Associated Papers
SPINT2 mutations in the Kunitz domain 2 found in SCSD patients inactivate HAI-2 as prostasin inhibitor via abnormal protein folding and N-glycosylation.
Huang N et al.
Human Molecular Genetics, 2024
PRSS8, encoding prostasin, is mutated in patients with autosomal recessive ichthyosis.
Shamseldin HE et al.
Human Genetics, 2023
Epithelial Sodium Channel-Mediated Sodium Transport Is Not Dependent on the Membrane-Bound Serine Protease CAP2/Tmprss4.
Keppner A et al.
Plos One, 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
Mutations of the serine protease CAP1/Prss8 lead to reduced embryonic viability, skin defects, and decreased ENaC activity.
Frateschi S et al.
The American Journal of Pathology, 2012
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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