MTO1 Inhibitors
Chemical inhibitors of MTO1 can exert their inhibitory effects through various mechanisms that ultimately compromise the protein's function by reducing the availability of ATP, which is essential for MTO1's role in mitochondrial tRNA modification. Rotenone, Piericidin A, and Sodium azide target different complexes of the mitochondrial electron transport chain, specifically complex I and IV, thereby disrupting the proton gradient required for ATP synthesis. This reduction in ATP levels can directly impede the ability of MTO1 to carry out its function, as ATP is a vital cofactor for the enzymatic modifications MTO1 catalyzes on mitochondrial tRNAs. Similarly, Oligomycin A and Aurovertin B bind to mitochondrial ATP synthase, inhibiting the conversion of ADP to ATP and indirectly inhibiting MTO1 by depriving it of the energy required for its tRNA modification activity. Antimycin A's inhibition of complex III and Carboxin's inhibition of complex II also contribute to a decrease in ATP production, thereby indirectly reducing MTO1 function.
TTFA and FCCP disrupt mitochondrial ATP production by inhibiting complex II and uncoupling oxidative phosphorylation, respectively. The inhibition of ATP production leads to an energy deficit that hampers the ability of MTO1 to effectively modify mitochondrial tRNAs. Zinc pyrithione disrupts mitochondrial electron transport, further contributing to a decrease in ATP synthesis and indirectly inhibiting the tRNA modification activity of MTO1. Iodoacetate targets glycolysis by irreversibly inhibiting GAPDH, which leads to a reduction in pyruvate production and, consequently, ATP synthesis, affecting the MTO1 activity. Azide, similar to Sodium azide, inhibits complex IV of the electron transport chain, causing a reduction in ATP synthesis and indirectly inhibiting the functional capacity of MTO1 by limiting the energy supply necessary for its role in mitochondrial tRNA modification. These chemical inhibitors, through their diverse mechanisms, all converge on the common endpoint of reducing ATP levels, which is critical for the functional inhibition of MTO1's enzymatic activity.
| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Rotenone | 83-79-4 | sc-203242 sc-203242A | 1 g 5 g | $89.00 $259.00 | 41 | |
Rotenone inhibits mitochondrial electron transport chain complex I, which indirectly leads to a decrease in cellular ATP levels. Since MTO1 is involved in the modification of mitochondrial tRNAs necessary for protein synthesis, reduced ATP levels can inhibit the function of MTO1 by limiting the energy required for its tRNA modification activity. | ||||||
Oligomycin A | 579-13-5 | sc-201551 sc-201551A sc-201551B sc-201551C sc-201551D | 5 mg 25 mg 100 mg 500 mg 1 g | $179.00 $612.00 $1203.00 $5202.00 $9364.00 | 26 | |
Oligomycin A inhibits mitochondrial ATP synthase, decreasing the ATP production. Because MTO1 requires ATP to catalyze the modification of mitochondrial tRNAs, inhibition of ATP synthase can indirectly inhibit the function of MTO1 by depleting its energy source. | ||||||
Antimycin A | 1397-94-0 | sc-202467 sc-202467A sc-202467B sc-202467C | 5 mg 10 mg 1 g 3 g | $55.00 $63.00 $1675.00 $4692.00 | 51 | |
Antimycin A inhibits mitochondrial complex III, which results in the reduction of ATP synthesis. The function of MTO1 is energy-dependent, thus lower levels of ATP can inhibit the tRNA modification process catalyzed by MTO1. | ||||||
Carboxine | 5234-68-4 | sc-234286 | 250 mg | $21.00 | 1 | |
Carboxin inhibits mitochondrial complex II, which may lead to reduced ATP production. Decreased ATP availability can inhibit MTO1's function by limiting the energy supply necessary for its tRNA modification activity. | ||||||
Sodium azide | 26628-22-8 | sc-208393 sc-208393B sc-208393C sc-208393D sc-208393A | 25 g 250 g 1 kg 2.5 kg 100 g | $43.00 $155.00 $393.00 $862.00 $90.00 | 8 | |
Sodium azide inhibits mitochondrial complex IV, disrupting ATP synthesis. The subsequent drop in ATP levels can inhibit MTO1 by impacting the energy-dependent tRNA modification process it facilitates. | ||||||
Aphidicolin | 38966-21-1 | sc-201535 sc-201535A sc-201535B | 1 mg 5 mg 25 mg | $84.00 $306.00 $1104.00 | 30 | |
Aurovertin B binds to mitochondrial ATP synthase, inhibiting ATP production. With reduced ATP levels, the activity of MTO1 is inhibited as it relies on ATP for mitochondrial tRNA modification functions. | ||||||
Piericidin A | 2738-64-9 | sc-202287 | 2 mg | $291.00 | 24 | |
Piericidin A is an inhibitor of mitochondrial complex I, leading to decreased ATP production. As MTO1's tRNA modification function is ATP-dependent, inhibition of ATP synthesis can result in functional inhibition of MTO1. | ||||||
2-Thenoyltrifluoroacetone | 326-91-0 | sc-251801 | 5 g | $37.00 | 1 | |
TTFA inhibits mitochondrial complex II, leading to reduced ATP synthesis. Inhibition of ATP production can indirectly inhibit MTO1 by limiting the energy crucial for its enzymatic activity on mitochondrial tRNAs. | ||||||
Zinc | 7440-66-6 | sc-213177 | 100 g | $48.00 | ||
Zinc pyrithione disrupts mitochondrial electron transport and ATP synthesis. By decreasing ATP availability, it can indirectly inhibit MTO1 activity, which is essential for mitochondrial tRNA modifications. | ||||||
FCCP | 370-86-5 | sc-203578 sc-203578A | 10 mg 50 mg | $94.00 $355.00 | 46 | |
FCCP uncouples mitochondrial oxidative phosphorylation, which leads to a decrease in ATP synthesis. The reduced availability of ATP can inhibit the energy-dependent functions of MTO1. | ||||||