Date published: 2025-9-13

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ZNF140 Inhibitors

Chemical inhibitors of ZNF140 include a range of compounds that disrupt its function through various cellular mechanisms. Palbociclib can hinder the activity of cyclin-dependent kinases 4 and 6, key regulators in the cell cycle whose downstream effects can lead to a reduction in the phosphorylation and subsequent activity of ZNF140. This action results in ZNF140 being less able to carry out its functions as a transcription factor. Similarly, Alsterpaullone targets cyclin-dependent kinases, though its effects are broader, still resulting in diminished phosphorylation states that are necessary for the full activity of ZNF140. Geldanamycin binds to heat shock protein 90 (Hsp90), a chaperone involved in the correct folding and stabilization of many proteins. By doing so, Geldanamycin can disrupt the proper folding and stability of ZNF140, leading to a functional inhibition. The proteasome inhibitor MG-132 can increase the levels of ubiquitinated proteins, which may sequester ZNF140 in non-functional complexes, effectively reducing its activity within the cell.

Trichostatin A and A-485 inhibit histone deacetylases and the p300/CBP histone acetyltransferase, respectively, which are enzymes that modify chromatin structure. These modifications can decrease the ability of ZNF140 to access and bind DNA, thereby inhibiting its transcriptional regulatory functions. The DNA intercalator Mitoxantrone can also change the structure of DNA, which can impede the binding of ZNF140 to its target genes, leading to a decrease in its transcriptional activity. 5-Azacytidine, by incorporating into DNA and RNA, can lead to a demethylation of gene promoters. This action may influence the DNA binding sites of ZNF140, reducing its ability to regulate gene expression. Chloroquine can disrupt endosomal and lysosomal pH, indirectly affecting the post-translational modification of ZNF140, which is essential for its activity. ICG-001, by inhibiting the Wnt/β-catenin signaling pathway, can exert an effect on the transcriptional regulation activities of ZNF140, considering that this pathway can interact with the regulatory functions of ZNF140. Bicalutamide, an androgen receptor antagonist, may alter interactions with nuclear receptor co-regulators, potentially disrupting the functional activity of ZNF140. Lastly, Triptolide, known for inhibiting transcription factors, can impair the regulatory roles ZNF140 plays in gene expression.

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