EC Number   |
General Information |
Reference |
|---|
   3.4.21.B6 | malfunction |
liver-specific PRSS8 enzyme knockout mice develop insulin resistance associated with the increase in hepatic Toll-like receptor 4, the knockout mice show an excessive response to lipopolysacchrides. Restoration of enzyme expression in livers of high-fat diet, knockout, and db/db mice decreases the TLR4 level and ameliorates insulin resistance, phenotypes, overview |
732562 |
| 3.4.21.B6 | malfunction |
loss of prostasin expression in the transitional cell carcinoma cell lines is correlated with loss of or reduced E-cadherin expression, loss of epithelial morphology, and promoter DNA hypermethylation and may have functional implications in tumor invasion and resistance to chemotherapy |
707872 |
| 3.4.21.B6 | malfunction |
matriptase and prostasin null mice have identical phenotypes. mice deficient for matriptase phenocopy mice deficient for epidermal prostasin and show impaired corneocyte differentiation, imparied lipid matrix formation, loss of profilaggrin processing and loss of tight junction formation and function. Together, these defects lead to a compromised epidermal barrier and result in fatal dehydration during the neonatal period. The proteolytic processing of prostasin as well as profilaggrin is greatly reduced in matriptase hypomorphic mice |
731623 |
| 3.4.21.B6 | malfunction |
prostasin null mice lack barrier formation and display fatal postnatal dehydration. But mice homozygous for a point mutation in the Prss8 gene, which causes the substitution of the active site serine within the catalytic histidine-aspartate-serine triad with alanine and renders prostasin catalytically inactive, develop barrier function and are healthy when followed for up to 20 weeks. Phenotypes, overview |
-, 732131 |
| 3.4.21.B6 | malfunction |
prostasin silencing in BPH-1 cells is associated with up-regulation of iNOS, ICAM-1, interleukin-6, and interleukin-8, and down-regulation of cyclin D1, as well as reduced proliferation and invasion |
710459 |
| 3.4.21.B6 | metabolism |
high-fat diet triggers the suppression of the enzyme expression by inducing endoplasmic reticulum stress and increases the Toll-like receptor 4 level in the liver. Serum enzyme levels are correlated to body mass index and homoeostasis model assessment-insulin resistance |
732562 |
| 3.4.21.B6 | metabolism |
matriptase and not prostasin is the primary effector protease of tight junction assembly in simple columnar epithelia |
732088 |
| 3.4.21.B6 | more |
spatial and temporal co-expression of matriptase and prostasin |
731623 |
| 3.4.21.B6 | physiological function |
HAI-1 but not HAI-2 is the prominent inhibitor for prostasin and matriptase in skin. The limited role for HAI-2 in the inhibition of matriptase and prostasin is the result of its primarily intracellular localization in basal and spinous layer keratinocytes, which probably prevents the HAI-2 from interacting with active prostasin or matriptase |
755167 |
| 3.4.21.B6 | physiological function |
knock-in mice expressing catalytically inactive prostasin display normal prenatal and postnatal survival. Catalytically inactive prostasin causes embryonic lethality in mice lacking its cognate inhibitors HAI-1 (SPINT1) or HAI-2 (SPINT2). Proteolytically inactive prostasin, unlike the wild-type protease, is unable to activate matriptase during placentation. All essential functions of prostasin in embryonic and postnatal development are compensated for by loss of HAI-1 |
753383 |
