Homozygous mice of the cyclin-dependent kinase inhibitor 1B (Cdkn1b) knock-out (also referred to as p27kip ) exhibit multi-organ hyperplasia and develop pituitary tumors. These mice may be useful in studies of tumorigenesis.
Dr. Matthew Fero, Fred Hutchinson Cancer Research Center
Mice deficient in p27kip are viable and larger than normal littermates, with increased cellularity of all tissues. The thymus and spleen are particularly enlarged. Homozygous (nullizygous) adult mice have a shortened lifespan due to the growth of benign intermediate lobe pituitary tumors. Female mice are infertile, with a follicular phase ovulatory block. Large doses of exogenous gonadotropin induce ovulation, but both implantation and intrauterine embryonic development is impaired. The mice demonstrate haploid-insufficient susceptibility to the development of adenomas in the pituitary, intestine and lung adenomas following exposure to gamma irradiation or chemical carcinogens.
This strain was generated by Dr. Matthew Fero at the Fred Hutchinson Cancer Research Center. The targeting construct contains a neo resistance gene and replaces the entire coding region of the Cdkn1b gene. 129S4/SvJaeSor-derived AK7 ES cells were used and the mutation was subsequently backcrossed to C57BL/6 mice.
|Allele Name||targeted mutation 1, Matthew Fero|
|Allele Type||Targeted (Null/Knockout)|
|Allele Synonym(s)||Cdkln1btm1Mlf; p27-; p27Kip1; p27Kip1-; p27kip1-null|
|Gene Symbol and Name||Cdkn1b, cyclin-dependent kinase inhibitor 1B|
|Strain of Origin||129S4/SvJaeSor|
|Molecular Note||Replacement of the entire coding region of the Cdkn1b gene with a neomycin cassette.|
|Mutations Made By|| |
Dr. Matthew Fero, Fred Hutchinson Cancer Research Center
Homozygote males are fertile, but homozygote females are not. Colony currently maintained by heterozygote X heterozygote matings. Coat color from breeding: Black
When using the p27- mouse strain in a publication, please cite the originating article(s) and include JAX stock #002781 in your Materials and Methods section.
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