DNA Damage/Repair Transformed MEF Cell Lines
Lambda-LIZ transgene harboring transformed MEF cell lines. Wild-type or null for: N-methylpurine DNA glycosylase (AAG), Mismatch repair endonuclease PMS2 (PMS2), DNA polymerase beta (Beta-pol), or Uracil-DNA glycosylase (UNG).
Highlights:
- Useful in toxicology and DNA repair research
- Enable evaluation of generations of gene mutations as a direct function of base excision repair or mismatch repair
- Wild-type, Beta-pol null, AAG null, PMS2 null, Beta-pol/PMS2 null, Beta-pol/AAG null, and UNG null lines available
- Also carry the lambda-LIZ transgene
Of great utility in toxicology and DNA repair research are cell lines derived from gene knockout mice enabling one to evaluate the formation and accumulation of gene mutations as a direct function of base excision repair (AAG, Beta-pol, UNG) and/or mismatch repair (PMS2). Of particular importance are lambda-LIZ transgenes. The utility of these fibroblast cell lines (derived embryos) stem from the deficiency in base excision repair, as a result of the null mutation in the AAG, Beta-pol, or UNG genes or a deficiency in mismatch repair, as a result of the null mutation in the PMS2 gene. In addition, in some cases, the cells have a double KO: AAG/Beta-pol or PMS2/Beta-pol.
From the laboratories of Samuel H. Wilson, MD and Robert W. Sobol, PhD, National Institute of Environmental Health Sciences/NIH.
Lambda-LIZ transgene harboring transformed MEF cell lines. Wild-type or null for: N-methylpurine DNA glycosylase (AAG), Mismatch repair endonuclease PMS2 (PMS2), DNA polymerase beta (Beta-pol), or Uracil-DNA glycosylase (UNG).
Highlights:
- Useful in toxicology and DNA repair research
- Enable evaluation of generations of gene mutations as a direct function of base excision repair or mismatch repair
- Wild-type, Beta-pol null, AAG null, PMS2 null, Beta-pol/PMS2 null, Beta-pol/AAG null, and UNG null lines available
- Also carry the lambda-LIZ transgene
Of great utility in toxicology and DNA repair research are cell lines derived from gene knockout mice enabling one to evaluate the formation and accumulation of gene mutations as a direct function of base excision repair (AAG, Beta-pol, UNG) and/or mismatch repair (PMS2). Of particular importance are lambda-LIZ transgenes. The utility of these fibroblast cell lines (derived embryos) stem from the deficiency in base excision repair, as a result of the null mutation in the AAG, Beta-pol, or UNG genes or a deficiency in mismatch repair, as a result of the null mutation in the PMS2 gene. In addition, in some cases, the cells have a double KO: AAG/Beta-pol or PMS2/Beta-pol.
From the laboratories of Samuel H. Wilson, MD and Robert W. Sobol, PhD, National Institute of Environmental Health Sciences/NIH.
| Catalog Number | Product | DataSheet | Size | AVAILABILITY | Price | Qty |
|---|
This product is for sale to Nonprofit customers only. For profit customers, please Contact Us for more information.
| Product Type: | Cell Line |
| Name: | DNA Damage/Repair Transformed MEF Cell Lines (92TAg, 88TAg, 308TAg, 127TAg, 151TAg, 283TAg, 207TAg, 210TAg) |
| Cell Type: | Transformed MEF |
| Source: | Mouse embryos |
| Growth Conditions: | DMEM high glucose (Invitrogen cat# 11960-044), FBS 10% (50ml), Pen/strep (5.5ml)(Invitrogen cat# 15070-063), Glutamx (11ml) (Invitrogen cat# 35050-061); Cells should be grown at 10% CO2 |
| Cryopreservation: | One million cells/ml and stored in 70% Media A/20% FBS/10% DMSO; one ml per vial. |
| Age: | 14.5-day-old |
| Mycoplasma Tested: | August 2016 - Negative |
| Storage: | Liquid nitrogen |
| Shipped: | Dry Ice |
- Sobol RW, Kartalou M, Almeida KH, Joyce DF, Engelward BP, Horton JK, Prasad R, Samson LD, Wilson SH: Base Excision Repair Intermediates Induce p53-independent Cytotoxic and Genotoxic Responses. J Biol Chem 2003, 278(41):39951-39959.
- Endres M, Biniszkiewicz D, Sobol RW, Harms C, Ahmadi M, Lipski A, Katchanov J, Mergenthaler P, Dirnagl U, Wilson SH, Meisel A, Jaenisch R: Increased postischemic brain injury in mice deficient in uracil-DNA glycosylase. Journal of Clinical Investigation 2004, 113(12):1711-1721.
If you publish research with this product, please let us know so we can cite your paper.
