Category Archives: Non-selective Adenosine

and C.P. cell function5. Indeed, CPs and IPs differentially modulate the abundance of transcription factors that regulate signaling pathways with prominent roles in cell differentiation, inflammation and neoplastic transformation (e.g., NF-kB, IFNs, STATs and Wnt)5. In cancer cells, genomic instability and oncogene addiction cause proteotoxic and oxidative stress6. Indeed, aneuploidy and variations in transcript levels produce imbalances in the stoichiometry of protein complexes and thereby lead to accumulation of misfolded proteins and formation of aggregates (proteotoxic stress)7,8,9. Moreover, oncogenic signaling and dysregulation Furilazole of mitochondrial function generate reactive oxygen species which damage DNA and proteins (oxidative stress). Proteasomes are key players in stress response since they degrade damaged (misfolded or oxidized) proteins10,11,12. Accordingly, cancer cells are presumed to be unduly dependent on proteasomal function13. Besides, tumors are commonly infiltrated by IFN–producing lymphocytes specific for neo-antigens14, and IFN- directly upregulates IP genes1. Hence, several factors could influence the abundance of proteasomes…

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