Protease, serine, 8 Proteine (PRSS8)

Human Protease, serine, 8 (PRSS8) Interaktionspartner

1. 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 Kunitz inhibitor from interacting with active prostasin or matriptase

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 and IL-13, down-regulates matriptase as well as prostasin through phosphorylation of the transcriptional regulator STAT6

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 and prostasin had a diurnal pattern parallel to ADH and aquaporin 2, confirming that, in healthy subjects, both prostasin and NCC relate to water balance.

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

11. Prostasin regulate the Lin28/Let-7 loop in ovarian cancer cells.

12. The higher frequency of C allele of prostasin gene at rs12597511 is associated with severe preeclampsia.

13. Prostasin repress cancer cells and contribute to chemoresistance by modulating the CASP/PAK2-p34/actin pathway.

14. Our study suggested that Axl and prostasin expression may be closely related to carcinogenesis, metastasis, and prognosis of ovarian adenocarcinoma.

15. urinary prostasin correlates with the aldosterone to renin ratio, and it is physiologically modulated by natriuresis in normotensive individuals

16. prostasin is a non-enzymatic co-factor for matriptase activation

17. Prostasin requires expression of endogenous matriptase to stimulate barrier formation since matriptase depletion by siRNA silencing abrogates prostasin barrier-forming activity.

18. Essential hypertension in Xinjiang Kazakhs is not associated with the 2827C>T polymorphism in the prostasin gene.

19. prostasin is present, mature and active on the apical surface of wild-type and cystic fibrosis bronchial epithelial cells

20. Study does not provide evidence of a major role of prostasin variation in blood pressure modulation.

Mouse (Murine) Protease, serine, 8 (PRSS8) Interaktionspartner

1. 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

2. a proteolysis-dependent function of activated prostasin in hair follicles, dependent on zymogen conversion by matriptase.

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

4. HAI-1 regulates the activity of activated matriptase, whereas HAI-2 has an essential role in regulating prostasin-dependent matriptase zymogen activation.

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

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

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

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

9. Mutations of the serine protease CAP1/Prss8 lead to reduced embryonic viability, skin defects, and decreased ENaC activity.

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

11. Deficiency of CAP1/Prss8 in alveolar epithelial cells induced in vitro a 40% decrease in epithelial sodium channel-mediated sodium currents.

12. 546 backcross progeny were typed for linked markers to position fr centromeric of Fgfr2, between D7Csu5 and D7Mit165; an interval that contains only 2.7 Mb and fewer than 70 genes

13. conditional allelle mutations at Prss8 can be generated by Cre- and FLP-mediated recombination

14. CAP1/Prss8 expression in the epidermis is crucial for the epidermal permeability barrier and is, thereby, indispensable for postnatal survival.

15. mutations in conserved residues of mCAP2 located in two protein-protein interacting domains significantly modulated ENaC activation

16. findings demonstrate that prostasin is expressed in bladder epithelium; expression is downregulated during inflammation produced by intraperitoneal LPS injection; prostasin may play a role in bladder inflammatory response by modulating cytokine signaling

17. Results suggest that cell-specific Gpld1- or peptidase-dependent pathways for prostasin secretion may control prostasin functions in a tissue-specific manner.

18. Results indicate that PN-1 could have a natriuretic role by inhibiting prostasin activity. Aldosterone and TGF-beta reciprocally regulate the expression of PN-1. PN-1 could represent a new factor that contributes to regulation of ENaC activity.

19. matriptase acts upstream of prostasin in a zymogen activation cascade that regulates terminal epidermal differentiation and is required for prostasin zymogen activation