Associated Papers
PRSS8, encoding prostasin, is mutated in patients with autosomal recessive ichthyosis.
Shamseldin HE et al.
Human Genetics, 2023
The Post-Translational Modification Networking in WNK-Centric Hypertension Regulation and Electrolyte Homeostasis.
Lin SC et al.
Biomedicines, 2022
Kidney-Specific CAP1/Prss8-Deficient Mice Maintain ENaC-Mediated Sodium Balance through an Aldosterone Independent Pathway.
Ehret E et al.
International Journal of Molecular Sciences, 2022
Transmembrane serine protease 2 (TMPRSS2) proteolytically activates the epithelial sodium channel (ENaC) by cleaving the channel's γ-subunit.
Sure F et al.
The Journal of Biological Chemistry, 2022
Zymogen-locked mutant prostasin (Prss8) leads to incomplete proteolytic activation of the epithelial sodium channel (ENaC) and severely compromises triamterene tolerance in mice.
Essigke D et al.
Acta Physiologica (oxford, England), 2021
Loss of HAI-2 in mice with decreased prostasin activity leads to an early-onset intestinal failure resembling congenital tufting enteropathy.
Szabo R et al.
Plos One, 2018
The serine protease hepsin mediates urinary secretion and polymerisation of Zona Pellucida domain protein uromodulin.
Brunati M et al.
Elife, 2015
The CAP1/Prss8 catalytic triad is not involved in PAR2 activation and protease nexin-1 (PN-1) inhibition.
Crisante G et al.
Faseb Journal : Official Publication of the Federation of American Societies for Experimental Biology, 2014
The membrane-anchored serine protease prostasin (CAP1/PRSS8) supports epidermal development and postnatal homeostasis independent of its enzymatic activity.
Peters DE et al.
The Journal of Biological Chemistry, 2014
Reduced prostasin (CAP1/PRSS8) activity eliminates HAI-1 and HAI-2 deficiency-associated developmental defects by preventing matriptase activation.
Szabo R et al.
Plos Genetics, 2012
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