Cathepsin C (CTSC) ELISA Kits

Human Cathepsin C (CTSC) Interaktionspartner

1. A novel homozygous missense variant in exon 2 of CTSC (NM_148170, c.G302C, p.Trp101Ser) predicted to disrupt protein structure and to be disease causing.

2. the study reveals that CTSC targeting plays a key role in the regulation of autophagy mediated colorectal cancer cell proliferation.

3. Mutations of CTSC gene are responsible for the phenotype of Papillon-Lefevre syndrome

4. expression markedly increased in the maternal vascular endothelium in subjects with preeclampsia compared with normal pregnant controls

5. A compound mutation consisting of a large deletion and a nonsense mutation, which provides a new insight in the mutation type of CTSC gene.

6. CTSC gene missense mutation is responsible for Papillo- Lefevre syndrome in a Turkish family.

7. analysis of fluorescent substrates provides a detailed S' specificity study of cathepsin C

8. Mutation screening of the CTSC gene from the two patients revealed the presence of the same homozygous nonsense mutation in Papillon-Lefevre syndrome and Haim-Munk syndromes. Phenotypic variants of the same rare disease caused by mutations of the cathepsin C (CTSC) gene.

9. Neutrophilic Cathepsin C Is Maturated by a Multistep Proteolytic Process and Secreted by Activated Cells during Inflammatory Lung Diseases.

10. CTSC was associated with albuminuria in type 2 diabetes patients.

11. Homozygous mutation 901G>A in exon 7 of CTSC gene is associated with Papillon-Lefevre syndrome.

12. Results identify a missense mutation in CTSC gene that segregate within a family with Papillon-Lefevre syndrome.

13. Papillon-Lefevre syndrome cause by homozygous nonsense mutation of cathepsin C gene.

14. CatC has a role in the selective tuning of innate and adaptive immune responses, relevant to a chronic immune disease, such as atherosclerosis.

15. cathepsin C in GCF does not seem to have an effect on the pathogenesis of periodontal diseases.

16. The present account of the 148.621 kb homozygous deletion on chromosome 11 is the first report of a mutational mechanism encompassing the whole CTSC gene.

17. CTSC mutations in 5 Iranian families with Papillon-Lefevre syndrome (PLS)analyzed; modeled the protein for mutations found in 2 of them; presence of this mutation provides evidence for founder CTSC mutations in PLS; this P35delL mutation leads to loss of a leucine residue; results indicate the phenotypes in these 2 patients likely due to CTSC mutations

18. Report novel deletion mutation in CTSC gene in Hungarian family with Papillon-Lefevre syndrome.

19. Cathepsin C gene 5'-untranslated region mutation in papillon-lefevre syndrome in 4 unrelated families in Slovenia

20. The novel loss-of function mutation of CTSC gene (c.203 T > G) found in Papillon-Lefevre Syndrome patients correlated with their diminished enzymatic activity.

Mouse (Murine) Cathepsin C (CTSC) Interaktionspartner

1. Cathepsin C regulates neutrophil elastase activation and E-cadherin cleavage in acute pancreatitis.

2. The data suggest that CatC promotes microglia M1 polarization and aggravates neuroinflammation via activation of Ca(2+)-dependent PKC/p38MAPK/NF-kappaB pathway.

3. During the active remyelinating phase, both CysF knockdown (CysFKD) and microglial-selective CatC overexpression (CatCOE) showed a worsening of the demyelination in Plp(4e/-) transgenic mice. Conversely, during the chronic demyelinating phase, CatC knockdown (CatCKD) ameliorated the demyelination. Our results suggest that the balance between CatC and CysF expression controls the demyelination and remyelination process.

4. Neutrophilic Cathepsin C Is Maturated by a Multistep Proteolytic Process and Secreted by Activated Cells during Inflammatory Lung Diseases.

5. A proteolytic cascade, involving cathepsins C and D, controls LLOMe-mediated necrosis.

6. Double immunofluorescence analysis showed that CTLA-2alpha was co-localized with cathepsin L, cathepsin C, and TINAGL1 in placenta.

7. CatC has a role in the selective tuning of innate and adaptive immune responses, relevant to a chronic immune disease, such as atherosclerosis.

8. Data indicate that all-trans retinoic acid (ATRA), which induces miR-23a expression, decreases cathepsin C (CTSC) expression and granzyme B activity leading to impaired NK cell cytotoxicity.

9. These results establish that DPPI is a major determinant of survival following Klebsiella pneumoniae lung infection and suggest that the survival disadvantage in DPPI(+/+) mice is in part due to processing of surfactant protein D by DPPI.

10. found no significant role for CtsC during mammary carcinogenesis but revealed squamous carcinogenesis to be functionally dependent on CtsC

11. Late stage cathepsin C, CXCL13 and Ki-67 overexpression correlate with regional neuropathology in a bovine spongiform encephalopathy transgenic murine model.

12. Proinflammatory cytokines induce expression and release of cathepsin C in microglial cells during neuroinflammatory progression.

13. The production of IL-1beta by macrophages, neutrophils, and mast cells in vitro is dependent on caspase-1 but not on cathepsin C.

14. NADPH oxidase in antimicrobial host defense against A. fumigatus and B. cepacia, whereas the proteases neutrophil elastase, cathepsin G, and lysosomal cysteine protease cathepsin C/ dipeptidyl peptidase I are dispensable

15. CatC is involved in limiting MCMV replication; however, this effect is independent of its role in promoting effector cytolytic activity.

16. Results indicate that mast cell dipeptidyl peptidase I (DPPI) harms the septic host and that DPPI is a novel potential therapeutic target for treatment of sepsis.

17. DPPI regulates a critical step in the development of collagen-induced arthritis that is independent of T cell and B cell functions.

18. Overall, our results indicate that although cathepsin C clearly generates the majority of granzyme B activity, some is still generated in its absence, pointing to alternative mechanisms for granzyme B processing and activation.

19. These findings suggest that DPPI and/or granule-associated serine proteases are necessary for neutrophil recruitment into the diseased aorta and that these proteases act to amplify vascular wall inflammation that leads to abdominal aortic aneurysms.

20. Role of DPPI and TIMP-3 in development of pulmonary fibrosis in early inflammation following bleomycin instillation.