Mirin

Pricing Availability   Qty
Description: MRN-ATM pathway inhibitor
Chemical Name: Z-5-(4-Hydroxybenzylidene)-2-imino-1,3-thiazolidin-4-one
Purity: ≥99% (HPLC)
Datasheet
Citations (5)
Reviews
Literature (2)

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

Mirin is also offered as part of the Tocriscreen 2.0 Max, Tocriscreen Kinase Inhibitor Library and Tocriscreen Epigenetics Library. Find out more about compound libraries available from Tocris.

Technical Data for Mirin

M. Wt 220.25
Formula C10H8N2O2S
Storage Store at +4°C
Purity ≥99% (HPLC)
CAS Number 1198097-97-0
PubChem ID 1206243
InChI Key YBHQCJILTOVLHD-YVMONPNESA-N
Smiles OC(C=C1)=CC=C1/C=C2/C(NC(S2)=N)=O

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
Solubility
DMSO 22.02 100

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.

Select a batch to recalculate based on the batch molecular weight:
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

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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.

View Related Products by Product Action

View all ATM and ATR Kinase Inhibitors

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:

Bothmer et al (2013) Mechanism of DNA resection during intrachromosomal recombination and immunoglobulin class switching. Regul Pept 210 115 PMID: 23254285

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

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


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Reviews for Mirin

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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!

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Cell Cycle and DNA Damage Research Product Guide

Cell Cycle and DNA Damage Research Product Guide

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Cell Cycle & DNA Damage Repair Poster

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. 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.