- Contains a targeted mutation of Cdkn2a (Ink4a/Arf) which introduced LoxP sites upstream of exon 2 and downstream of exon 3.
- Cross with the tissue-specific Cre of your choice to develop a tumor model
- The cell cycle inhibitory protein Cdkn2a is frequently disrupted in various types of human cancer, and germline mutations of this locus can confer susceptibility to melanoma and other tumors.
- After deletion of the gene via crossing to a tissue-specific Cre line, mice can develop tumors, giving rise to various sarcomas, carcinomas, lymphomas, and metastatic melanoma
Genetic Background: C57BL/6 Background
Origin: The Floxed Ink4a/Arf Mouse was developed in 2001 in the laboratory of Dr. Anton Berns of the Netherlands Cancer Institute (NKI). The Cdkn2a mutation was generated by insertion of loxP sites 1 kb upstream of Ink4a exon 2 and 1.5 kb downstream of exon 3. Targeted IB10 (129/Ola) embryonic stem cells were injected into C57BL/6 blastocysts and resulting chimeras were crossed with FVB/N mice. Sibling progeny were crossed to generate Cdkn2a homozygous floxed mice. The line was backcrossed to C57BL/6/J. Taconic received stock in 2011. The line was derived by embryo transfer and was maintained by incrossing mice homozygous for the floxed allele.
Krimpenfort P, Quon KC, Mooi WJ, Loonstra A, Berns A. (2001) Loss of p16Ink4a confers susceptibility to metastatic melanoma in mice. Nature. 413(6851):83-6