Txl-2 inhibitors encompass a diverse array of chemical compounds that reduce the functional activity of Txl-2 through their effects on different cellular mechanisms, primarily targeting processes integral to cell cycle progression and DNA synthesis, where Txl-2 is functionally important. For instance, microtubule-interfering agents such as Paclitaxel, Vinblastine, and Colchicine stabilize or disrupt microtubule dynamics, leading to cell cycle arrest. This blockade of proper microtubule function diminishes the activity of Txl-2 as it is reliant on the progression of the cell cycle. Similarly, DNA-damaging agents such as Etoposide, Camptothecin, and Bleomycin inhibit enzymes like topoisomerase or induce DNA strand breaks, which initiate cell cycle arrest and apoptosis. These disruptions in DNA integrity and replication indirectly inhibit Txl-2 by preventing the cellular processes that require Txl-2 activity.
Furthermore, compounds like Mithramycin A and Mitomycin C interfere with DNA and RNA synthesis by binding to DNA or forming cross-links, which inhibit transcription and replication, indirectly leading to a decrease in Txl-2 activity. DNA synthesis inhibitors such as Hydroxyurea, Methotrexate, and Gemcitabine exert their effects by limiting the availability of nucleotides or acting as nucleoside analogs, resulting in reduced DNA synthesis and cell cycle arrest. The consequent disruption in DNA replication processes and transcriptional events that Txl-2 is involved in leads to its functional inhibition. Cyclophosphamide, another DNA cross-linking agent, further contributes to the inhibition of Txl-2 by inducing DNA damage and halting cell cycle progression. Collectively, these Txl-2 inhibitors operate through indirect mechanisms that intersect with the cellular pathways and processes crucial for Txl-2 activity, ultimately leading to its diminished function without directly altering Txl-2 transcription or translation.
SEE ALSO...
Items 1 to 10 of 12 total
Display:
| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Taxol | 33069-62-4 | sc-201439D sc-201439 sc-201439A sc-201439E sc-201439B sc-201439C | 1 mg 5 mg 25 mg 100 mg 250 mg 1 g | $40.00 $73.00 $217.00 $242.00 $724.00 $1196.00 | 39 | |
Paclitaxel stabilizes microtubules and prevents their depolymerization, which can diminish cell division and mitotic signaling. This microtubule-stabilizing action would indirectly lead to the inhibition of Txl-2 by disrupting cellular processes Txl-2 is involved in, such as cell cycle progression. | ||||||
Etoposide (VP-16) | 33419-42-0 | sc-3512B sc-3512 sc-3512A | 10 mg 100 mg 500 mg | $32.00 $170.00 $385.00 | 63 | |
Etoposide inhibits the enzyme topoisomerase II, leading to DNA damage and triggering cell cycle arrest. This DNA damage response would indirectly inhibit Txl-2 by hampering the cell division cycle where Txl-2 is functionally important. | ||||||
Camptothecin | 7689-03-4 | sc-200871 sc-200871A sc-200871B | 50 mg 250 mg 100 mg | $57.00 $182.00 $92.00 | 21 | |
Camptothecin is a topoisomerase I inhibitor that induces DNA damage and subsequent cell cycle arrest. This would result in the inhibition of Txl-2 activity as the cell cycle is an important process for Txl-2 function. | ||||||
Vinblastine | 865-21-4 | sc-491749 sc-491749A sc-491749B sc-491749C sc-491749D | 10 mg 50 mg 100 mg 500 mg 1 g | $100.00 $230.00 $450.00 $1715.00 $2900.00 | 4 | |
Vinblastine disrupts microtubule assembly, leading to cell cycle arrest and apoptosis. This disruption would ultimately inhibit the activity of Txl-2 by arresting the cell cycle and preventing cell division. | ||||||
Colchicine | 64-86-8 | sc-203005 sc-203005A sc-203005B sc-203005C sc-203005D sc-203005E | 1 g 5 g 50 g 100 g 500 g 1 kg | $98.00 $315.00 $2244.00 $4396.00 $17850.00 $34068.00 | 3 | |
Colchicine binds to tubulin, inhibiting microtubule polymerization, which leads to cell cycle arrest and apoptosis. This inhibition of the microtubule function would lead to an indirect decrease in Txl-2 activity by blocking cell division. | ||||||
Mithramycin A | 18378-89-7 | sc-200909 | 1 mg | $54.00 | 6 | |
Mithramycin A binds to DNA and inhibits RNA synthesis, which can lead to cell cycle arrest. This inhibition of RNA synthesis would reduce the activity of Txl-2 by affecting transcriptional processes necessary for its function. | ||||||
Bleomycin Sulfate | 9041-93-4 | sc-200134 sc-200134A sc-200134B sc-200134C | 10 mg 50 mg 100 mg 500 mg | $206.00 $612.00 $1020.00 $2856.00 | 38 | |
Bleomycin causes DNA strand breaks, leading to cell cycle arrest and cell death. This DNA damage response indirectly reduces Txl-2 activity by interfering with cellular processes that Txl-2 is involved in, particularly cell division. | ||||||
Mitomycin C | 50-07-7 | sc-3514A sc-3514 sc-3514B | 2 mg 5 mg 10 mg | $65.00 $99.00 $140.00 | 85 | |
Mitomycin C cross-links DNA, which prevents DNA replication and transcription, leading to cell cycle arrest. This action indirectly inhibits Txl-2 by affecting the replication and transcription processes Txl-2 is involved in. | ||||||
Cyclophosphamide | 50-18-0 | sc-361165 sc-361165A sc-361165B sc-361165C | 50 mg 100 mg 500 mg 1 g | $76.00 $143.00 $469.00 $775.00 | 18 | |
Cyclophosphamide forms DNA cross-links, leading to DNA damage and cell cycle arrest. This would indirectly inhibit Txl-2 activity as it disrupts the progression of the cell cycle, a key process for Txl-2. | ||||||
Hydroxyurea | 127-07-1 | sc-29061 sc-29061A | 5 g 25 g | $76.00 $255.00 | 18 | |
Hydroxyurea inhibits ribonucleotide reductase, decreasing the availability of deoxyribonucleotides and causing cell cycle arrest. This would lead to a decrease in Txl-2 activity by disrupting DNA synthesis and cell division. | ||||||