Date published: 2025-9-15

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ZNF235 Inhibitors

Chemical inhibitors of ZNF235 can act through various mechanisms to modulate the activity of this protein. Alsterpaullone, Purvalanol A, and Roscovitine are cyclin-dependent kinase inhibitors that can interrupt the cell cycle progression. By doing so, they can indirectly inhibit the functioning of ZNF235, which is likely dependent on the cell cycle's precise regulation for its role in DNA damage response and cell division. Similarly, SP600125, by inhibiting c-Jun N-terminal kinase, can impact the transcriptional regulation activities of ZNF235, as this kinase is part of stress signaling pathways that influence transcription factors. LY294002 and Wortmannin, both phosphoinositide 3-kinase inhibitors, can disrupt downstream processes that ZNF235 might influence, especially those related to transcriptional regulation associated with growth and survival pathways.

Moreover, Rapamycin, which targets the mTOR signaling pathway, can affect cell growth and proliferation signals that are crucial for ZNF235's function. PD98059 and U0126, selective inhibitors of the MAPK/ERK pathway, can disrupt the signaling necessary for ZNF235's transcription factor activity, particularly with regard to extracellular signals that utilize this pathway. SB203580 targets p38 MAP kinase and can inhibit ZNF235's role in gene regulation in response to stress signals mediated by this kinase. Lastly, Sorafenib and Sunitinib, which inhibit various tyrosine protein kinases and receptor tyrosine kinases respectively, can decrease the activity of ZNF235 by inhibiting signaling pathways that ZNF235 may be involved in, especially those related to cell signaling and regulation.

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