung alveolar fluid clearance and has been unveiled as diagnostic marker for specific cancer types. Here, we show that a constitutive knockout of CAP1/Prss8 leads to embryonic lethality. These embryos presented no specific defects, but it is during this period, and in particular at E13.5, that wildtype placentas show an increased expression of CAP1/Prss8, thus suggesting a placental defect in the knockout situation. The placentas of knockout embryos exhibited significantly reduced vascular development and incomplete cellular maturation. In contrary, epiblast-specific deletion of CAP1/Prss8 allowed development until birth. These CAP1/Prss8-deficient newborns presented abnormal epidermis, and died soon after birth due to impaired skin function. We thus conclude that a late placental insufficiency might be the primary cause of embryonic lethality in CAP1/Prss8 knockouts. This study highlights a novel and crucial role for CAP1/Prss8 in placental development and function.
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