- 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. Color:
Black Species:
Mouse Initial Publication:
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.
