RMI1 Activators
RMI1, or RecQ Mediated Genome Instability 1, is an integral protein that plays a pivotal role in the maintenance of genome stability. It is a part of the BTR complex, which includes other proteins like BLM helicase and Topoisomerase IIIα. The primary function of RMI1 within this complex is to ensure the proper processing of recombination intermediates during DNA replication and repair. It assists in stabilizing the complex and orchestrates the resolution of double Holliday junctions, a crucial step in homologous recombination to prevent chromosomal breakage and rearrangement. Given its significant role in safeguarding the integrity of the genome, RMI1 is a focal point in the cellular response to DNA damage and the replication stress response.
Understanding the regulation of RMI1 is of scientific interest, particularly the identification of chemical compounds that could potentially induce its expression. Certain chemicals have been hypothesized to stimulate the expression of RMI1 indirectly by imposing stress on the DNA replication and repair systems. For instance, compounds such as doxorubicin and etoposide are known to cause DNA strand breaks, which could lead to the recruitment and increased expression of RMI1 as the cell mobilizes its repair mechanisms. Other chemicals like hydroxyurea and cisplatin create replication stress or form DNA adducts, respectively, potentially prompting a similar upregulation of RMI1. Additionally, agents such as hydrogen peroxide and methyl methanesulfonate can inflict oxidative damage or alkylation on the DNA, which may also trigger the cell to enhance RMI1 expression to combat this damage. Environmental toxins like arsenic trioxide and aflatoxin B1 are also implicated in generating DNA lesions that necessitate a robust DNA repair response, potentially involving RMI1. While the direct induction of RMI1 by these compounds is a complex process that would require further empirical investigation, the link between DNA damage and the necessity for DNA repair proteins implicates these compounds as potential activators of RMI1 expression.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Doxorubicin | 23214-92-8 | sc-280681 sc-280681A | 1 mg 5 mg | $173.00 $418.00 | 43 | |
Doxorubicin introduces double-strand breaks in DNA, which may lead to an upsurge in the transcriptional activity of genes involved in DNA repair, including RMI1, as part of the homologous recombination repair pathway. | ||||||
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 interferes with the DNA enzyme topoisomerase II, causing DNA strand breaks. In response, the cell may enhance the expression of RMI1 to facilitate the repair of these breaks and maintain chromosomal stability. | ||||||
Hydroxyurea | 127-07-1 | sc-29061 sc-29061A | 5 g 25 g | $76.00 $255.00 | 18 | |
Hydroxyurea inhibits ribonucleotide reductase, leading to a depletion of deoxyribonucleotide pools, thereby stalling DNA replication forks. This replication stress might stimulate the upregulation of RMI1 to protect and repair the replication machinery. | ||||||
Cisplatin | 15663-27-1 | sc-200896 sc-200896A | 100 mg 500 mg | $76.00 $216.00 | 101 | |
Cisplatin forms intrastrand DNA crosslinks that obstruct replication and transcription. In response to this genotoxic stress, RMI1's expression could be increased to facilitate the removal of crosslinks and restore genomic integrity. | ||||||
Camptothecin | 7689-03-4 | sc-200871 sc-200871A sc-200871B | 50 mg 250 mg 100 mg | $57.00 $182.00 $92.00 | 21 | |
Camptothecin traps topoisomerase I on DNA, preventing re-ligation of the DNA strands and leading to single-strand breaks. The cell may respond by enhancing RMI1 expression to assist in the resolution of these topological stressors. | ||||||
Methyl methanesulfonate | 66-27-3 | sc-250376 sc-250376A | 5 g 25 g | $55.00 $130.00 | 2 | |
Methyl methanesulfonate alkylates DNA bases, particularly guanine, which can cause inappropriate base pairing and DNA breaks. The cellular mechanism to cope with this type of lesion likely involves the upregulation of RMI1 as part of the base excision repair and homologous recombination pathways. | ||||||
Benzo[a]pyrene | 50-32-8 | sc-257130 | 1 g | $439.00 | 4 | |
Benzo[a]pyrene is metabolically activated to form reactive diol epoxide intermediates that bind to DNA, leading to bulky adducts. This can stimulate the cellular DNA repair machinery to increase RMI1 expression to aid in the removal of these adducts. | ||||||
Arsenic(III) oxide | 1327-53-3 | sc-210837 sc-210837A | 250 g 1 kg | $87.00 $224.00 | ||
Arsenic trioxide generates reactive oxygen species and interferes with DNA repair enzymes, leading to oxidative DNA damage. The antioxidant defense and repair systems might respond by stimulating the synthesis of RMI1. | ||||||
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 generates interstrand cross-links within DNA, which are complex lesions that block replication. To overcome this blockade, the expression of RMI1 might be stimulated as part of the Fanconi anemia pathway, which is involved in interstrand cross-link repair. | ||||||
Hydrogen Peroxide | 7722-84-1 | sc-203336 sc-203336A sc-203336B | 100 ml 500 ml 3.8 L | $30.00 $60.00 $93.00 | 27 | |
Hydrogen peroxide is a reactive oxygen species that can oxidize bases and cause single-strand breaks in DNA. These oxidative lesions may cause a cellular response that includes the increased synthesis of RMI1 to coordinate the repair process. | ||||||