PRELI Inhibitors

PRELI is a mitochondrial protein that plays an essential role in regulating mitochondrial morphology, homeostasis, and function. It is intricately involved in cellular energy metabolism, making it susceptible to a range of chemical inhibitors targeting mitochondrial pathways. For instance, Oligomycin A is an ATP synthase inhibitor that hampers mitochondrial ATP production, thereby affecting PRELI's function in maintaining mitochondrial health. Likewise, Cyclosporin A and Rotenone also target the mitochondria but do so by blocking the permeability transition pore and inhibiting complex I, respectively. FCCP acts as an uncoupler, thus affecting PRELI's role in mitochondrial homeostasis by disrupting oxidative phosphorylation. Mdivi-1 inhibits mitochondrial division, which alters the mitochondrial morphology that PRELI seeks to maintain.

Moreover, the function of PRELI also intersects with glycolytic pathways, evidenced by the inhibitory effects of 2-Deoxy-D-glucose, an inhibitor of glycolysis. Other inhibitors like Myxothiazol and Antimycin A target mitochondrial complex III, while Azide and DCCD focus on cytochrome oxidase and ATP synthase, respectively. These inhibitors can compromise PRELI's ability to sustain mitochondrial function effectively. In the realm of protein processing and transport, Tunicamycin and Brefeldin A can also impact PRELI. Tunicamycin inhibits N-linked glycosylation, and Brefeldin A disrupts ER-to-Golgi transport, both of which are crucial pathways where PRELI might be involved in protein sorting or processing. In summary, the chemical inhibitors targeting PRELI operate via diverse mechanisms to impair its function, most notably in mitochondrial integrity and cellular energy metabolism.