FAM9C Inhibitors

Inhibitors of FAM9C operate through various biochemical mechanisms to decrease its functional activity. By targeting the ATP binding sites of kinases, certain inhibitors can prevent the phosphorylation events that are crucial for the activity of FAM9C, leading to its functional inhibition. Other inhibitors specifically halt cell cycle progression by targeting cyclin-dependent kinases, which could reduce the expression levels of FAM9C during critical phases such as the G1-S transition. Histone deacetylase inhibitors contribute to this process by altering chromatin structure, thereby indirectly reducing the transcription of genes, including that of FAM9C. Further down the cell signaling pathways, the intervention into the PI3K/AKT and the MAPK/ERK pathways by respective pathway inhibitors can decrease the stability or expression of FAM9C, assuming its involvement in these pathways. This is facilitated by alteration of the phosphorylation status of downstream proteins and by affecting cell cycle regulators, which in turn, impacts the levels and function of FAM9C. In addition to interference with signaling cascades, some inhibitors disrupt intracellular protein transport mechanisms, potentially affecting the proper processing and trafficking of FAM9C. Disruption of the proteostasis network, through the inhibition of proteasome activity, may also lead to an accumulation of ubiquitinated proteins, thereby affecting the degradation pathway of FAM9C if it is a target for ubiquitination. Inhibition of molecular chaperones like HSP90 can impair the folding of a range of client proteins, among which FAM9C might be affected, leading to reduced stability and activity. The inhibition of kinases within specific families can also alter the phosphorylation status of proteins within signaling pathways that involve FAM9C, indirectly influencing its activity. Lastly, by disturbing calcium homeostasis through the inhibition of calcium ATPases, cellular processes dependent on calcium signaling can be indirectly inhibited, which may impinge upon the functional activity of FAM9C if it is reliant on such signaling mechanisms.