serpin Peptidase Inhibitor, Clade B (Ovalbumin), Member 9 (SERPINB9) ELISA Kits

Pig (Porcine) serpin Peptidase Inhibitor, Clade B (Ovalbumin), Member 9 (SERPINB9) interaction partners

1. Cloning of pig serine proteinase inhibitor 9.

Mouse (Murine) serpin Peptidase Inhibitor, Clade B (Ovalbumin), Member 9 (SERPINB9) interaction partners

1. These findings add support for role for Sb9 cross-presentation, and indicate that high Sb9 expression is a novel marker of cross-presentation capable dendritic cells

2. Data suggest that reactive oxygen species (ROS) generated within cytotoxic lymphocytes by receptor stimulation are required for lysosomal permeabilization and release of GzmB (granzyme B) into the cytosol and for inactivation of serpin B9.

3. our data demonstrate, for the first time, a novel role for Spi6 in Regulatory T cell homeostasis

4. Data indicate that Serpinb9 (Spi6)-deficient dendritic cells appear to process antigen faster.

5. the negative regulation of DC priming of CD8 T lymphocyte immunity by CTL killing is mitigated by the physiological inhibition of GrB by Spi6.

6. SPI6 protects mesenchymal stem cells from GrB-mediated killing and plays a pivotal role in their survival in vivo.

7. Data show that increased activation-induced apoptosis resulted in impaired survival and a decreased clonal burst size of Spi6 KO iNKT cells, which could be corrected by GrB deficiency.

8. SPI-CI is a novel immune escape molecule that acts in concert with SPI-6 to prevent cytotoxic lymphocyte-mediated killing of tumor cells.

9. Estrogen induction of PI-9 may reduce the ability of cytolytic lymphocytes-mediated immune surveillance to destroy newly transformed cells

10. In mCAP3, an intact catalytic triad was necessary for activation of ENaC but not for intramolecular cleavage of the protease.

11. protects hepatocytes against excessively vigorous granzyme B-dependent killing but may also delay immune clearance of virally infected hepatocytes

12. deficiency in a weak intracellular inhibitor of neutrophil elastase results in an acute inflammatory response that protects from P. aeruginosa but does not cause lung disease

13. SPI-6 is selectively up-regulated in hepatocytes in response to infiltration of the liver by NK cells that express perforin and enzymatically active granzyme B.

14. Increased SPI-6 expression is not sufficient to confer lipopolysaccharide-treated dendritic cells with resistance to direct killing in vivo.

Human serpin Peptidase Inhibitor, Clade B (Ovalbumin), Member 9 (SERPINB9) interaction partners

1. Data show that the serine protease inhibitor B9 (serpinB9) mediated caspase-1 inhibition regulates IL-1beta release in monocytes.

2. Treatment with estrogens further increased PI-9 level while decreased that of ERalpha66 isoform thus excluding the involvement of this receptor isoform in the event. Moreover, our studies also provided evidence that tertiary tumorspheres express elevated levels of CXCR4 and phospho-p38, suggesting that the high PI-9 content might be ascribed to the activation of the proliferative CXCR4/phospho-p38 axis.

3. We filtered four OSCC genes including SERPINB9, SERPINE2, GAK, and HSP90B1 through the gene global prioritization score (P < 0.005).

4. Data show that oropharyngeal squamous cell carcinomas (OPSCCs) express granzyme inhibitors SERPINB1, SERPINB4 and SERPINB9 for cytotoxicity and the expression was not different between human papillomavirus (HPV)-positive and HPV-negative tumors.

5. Pediatric CNS-PNETs evade immune recognition by downregulating cell surface MHC-I and CD1d expression. Intriguingly, expression of SERPINB9, SERPINB1, and SERPINB4 is acquired during tumorigenesis in 29%, 29%, and 57% of the tumors

6. Data suggest that reactive oxygen species (ROS) generated within cytotoxic lymphocytes by receptor stimulation are required for lysosomal permeabilization and release of GzmB (granzyme B) into the cytosol and for inactivation of serpin B9.

7. Increased intracellular PI-9 activity in mononuclear phagocytes from HIV-infected patients contributes to successful intracellular infection by virulent Mycobacterium tuberculosis.

8. The GrB-Sb9 nexus may therefore represent an additional mechanism of limiting lymphocyte lifespan and populations.

9. Suppression of granzyme B initiated apoptosis in protease inhibitor-9-expressing leukemia cells.

10. SerpinB9 expression in human renal tubular epithelial cells is induced by triggering of the viral dsRNA sensors TLR3, MDA5 and RIG-I during subclinical rejection.

11. lung cancer cells utilise their increased PI-9 expression to protect from granzyme B-mediated cytotoxicity as an immune evasion mechanism

12. Inhibition of Granzyme B by PI-9 protects prostate cancer cells from apoptosis.

13. Reduced proteinase inhibitor 9 expression in human vascular smooth muscle cells is associated with atherosclerotic disease progression.

14. PI-9 induction within human mononuclear phagocytes by virulent Mycobacterium tuberculosis serves to protect these primary targets of infection from elimination by apoptosis and thereby promotes intracellular survival of the organism.

15. constitutive expression of serine protease inhibitor 9 (PI-9) on human peripheral blood-and bone marrow-derived mesenchymal stem cells is a major defense mechanism against granzyme B-mediated destruction by NK cells

16. upregulated expression of PI-9 in NSCLC cells may serve to protect them from apoptosis induced by GrB

17. Expression levels of apoptosis-related proteins caspase 3, Bcl-2, and PI9 predict clinical outcome in anaplastic large cell lymphoma.

18. The presence and subcellular localization of proteinase inhibitor 9 in leukocytes and dendritic cells are consistent with a protective role against ectopic or misdirected granzyme B during an immune response.

19. a high expression of PI-9 by tubular epithelial cells can serve as one of the factors protecting renal allografts from rejection in spite of the presence of inflammatory cell infiltrates.

20. proteinase inhibitor 9 was effectively hydrolyzed and inactivated by human granzyme M, raising the possibility that this orphan granzyme bypasses proteinase inhibitor 9 inhibition of granzyme B