our present study revealed that KMT2A epigenetically promotes cancer progression by targeting CTSZ which has specific functions in cancer invasion and metastasis.
results indicate that altered expression and localization of cathepsin Z in hepatocytes are characteristic features of primary biliary cholangitis (PBC) and other cholestatic liver diseases and are implicated in the progression of PBC.
expression of cathepsin B and X was detected in stromal cells and cancer cells throughout the glioblastoma (GBM) sections whereas cathepsin K expression was more restricted to arteriole-rich regions in the GBM sections. Metabolic mapping showed that cathepsin B but not cathepsin K is active in GSC niches.
we evaluated the involvement of cathepsin B and X in the TGF-b1 signaling pathway one of the key signaling mechanisms triggering epithelial-mesenchymal transition in cancer. In MCF-7 cells the expression of cathepsin B was shown to depend on their activation with TGF-b1 while for cathepsin X a TGF-b1 independent mechanism of induction during EMT is indicated.
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