Chemical inhibitors of ZNF264 include a range of compounds that interfere with various cellular signaling pathways and processes, thereby impeding the functional activity of ZNF264. Palbociclib, ribociclib, and abemaciclib are inhibitors of CDK4/6, enzymes that play a crucial role in cell cycle progression. The inhibition of CDK4/6 can lead to decreased phosphorylation and activation of proteins that ZNF264 might regulate, thereby reducing ZNF264's ability to modulate gene expression. These inhibitors may thus indirectly prevent ZNF264 from fulfilling its role in the cell. Similarly, omipalisib targets PI3K and mTOR pathways, which are integral to cell survival and proliferation. Through the inhibition of these pathways, omipalisib can influence post-translational modifications of proteins that interact with ZNF264, potentially diminishing ZNF264's regulatory effects.
Further, the chemical rapamycin, a well-known inhibitor of the mTOR pathway, can influence the stability and function of ZNF264 by modifying the signaling cascades ZNF264 is involved in. Sorafenib, a multi-tyrosine kinase inhibitor, can impede various kinases that might phosphorylate proteins associated with ZNF264, ultimately hindering ZNF264's involvement in gene regulation networks. Ulixertinib and cobimetinib target the ERK and MEK pathways, respectively, which can have downstream effects on the signaling pathways that ZNF264 is part of, possibly leading to its functional inhibition. Trametinib, also a MEK inhibitor, can disrupt the MEK/ERK pathway and thereby influence ZNF264's activity in a similar manner.
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