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Discontinued ProductNSC 319726 (Cat. No. 5065) has been withdrawn from sale for commercial reasons.
Biological Activity for NSC 319726
NSC 319726 is a reactivator of mutant p53. Restores wild type p53 structure and function to the p53R175 mutant. Inhibits growth of fibroblasts expressing the p53R175 mutation (IC50 = 8 nM). Also inhibits growth of xenograft tumors expressing the p53R175 mutation in vivo.
Technical Data for NSC 319726
|Storage||Store at -20°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.
References for NSC 319726
References are publications that support the biological activity of the product.
Yu et al (2012) Allele-specific p53 mutant reactivation. Cancer Cell 21 614 PMID: 22624712
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Keywords: NSC 319726, NSC 319726 supplier, NSC319726, mutant, p53, reactivators, activators, p53R175, transcription, factors, cell, cycle, apoptosis, 5065, Tocris Bioscience
Citations for NSC 319726
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Currently there are no citations for NSC 319726.
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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 Guide
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.