Date published: 2025-9-17

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ZCCHC11 Inhibitors

ZCCHC11 inhibitors are a class of chemical compounds that specifically target zinc finger CCHC-type containing protein 11 (ZCCHC11), a protein involved in RNA metabolism, particularly in RNA modification and regulation. ZCCHC11, also known as terminal uridylyltransferase 1 (TUT1), is part of a family of enzymes that add uridine residues to the 3' ends of RNA molecules in a process known as uridylation. This modification plays a key role in determining the stability and degradation of various RNA species, such as microRNAs (miRNAs) and mRNAs. ZCCHC11 contains CCHC zinc finger motifs, which are critical for its ability to bind RNA substrates and perform catalytic functions. Inhibitors of ZCCHC11 function by disrupting its RNA-binding ability or interfering with the catalytic activity of the enzyme, resulting in altered RNA modification and turnover, which can influence gene expression and cellular processes dependent on RNA stability.

The mechanisms by which ZCCHC11 inhibitors operate are diverse, depending on the structure and chemical properties of the compounds. Some inhibitors may bind to the catalytic domain of ZCCHC11, blocking its ability to add uridine residues to RNA molecules, thereby preventing uridylation. Other inhibitors may target the zinc finger domains that are essential for ZCCHC11's interaction with RNA, potentially by chelating the zinc ions required for maintaining the structural integrity of these motifs. By destabilizing the zinc finger domains, these inhibitors prevent ZCCHC11 from binding to its RNA substrates, further impairing its role in RNA modification. In addition, some inhibitors may act by disrupting protein-protein interactions necessary for ZCCHC11 to function within larger RNA regulatory complexes. Studying ZCCHC11 inhibitors provides valuable insights into the mechanisms of RNA regulation, the importance of RNA modifications such as uridylation, and the broader role of RNA-binding proteins in controlling gene expression and maintaining cellular homeostasis.

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