CTAGE2 Inhibitors

Chemical inhibitors of CTAGE2 can disrupt its function through various mechanisms related to cell cycle regulation and proteasomal activity. Alisertib, ZM447439, and Volasertib target and inhibit Aurora kinases, which are essential regulators of mitosis. The inhibition of these kinases by these chemicals can arrest the cell cycle, potentially leading to an inhibition of CTAGE2. Similarly, Paclitaxel (Taxol) stabilizes microtubules and prevents their disassembly, which is also crucial for mitosis. This action can obstruct the function of CTAGE2. Monastrol and S-Trityl-L-cysteine specifically inhibit the kinesin Eg5, leading to defects in spindle bipolarity, which would be detrimental to CTAGE2 function.

Additionally, proteasome inhibitors like Marizomib, Bortezomib, and MG132 can impede CTAGE2 by preventing the degradation of polyubiquitinated proteins, which may be fundamental to the function of CTAGE2. Nocodazole disrupts microtubule polymerization, which can lead to cell cycle arrest, again potentially inhibiting CTAGE2. Furthermore, Purvalanol A, a cyclin-dependent kinase inhibitor, halts cell cycle progression, which would impact CTAGE2 function. Lastly, BI 2536, another potent Plk1 inhibitor, can lead to mitotic arrest, which would impede the function of CTAGE2, as the disruption of Plk1 activity would affect mitotic progression and thus the function of CTAGE2 in this process.