Date published: 2025-9-17

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C19orf24 Inhibitors

C19orf24 inhibitors encompass a diverse set of chemical compounds that target various cellular pathways and processes which are either directly or indirectly associated with the activity and function of C19orf24. Kinase inhibitors like staurosporine exert their effects by inhibiting the kinase activity that is paramount for the phosphorylation and subsequent activation of numerous proteins, potentially including C19orf24. By impeding this phosphorylation, staurosporine can lead to a decrease in C19orf24 activity. Similarly, LY294002 operates by specifically obstructing PI3K, which is crucial for AKT signaling, a pathway that might affect the stability or localization of C19orf24, thus indirectly inhibiting its functionality. This inhibition could result in lesser phosphorylation of substrates required for C19orf24's activation or stabilization.

The functional mechanisms of other compounds, such as rapamycin, also indirectly impact C19orf24 activity. Rapamycin's inhibition of the mTOR pathway disrupts protein synthesis and other survival pathways that could be essential for C19orf24's role within the cell. Inhibition by rapamycin might lead to a reduction in cellular resources necessary for C19orf24 function. Furthermore, the glycolysis inhibitor 2-Deoxy-D-glucose can indirectly affect C19orf24 by reducing the cellular energy pool, which is vital for the activity of numerous proteins. On the other hand, Alisertib targets Aurora kinase A, which is involved in the cell cycle. Disruption of the cell cycle can indirectly affect proteins like C19orf24, which may be regulated in a cell cycle-dependent manner. The MEK inhibitors U0126 and PD0325901 may lead to decreased activity of the MAPK/ERK pathway, which is known to be involved in a wide array of cellular functions, including those that could impinge upon C19orf24 functionality. By dampening this pathway, these inhibitors could reduce the activity of C19orf24 by limiting the signaling that contributes to its proper function.

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