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Contains a disruption of the p53 tumor suppressor gene, the most commonly mutated gene in human cancers
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Useful for studying p53 gene function or screening potential cancer intervention therapies
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Homozygous TSG-p53® mice are totally deficient in p53 protein and prone to the development of spontaneous tumors, primarily lymphomas and sarcomas
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Heterozygous TSG-p53® mice carry one normal p53 allele and have a low rate of spontaneous tumor development
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Differs from Model P53N5-T in that P53N12-T has been backcrossed for an additional seven generations, thereby reducing genes from the 129 strain
Genetic Background:
C57BL/6 Background Origin:
The TSG-p53® mouse was developed in the laboratory of Lawrence A. Donehower and Allan Bradley at the Baylor College of Medicine. The model was created by targeting the Trp53 gene in AB1 ES cells and injecting the targeted cells into C57BL/6 blastocysts. Resultant chimeras were backcrossed to C57BL/6J for two generations (N2). Taconic received stock in 1991. The mice were backcrossed to N3 for caesarean derivation and to N4 immediately after derivation. In 1995, backcrossing of the N4 heterozygote to C57BL/6NTac mice recommenced at Taconic and continued to twelve generations (N12). The line was embryo transfer derived in 1998. Heterozygous and homozygous mice are maintained at N12 through mating of homozygous male mice with heterozygous females. Availability:
Available for immediate cryorecovery Genetics:
Wild type for Nnt mutation Color:
Black Species:
Mouse Initial Publication:
Donehower LA, Harvey M, Slagle BL, McArthur MJ, Montgomery CA, Jr, Butel JS, Bradley A. (1992)
Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumors.
Nature, 356:215-221.
