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说明： MRN-ATM pathway inhibitor
化学名： Z-5-(4-Hydroxybenzylidene)-2-imino-1,3-thiazolidin-4-one
纯度： ≥99% (HPLC)
生物活性 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.
化合物库 for Mirin
Mirin is also offered as part of the Tocriscreen 2.0 Max, Tocriscreen Kinase Inhibitor Library and Tocriscreen Epigenetics Library. 了解 Tocris 化合物库的更多信息。
技术数据 for Mirin
| 分子量 | 220.25 |
| 公式 | C10H8N2O2S |
| 储存 | Store at +4°C |
| 纯度 | ≥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 |
上方提供的技术数据仅供参考。批次相关数据请参见分析证书。
Tocris products are intended for laboratory research use only, unless stated otherwise.
溶解性数据 for Mirin
| 溶剂 | 最高浓度 mg/mL | 最高浓度 mM | |
|---|---|---|---|
| 溶解性 | |||
| DMSO | 22.02 | 100 |
制备储备液 for Mirin
以下数据基于产品分子量 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.
| 浓度/溶剂体积/质量 | 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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产品说明书 for Mirin
参考文献 for Mirin
参考文献是支持产品生物活性的出版物。
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.
按产品操作查看相关产品
关键词: 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 篇 Mirin 的引用文献
引用文献是使用了 Tocris 产品的出版物。 Mirin 的部分引用包括：
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
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
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该领域的文献
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!
*请注意，Tocris 仅会向正规科研企业/机构地址发送文献。
Cell Cycle and DNA Damage Research Product Guide
This product guide provides a review of the cell cycle and DNA damage research area and lists over 150 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. 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.