The chemical class referred to as Spartan inhibitors encompasses a range of compounds that can influence the function of the Spartan protein, a crucial actor in the cellular DNA repair machinery. These inhibitors do not directly target Spartan's proteolytic activity; instead, they modulate the protein's function through their impact on various cellular processes, particularly those related to the DNA damage response and proteostasis. The Spartan protein is known to be involved in the specialized task of repairing DNA-protein crosslinks (DPCs), which are complex lesions that impede critical cellular processes such as transcription and replication. Spartan facilitates the removal of these crosslinks, thus safeguarding genomic integrity.
The effectiveness of Spartan inhibitors is rooted in their capacity to induce cellular states that challenge the DNA repair pathways. When cellular DNA repair mechanisms are overwhelmed due to an excess of DNA lesions, Spartan's role becomes more demanding. The inhibitors in this class can induce a wide range of DNA damages, from crosslinks to double-strand breaks, which places a higher workload on Spartan. Additionally, some compounds can lead to replication stress by inhibiting enzymes that are essential for DNA synthesis and repair, further taxing the repair systems and Spartan's role within them. The cellular response to these induced stresses includes activation of various signaling pathways that govern the cell cycle, DNA repair, and proteolysis. Through these pathways, Spartan is called upon to address the damage and assist in restoring genomic stability. The action of Spartan inhibitors is also indirectly linked to the ubiquitin-proteasome system, where proteasome inhibitors can lead to an accumulation of ubiquitinated proteins, affecting Spartan's associated processes. By altering the turnover and degradation of proteins, these inhibitors can create a cellular environment that requires heightened activity of DNA repair proteins, including Spartan. As a result, Spartan's function can be influenced by the altered proteostasis, and its ability to maintain genomic integrity can be modulated. The regulation and modulation of Spartan through these indirect inhibitors are complex, involving a network of cellular responses that ultimately affect the protein's ability to carry out its repair function. These inhibitors, therefore, play a role in modulating the cellular pathways that Spartan is part of, which is a reflection of their diverse mechanisms of action and the interconnected nature of cellular signaling and repair pathways.
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Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
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Camptothecin | 7689-03-4 | sc-200871 sc-200871A sc-200871B | 50 mg 250 mg 100 mg | $57.00 $182.00 $92.00 | 21 | |
Inhibits Topoisomerase I, causing DNA damage and replication stress, which could possibly inhibit Spartan for damage resolution. | ||||||
Aphidicolin | 38966-21-1 | sc-201535 sc-201535A sc-201535B | 1 mg 5 mg 25 mg | $82.00 $300.00 $1082.00 | 30 | |
An inhibitor of DNA polymerase α, leading to stalled replication forks and could possibly increase the need for Spartan-mediated repair. | ||||||
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 | |
Causes DNA double-strand breaks by inhibiting Topoisomerase II, possibly leading to an increased workload for Spartan in the DNA damage response that could possibly inhibit its function. | ||||||
Bortezomib | 179324-69-7 | sc-217785 sc-217785A | 2.5 mg 25 mg | $132.00 $1064.00 | 115 | |
Another proteasome inhibitor that can increase cellular protein damage and stress, which could possibly impact Spartan activity. | ||||||
Olaparib | 763113-22-0 | sc-302017 sc-302017A sc-302017B | 250 mg 500 mg 1 g | $206.00 $299.00 $485.00 | 10 | |
A PARP inhibitor that can lead to the accumulation of DNA damage and could possibly affect Spartan by increasing DNA repair demands. | ||||||
UCN-01 | 112953-11-4 | sc-202376 | 500 µg | $246.00 | 10 | |
Inhibits several kinases involved in cell cycle control and DNA damage response, which could possibly require Spartan activity. |