Protease, serine, 8 Proteins (PRSS8)

Human Protease, serine, 8 (PRSS8) interaction partners

1. limited role for HAI-2 (show SPINT2 Proteins) in the inhibition of matriptase (show ST14 Proteins) and prostasin is the result of its primarily intracellular localization in basal and spinous layer keratinocytes, which probably prevents the Kunitz inhibitor from interacting with active prostasin or matriptase (show ST14 Proteins)

2. PRSS8 was downregulated in glioma tissues.PRSS8 role in the glioma cell proliferation, migration, and invasion.

3. PRSS8 acts as a tumor suppressor in colorectal cancer

4. Data show that PRSS8 was reduced in esophageal squamous cell carcinomas (ESCC) tissues and the reduction of PRSS8 was associated with poor differentiation and shorter survival time.

5. Studies in colonic T84 cell monolayers revealed that barrier disruption by the colitis-associated Th2-type cytokines, IL-4 (show IL4 Proteins) and IL-13 (show IL13 Proteins), down-regulates matriptase (show ST14 Proteins) as well as prostasin through phosphorylation of the transcriptional regulator STAT6 (show STAT6 Proteins)

6. PRSS8 may serve as a tumour suppressor in hepatocellular carcinoma progression.

7. Overexpression of PRSS8 mRNA and high levels of prostasin in multiple subtypes of early stage ovarian tumors may provide clinical biomarkers for early detection of ovarian cancer.

8. It is concluded that prostasin protein level change is less likely to be causally involved in placental dysfunction in preeclampsia.

9. In urinary exosomes, NCC (show SLC12A3 Proteins) and prostasin had a diurnal pattern parallel to ADH (show AVP Proteins) and aquaporin 2 (show AQP2 Proteins), confirming that, in healthy subjects, both prostasin and NCC (show SLC12A3 Proteins) relate to water balance.

10. Polymorphism of the prostasin gene is closely associated with poor pregnancy outcomes of early-onset severe preeclampsia.

Mouse (Murine) Protease, serine, 8 (PRSS8) interaction partners

1. Studies in colonic T84 cell monolayers revealed that barrier disruption by the colitis-associated Th2-type cytokines, IL-4 (show IL4 Proteins) and IL-13 (show IL13 Proteins), down-regulates matriptase (show ST14 Proteins) as well as prostasin through phosphorylation of the transcriptional regulator STAT6 (show STAT6 Proteins)

2. a proteolysis-dependent function of activated prostasin in hair follicles, dependent on zymogen conversion by matriptase (show ST14 Proteins).

3. The claudin-4 (show CLDN4 Proteins)-mediated chloride conductance can be regulated endogenously by a protease-channel-activating protease 1 (cap1).

4. HAI-1 (show SPINT1 Proteins) regulates the activity of activated matriptase (show ST14 Proteins), whereas HAI-2 (show SPINT2 Proteins) has an essential role in regulating prostasin-dependent matriptase (show ST14 Proteins) zymogen activation.

5. a novel inhibitory interaction between CAP1/Prss8 and nexin-1 (show SERPINE2 Proteins), opening the search for specific CAP1/Prss8 antagonists that are independent of its catalytic activity

6. Data indicate that liver-specific serine protease (show F2 Proteins) prostasin (PRSS8) knockout (LKO) mice develop insulin (show INS Proteins) resistance associated with the increase in hepatic Toll-like receptor 4 (TLR4 (show TLR4 Proteins)).

7. Data indicate that serine protease (show F2 Proteins) prostasin (CAP1/PRSS8) supports terminal epidermal differentiation through a non-catalytic mechanism.

8. mutations in Prss8 restored placentation and normal development of HAI-1 (show SPINT1 Proteins)-deficient embryos and prevented early embryonic lethality, mid-gestation lethality due to placental labyrinth failure, and neural tube defects in HAI-2 (show SPINT2 Proteins)-deficient embryos.

9. Mutations of the serine protease (show F2 Proteins) CAP1/Prss8 lead to reduced embryonic viability, skin defects, and decreased ENaC (show SCNN1A Proteins) activity.

10. The T to A mutation at residue 170 (Val to Asp (show C3 Proteins)) in Prss8 is responsible for the mutant frizzy (fr) phenotype.