1. An inactivating caspase 11 passenger mutation originating from the 129 murine strain in mice targeted for c-IAP1
- Author
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Elizabeth D. Hughes, J. Michael Younger, Colin S. Duckett, Philip A. Barker, Danielle Marcotte, Thomas L. Saunders, and Niall S. Kenneth
- Subjects
Mice, 129 Strain ,Caspase 1 ,Caspase-11 ,Inhibitor of apoptosis ,Biochemistry ,Cell Line ,Inhibitor of Apoptosis Proteins ,Mice ,03 medical and health sciences ,0302 clinical medicine ,Animals ,Molecular Biology ,Gene ,Caspase ,030304 developmental biology ,0303 health sciences ,biology ,NLRP1 ,Cell Biology ,Molecular biology ,Caspases, Initiator ,Enzyme Activation ,Cell culture ,Caspases ,030220 oncology & carcinogenesis ,Mutation ,biology.protein ,Caspase 10 - Abstract
A recent study revealed that ES (embryonic stem) cell lines derived from the 129 murine strain carry an inactivating mutation within the caspase 11 gene (Casp4) locus [Kayagaki, Warming, Lamkanfi, Vande Walle, Louie, Dong, Newton, Qu, Liu, Heldens, Zhang, Lee, Roose-Girma and Dixit (2011) Nature 479, 117–121]. Thus, if 129 ES cells are used to target genes closely linked to caspase 11, the resulting mice might also carry the caspase 11 deficiency as a passenger mutation. In the present study, we examined the genetic loci of mice targeted for the closely linked c-IAP (cellular inhibitor of apoptosis) genes, which were generated in 129 ES cells, and found that, despite extensive backcrossing into a C57BL/6 background, c-IAP1−/− animals are also deficient in caspase 11. Consequently, data obtained from these mice should be re-evaluated in this new context.
- Published
- 2012
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