NF-YB Inhibitors

NF-YB inhibitors, in a broad sense, include a range of compounds that indirectly influence the activity of NF-YB by targeting the NF-Y complex or its regulatory mechanisms. NF-YB, as a part of the NF-Y trimeric complex, is crucial for DNA binding and transcriptional regulation of various genes. The inhibitors listed here affect NF-YB primarily through indirect mechanisms, such as DNA interaction interference, modulation of chromatin structure, or influencing the expression of NF-Y subunits. Compounds like Mithramycin A, Echinomycin, Distamycin A, and Chromomycin A3 function by binding to DNA sequences, particularly those rich in GC content. This binding can disrupt the interaction between the NF-Y complex and its DNA binding sites, particularly the CCAAT box, which is crucial for NF-YB function. By altering the DNA binding capability of NF-Y, these compounds indirectly modulate the transcriptional regulatory role of NF-YB. Other inhibitors such as Olaparib, Trichostatin A, and Vorinostat affect NF-YB through changes in DNA repair pathways and chromatin remodeling. These compounds do not target NF-YB directly but influence the transcriptional environment in which NF-YB operates. For example, histone deacetylase inhibitors like Trichostatin A and Vorinostat modify the chromatin structure, potentially impacting the accessibility of NF-Y to its DNA targets. Additionally, compounds like Rocaglamide and Thiostrepton, although not direct inhibitors of NF-YB, can influence its activity by affecting the expression of NF-Y subunits or interacting proteins like FOXM1. Curcumin, known for its broad spectrum of biological activities, might also affect NF-YB indirectly by modulating various cellular signaling pathways.