Date published: 2025-9-21

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ZNF570 Inhibitors

Chemical inhibitors of ZNF570 can function through various mechanisms to inhibit this zinc finger protein's activity within cellular processes. Palbociclib and PD0332991 are selective inhibitors of CDK4/6, enzymes critical for cell cycle progression. By blocking these kinases, Palbociclib and PD0332991 can arrest the cell cycle, thereby inhibiting ZNF570's function if it is indeed involved in cell cycle regulation. Similarly, Nutlin-3 activates p53 by inhibiting MDM2, leading to an increase in p21, a cyclin-dependent kinase inhibitor that causes cell cycle arrest. This arrest can limit the function of ZNF570 if it is involved in the p53 signaling pathway. Vorinostat and Trichostatin A, both histone deacetylase (HDAC) inhibitors, lead to chromatin remodeling, which can suppress the function of transcription factors and other proteins associated with gene expression, including potentially ZNF570, if it is linked to chromatin modifications.

Furthermore, MG132, a proteasome inhibitor, can prevent the degradation of proteins that regulate ZNF570 activity, thereby indirectly maintaining inhibitors of ZNF570 in the cell and reducing ZNF570 activity. In the context of growth factor signaling, Lapatinib, an EGFR/HER2 inhibitor, can suppress downstream signaling pathways that ZNF570 may be part of, leading to its functional inhibition. LY294002, a PI3K inhibitor, blocks the AKT signaling pathway, which can inhibit ZNF570 if it is involved in this pathway. Additionally, U0126 and SB203580, which are inhibitors of MEK and p38 MAPK respectively, can inhibit the MAPK/ERK and p38 MAPK pathways. If ZNF570 functions within these pathways, its activity would be inhibited. SP600125, a JNK inhibitor, can also inhibit ZNF570 by obstructing the JNK signaling if ZNF570 operates within this pathway. Lastly, Rapamycin inhibits mTOR, a key regulator of cell growth and proliferation, which could lead to the inhibition of ZNF570 if it is involved in the mTOR signaling pathway.

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