MRP-L21 Inhibitors

Omeprazole, a proton pump inhibitor, decreases the acidic environment of the stomach. Within mitochondria, it may disrupt the inner mitochondrial membrane potential, crucial for ATP synthesis. The compromised ATP production can indirectly inhibit MRP-L21's role in mitochondrial protein synthesis as the process is ATP-dependent.

Bortezomib, a proteasome inhibitor, prevents the breakdown of misfolded proteins. By causing proteotoxic stress, it can lead to the misfolding of newly synthesized mitochondrial proteins, including MRP-L21, impeding its proper assembly into the mitochondrial ribosome.

Metformin activates AMP-activated protein kinase (AMPK), which enhances cellular energy efficiency. Activation of AMPK can reduce the translation of mitochondrial-encoded proteins, potentially decreasing the need for MRP-L21 in the mitochondrial ribosome complex.

Chloroquine accumulates in lysosomes and inhibits lysosomal enzymes. By interfering with autophagy, it can lead to the accumulation of damaged mitochondria. This can indirectly inhibit MRP-L21 by impairing the organelle where it operates.

Rapamycin inhibits the mTOR pathway, which is involved in cell growth and protein synthesis. Inhibition of mTOR can downregulate mitochondrial biogenesis and, as a consequence, may reduce the incorporation of MRP-L21 into the mitochondrial ribosomes.

Paclitaxel stabilizes microtubules and disrupts their dynamics, which is essential for mitosis. By interfering with cell division, it indirectly affects all cellular replication processes, including the synthesis of mitochondrial proteins that require MRP-L21.

Ritonavir, an HIV protease inhibitor, has been shown to affect mitochondrial function. It can inhibit the activity of mitochondrial DNA polymerase, potentially decreasing the synthesis of mitochondrial-encoded proteins that would require assembly with MRP-L21.

Valinomycin is a potassium ionophore that disrupts mitochondrial membrane potential. By dissipating the electrochemical gradient, it inhibits ATP synthesis, indirectly affecting the mitochondrial translation process involving MRP-L21.

Thapsigargin inhibits the sarco/endoplasmic reticulum Ca2+ ATPase (SERCA), leading to a depletion of ER calcium stores. This can trigger a cellular stress response, potentially affecting mitochondrial function and indirectly inhibiting MRP-L21's role in protein synthesis.

Rotenone is an inhibitor of mitochondrial complex I. By inhibiting electron transport, it decreases ATP production, which is necessary for the assembly and functioning of MRP-L21 within the mitochondrial ribosome.