Cystatin F (Leukocystatin) (CST7) ELISA Kits

Human Cystatin F (Leukocystatin) (CST7) interaction partners

1. Cystatin F was identified as the key subunit of family 2 cystatins in survival analysis. Pancreatic ductal adenocarcinoma (PDAC) patients who harbored a higher expression level of CST7 had a lower risk in overall survival. The prognostic nomogram indicated that the CST7 expression model effectively predicted the outcomes of patients with earlystage PDAC.

2. during monocyte to macrophage differentiation, the endosomal/lysosomal proteolytic activity can be regulated by cystatin F whose expression is under the control of transcriptional factor C/EBP alpha.

3. Regulation of cathepsins S and L by cystatin F during maturation of dendritic cells.

4. Transgenic cystatin F is expressed in model mice only during demyelination; in chronic demyelination, remyelinating ability is lost.

5. cystatin F is an intracellular cysteine peptidase inhibitor with readily regulated expression

6. CST7 is secreted, but artificial modification of its C-terminus can induce its endocytic targeting.

7. Cystatin F was not colocalized with cystatin C shich suggests distinct functions for these two cysteine protease inhibitors in U937 cells.

8. analysis of reduction-dependent activation of human cystatin F

9. A latent protease inhibitor which is itself regulated by proteolysis in the endocytic pathway.

10. Data demonstrate the addition of N-linked sugars to an Asn-X-Cys motif in cystatin F and suggest that the mannose 6-phosphate sorting machinery is used to divert cystatin F from the secretory pathway and to mediate its uptake from extracellular pools.

Mouse (Murine) Cystatin F (Leukocystatin) (CST7) interaction partners

1. These results indicate that hypoxia BV2 cells highly express Cystatin F, which is involved in A2A R activation-mediated neuroinflammation via the PKA/CREB and PKC/CREB or ERK1/2 signaling pathways.

2. High CST7 expression is associated with Alzheimer's disease.

3. Our results validate cystatin F as a useful biomarker of early pathogenesis in experimental models of prion disease, and point to unexpected species-specific differences in the transcriptional responses to prion infections.

4. 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.

5. The cystatin F expression in the activated microglia is closely associated with the effect of the A2A receptors, which may be related to the neuroinflammatory responses occurring during the pathological process.

6. an inhibitory activity other than cystatin F quenches CatL activity in activated macrophages

7. Expression of cystatin F indicates ongoing demyelination and remyelination; absence of cystatin F expression indicates cessation of remyelination in the demyelinating area.

8. The embryo's cystatin C and F expression functions as a protective mechanism against the maternal proteinase cathepsin S.