The class of chemicals known as REV1 activators encompasses a diverse range of compounds that indirectly influence the activity of the DNA repair protein REV1. These chemicals do not activate REV1 directly; rather, their actions induce cellular states or DNA damage that necessitates the involvement of REV1 as part of the cellular DNA repair machinery. The primary mechanism through which these chemicals exert their influence is by inducing various forms of DNA damage or stress, thereby activating DNA repair pathways where REV1 is a critical component.
REV1 is integral to the Translesion Synthesis (TLS) pathway, a mechanism that allows DNA replication to continue past sites of damage. Chemicals like cisplatin and hydroxyurea induce DNA lesions or replication stress, respectively, leading to the activation of pathways that require REV1's function. Other compounds, such as camptothecin and etoposide, inhibit topoisomerases, resulting in DNA strand breaks that engage REV1 in the repair process. Similarly, PARP inhibitors like olaparib create conditions where double-strand breaks occur, indirectly involving REV1 in the repair mechanisms. Additionally, some chemicals in this class target key proteins in the DNA damage response pathways. For instance, ATR, ATM, and CHK1 inhibitors disrupt the normal signaling processes in response to DNA damage. The disruption of these pathways can lead to an increased reliance on REV1's role in DNA repair, especially under conditions where alternative repair mechanisms are impaired or overwhelmed.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Cisplatin | 15663-27-1 | sc-200896 sc-200896A | 100 mg 500 mg | $138.00 $380.00 | 101 | |
Induces DNA damage necessitating DNA repair mechanisms, including the TLS pathway, indirectly upregulating REV1 activity. | ||||||
Hydroxyurea | 127-07-1 | sc-29061 sc-29061A | 5 g 25 g | $78.00 $260.00 | 18 | |
Inhibits ribonucleotide reductase, leading to replication stress and activation of the ATR-Chk1 pathway, indirectly increasing REV1 activity. | ||||||
Aphidicolin | 38966-21-1 | sc-201535 sc-201535A sc-201535B | 1 mg 5 mg 25 mg | $84.00 $306.00 $1104.00 | 30 | |
Inhibits DNA polymerases α, δ, and ε, inducing replication stress and stalling DNA replication forks, thereby activating the ATR-Chk1 pathway and indirectly upregulating REV1. | ||||||
Camptothecin | 7689-03-4 | sc-200871 sc-200871A sc-200871B | 50 mg 250 mg 100 mg | $58.00 $186.00 $94.00 | 21 | |
A topoisomerase I inhibitor that induces DNA double-strand breaks, engaging REV1 in the repair process as part of the HR and NHEJ pathways. | ||||||
Etoposide (VP-16) | 33419-42-0 | sc-3512B sc-3512 sc-3512A | 10 mg 100 mg 500 mg | $51.00 $231.00 $523.00 | 63 | |
A topoisomerase II inhibitor generating DNA double-strand breaks, engaging REV1 in the DNA damage response, particularly in HR and NHEJ pathways. | ||||||
Olaparib | 763113-22-0 | sc-302017 sc-302017A sc-302017B | 250 mg 500 mg 1 g | $210.00 $305.00 $495.00 | 10 | |
A PARP inhibitor disrupting the repair of single-strand breaks, leading to double-strand breaks and potentially involving REV1 in TLS during complex DNA repair processes. | ||||||
Methyl methanesulfonate | 66-27-3 | sc-250376 sc-250376A | 5 g 25 g | $56.00 $133.00 | 2 | |
Induces alkylating damage in DNA, leading to the formation of adducts and mismatches, with REV1 participating in the repair of such lesions. | ||||||
Bleomycin Sulfate | 9041-93-4 | sc-200134 sc-200134A sc-200134B sc-200134C | 10 mg 50 mg 100 mg 500 mg | $210.00 $624.00 $1040.00 $2913.00 | 38 | |
Induces DNA strand breaks and oxidative damage, with REV1 involved in the repair as part of the NHEJ and HR pathways. | ||||||
VE 821 | 1232410-49-9 | sc-475878 | 10 mg | $360.00 | ||
Disrupts the ATR-Chk1 pathway, indirectly affecting DNA damage response mechanisms and potentially increasing the reliance on REV1 in DNA repair processes. | ||||||
ATM Kinase Inhibitor | 587871-26-9 | sc-202963 | 2 mg | $110.00 | 28 | |
Inhibits ATM kinase, affecting pathways where REV1 is involved, particularly under DNA repair stress conditions. | ||||||