Chemical inhibitors of FAM111B can achieve functional inhibition through their action on the cell cycle, which is a biological process where FAM111B plays a critical role. Alsterpaullone, Roscovitine, Purvalanol A, Olomoucine, Indirubin, Flavopiridol, Dinaciclib, and Milciclib are all inhibitors of cyclin-dependent kinases (CDKs), a group of enzymes that are pivotal for the progression of cells through the cell cycle. FAM111B is implicated in the regulation of DNA replication and chromatin organization, which are processes that are tightly coupled to the cell cycle. By inhibiting CDKs, these chemicals can disrupt the progression of the cell cycle at various checkpoints. This action can impede the activity of FAM111B by preventing the cell cycle-dependent steps that FAM111B is known to regulate. For instance, Flavopiridol and Milciclib can induce a broad inhibition of CDKs, leading to a potential halt in cell cycle phases where FAM111B is necessary for the maintenance of DNA integrity and replication fidelity.
Additionally, chemicals like Harmine, PD0332991, Ribociclib, and AT7519 target specific CDKs or related kinases such as dual-specificity tyrosine phosphorylation-regulated kinase (DYRK). Harmine can inhibit DYRK, a kinase implicated in cell cycle control, thereby affecting the cell cycle and subsequently the functional role of FAM111B. PD0332991 and Ribociclib, by selectively inhibiting CDK4 and CDK6, can alter the cell cycle dynamics, indirectly inhibiting the role of FAM111B in DNA replication and checkpoint control. AT7519, as a multi-CDK inhibitor, can also exert an influence on FAM111B's activity by disrupting the cell cycle and other CDK-dependent processes.
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