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Biological Activity for Mirin
Mirin is a Mre11-Rad50-Nbs1 (MRN)-ATM pathway inhibitor that blocks the 3' and 5' exonuclease activity associated with Mre11. Prevents ATM activation in response to double strand breaks (IC50 = 12 μM) and induces G2 cell cycle arrest. Also blocks homology-directed repair in vitro.
Compound Libraries for Mirin
Technical Data for Mirin
|Storage||Store at +4°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
Solubility Data for Mirin
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions for Mirin
The following data is based on the product molecular weight 220.25. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||4.54 mL||22.7 mL||45.4 mL|
|5 mM||0.91 mL||4.54 mL||9.08 mL|
|10 mM||0.45 mL||2.27 mL||4.54 mL|
|50 mM||0.09 mL||0.45 mL||0.91 mL|
References for Mirin
References are publications that support the biological activity of the product.
Dupre et al (2008) A forward chemical genetic screen reveals an inhibitor of the Mre11-Rad50-Nbs1 complex. Nat.Chem.Biol. 4 119 PMID: 18176557
Stivers (2008) Small molecule versus DNA repair mechanisms. Nat.Chem.Biol. 4 86 PMID: 18202674
Garner et al (2009) Corrected structure of mirin, a small-molecule inhibitor of the Mre11-Rad50-Nbs1 complex. Nat.Chem.Biol. 5 129 PMID: 19219009
If you know of a relevant reference for Mirin, please let us know.
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Keywords: Mirin, Mirin supplier, MRN-ATM, pathway, inhibitors, inhibits, exonuclease, activity, Mre11-Rad50-Nbs1, Esterases, ATM, activation, Checkpoint, Control, Kinases, &, ATR, Kinase, Exonucleases, 3190, Tocris Bioscience
5 Citations for Mirin
Citations are publications that use Tocris products. Selected citations for Mirin include:
Hampp et al (2016) DNA damage tolerance pathway involving DNA polymerase ? and the tumor suppressor p53 regulates DNA replication fork progression Proc Natl Acad Sci U S A. 113 E4311 PMID: 27407148
Bothmer et al (2013) Mechanism of DNA resection during intrachromosomal recombination and immunoglobulin class switching. Regul Pept 210 115 PMID: 23254285
Berte et al (2016) Targeting Homologous Recombination by Pharmacological Inhibitors Enhances the Killing Response of Glioblastoma Cells Treated with Alkylating Drugs. Mol Cancer Ther 15 2665 PMID: 27474153
Hollingworth et al (2017) Localization of Double-Strand Break Repair Proteins to Viral Replication Compartments following Lytic Reactivation of Kaposi's Sarcoma-Associated Herpesvirus. J Virol 91 PMID: 28855246
Lee and Dunphy (2013) The Mre11-Rad50-Nbs1 (MRN) complex has a specific role in the activation of Chk1 in response to stalled replication forks. Mol Biol Cell 24 1343 PMID: 23468519
Do you know of a great paper that uses Mirin from Tocris? Please let us know.
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Literature in this Area
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!
*Please note that Tocris will only send literature to established scientific business / institute addresses.
Cell Cycle and DNA Damage Research Product GuideNew
This product guide provides a review of the cell cycle and DNA damage research area and lists over 170 products, including research tools for:
- Cell Cycle and Mitosis
- DNA Damage Repair
- Targeted Protein Degradation
- Ubiquitin Proteasome Pathway
- Chemotherapy Targets
Cell Cycle & DNA Damage Repair Poster
In normal cells, each stage of the cell cycle is tightly regulated, however in cancer cells many genes and proteins that are involved in the regulation of the cell cycle are mutated or over expressed. Adapted from the 2015 Cancer Product Guide, Edition 3, this poster summarizes the stages of the cell cycle and DNA repair. It also highlights strategies for enhancing replicative stress in cancer cells to force mitotic catastrophe and cell death.