General Information

Development

p53 is an oncogene with broad and powerful functions, and more than half of all tumor patients carry p53 mutations. When a gene deletion or mutation results in a loss of p53 activity, cells lose the ability to control their growth and death, leading to immortalization and ultimately cancer.

In order to study the occurrence and development of p53 gene-related cancers and to explore new therapeutic modalities, Vitonda used CRISPR-Cas9-Nickase technology to knock out the coding sequence of exon 3 and onwards (or undergo a code-shifting mutation) in C57BL/6 mice to obtain p53 knockout mice. The first constructed mouse with 82 bp deleted was selected to establish a p53 knockout C57BL/6 mouse line according to the inbred line mating pattern.

Genotype identification information

Fig 1. Genetic assay of p53 KO mice

Wild type: 8244, 46; Heterozygous: 8245, 48, 49; Homozygous: 8250

p53 KO Mice Applications

1. Breast cancer, lymphoma, pancreatic cancer, colorectal cancer and non-small cell lung cancer research

2. Anti-tumor small molecule drug screening

Reference

1. Muller PA, Vousden KH. p53 mutations in cancer. Nat Cell Biol. 2013, 15(1):2-8.

2. Lawrence A. Donehower, Michele Harvey, et al. Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours. Nature. 1992, 356:215–221.