Sodium retention in nephrotic syndrome is independent of the activation of the membrane-anchored serine protease prostasin (CAP1/PRSS8) and its enzymatic activity.
Genetic Prss8 deficiency caused colitis and an inflamed rectum at an early age and intestinal tumors at a late age with increased intestinal cell proliferation and migration but decreased cell differentiation. Increased PRSS8 inhibited cancer growth and metastasis in nude mice and inhibited cancer cell migration invasion colony and tumor sphere formation.PRSS8 targeted Wnt/beta-catenin stem-cell and EMT signaling.
Studies in colonic T84 cell monolayers revealed that barrier disruption by the colitis-associated Th2-type cytokines IL-4 and IL-13 down-regulates matriptase as well as prostasin through phosphorylation of the transcriptional regulator STAT6
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