YME1L1 Inhibitors

Alisertib is an Aurora kinase A inhibitor. Aurora kinase A is involved in mitochondrial fission, which is a process YME1L1 participates in. By inhibiting Aurora kinase A, alisertib can indirectly inhibit the mitochondrial fission process, potentially reducing the functional role of YME1L1, as it is a protein that integrates mitochondrial dynamics.

Mdivi-1 is a selective inhibitor of mitochondrial division DRP1. YME1L1 is known to interact with components of the mitochondrial fission machinery, and its activity is related to the proper balance between mitochondrial fission and fusion. By inhibiting DRP1, Mdivi-1 can disrupt the mitochondrial fission process, which may indirectly inhibit the function of YME1L1 by preventing the fission with which YME1L1 is associated.

Sorafenib targets multiple kinases, some of which are involved in mitochondrial dynamics. Inhibition of these kinases can lead to altered mitochondrial morphology and function, which could indirectly inhibit YME1L1 by disrupting the mitochondrial context in which YME1L1 operates.

Oligomycin A is an inhibitor of ATP synthase in mitochondrial membranes. YME1L1 is involved in the maintenance of the mitochondrial network and its function can be influenced by changes in the mitochondrial membrane potential and ATP synthesis. By inhibiting ATP synthase, oligomycin A can alter the mitochondrial membrane potential, potentially inhibiting the function of YME1L1 due to changes in the mitochondrial environment where YME1L1 exerts its function.

Chloroquine is known to accumulate in lysosomes and mitochondria, altering their function. It can cause mitochondrial DNA damage and disrupt the electron transport chain. Since YME1L1 is a mitochondrial protein involved in maintaining mitochondrial network and genome stability, chloroquine's impact on mitochondrial function can indirectly inhibit YME1L1 activity by impairing the integrity of the mitochondrial environment.

Antimycin A is a complex III inhibitor of the electron transport chain. By inhibiting complex III, it can cause a buildup of reactive oxygen species (ROS) and alter mitochondrial membrane potential. Since YME1L1 is associated with the regulation of mitochondrial biogenesis and morphology, the changes in mitochondrial function caused by antimycin A could indirectly inhibit YME1L1 by disturbing mitochondrial homeostasis.

Rotenone is an inhibitor of complex I of the mitochondrial electron transport chain. YME1L1's function is related to the regulation of mitochondrial biogenesis and morphology. By disrupting complex I, rotenone can lead to mitochondrial dysfunction, which may indirectly inhibit the activity of YME1L1 by compromising the mitochondria's structural and functional integrity where YME1L1 operates.

CCCP is a protonophore that dissipates the mitochondrial membrane potential. YME1L1's regulatory role in mitochondrial biogenesis and morphology is dependent on an intact mitochondrial membrane potential. Disruption of this potential by CCCP could lead to an indirect inhibition of YME1L1 by impairing the mitochondrial function and structure that YME1L1 is involved in.

Bongkrekic acid is an inhibitor of the mitochondrial adenine nucleotide translocator (ANT). YME1L1 is associated with mitochondrial health and function, which can be compromised by the inhibition of ANT as it is crucial for ADP/ATP exchange across the mitochondrial inner membrane.