- decreased susceptibility to autoimmune diabetes / MGI
- periinsulitis / MGI
- decreased physiological sensitivity to xenobiotic / MGI
- decreased hematocrit / MGI
- abnormal liver physiology / MGI
- abnormal T cell differentiation / MGI
- abnormal cytokine secretion / MGI
- increased autoantibody level / MGI
- decreased susceptibility to parasitic infection / MGI
FVB/N(Cg)-H2b Tg(KRT14-HPV16)wt1Dh/Orl
Status | Under development - register interest |
EMMA ID | EM:15289 |
International strain name | FVB/N(Cg)-H2b Tg(KRT14-HPV16)wt1Dh/Orl |
Alternative name | Tg(KRT14-HPV16)wt1Dh |
Strain type | Other |
Allele/Transgene symbol | H2b, |
Gene/Transgene symbol | H2 |
Information from provider
Provider | Douglas Hanahan |
Provider affiliation | SV, EPFL/ISREC/Ludwig Lausanne |
Genetic information | The transgene is composed of 2 kb of the human K14 promoter/enhancer, regulating expression of the entire early region of HPV16. |
Phenotypic information | Homozygous:NAHeterozygous:During development the mice develop skin hyperplasia (ear) at 1 month of age, considered as DG1 in Switzerland for the animal experimentation criteria. Later the severity evolves, and the mice present skin dysplasia (3 months of age, DG1) followed by skin pruritus and ulcers (6 months of age, DG2, max degree at EPFL Lausanne). Finally, the mice develop some spontaneous skin cancer in 21% of mice between 8-12 months (DG3, not reached at EPFL Lausanne; Coussens et al., Am J Pathol. 1996,149(6):1899-917 - PMID:8952526) |
Breeding history | The K14HPV16/H2b line was generated by crossing K14HPV16-FVB/N (H2q) mice with C57BL/6 (H2b) mice to introduce the entire H2b locus, followed by backcrossing to FVB/N to render the mice congenic for H2b but otherwise genetically FVB/N. F1 mice were backcrossed for 11 generations to FVB/N, selecting for the H2b locus in every generation by flow cytometry analyses of H2Kb and H2Db. Afterwards, mice were intercrossed to generate homozygous H2b mice, expressing H2Kb and H2Db, but not H2Kq and H2D/Lq. The strain should be regarded as a double mutant strain as it carries the Tg(KRT14-HPV16)wt1Dh transgene and the H2b mutation inserted by previous backcrossing with C57BL/6 to FVB. The strain FVB.Cg-Tg(KRT14-HPV16)wt1Dh/Nci available through the NCI mouse repository (https://www.findmice.org/summary?gaccid=MGI:3047406) corresponds to our K14HPV16 old model with a full FVB/N background. As explained above and in Galliverti et al. (Cancer Immunol Res. 2018, 2020), our mice have been crossed with C57BL/6 mice to introduce the H2b locus. |
References | None available |
Homozygous fertile | not known |
Homozygous viable | not known |
Homozygous matings required | yes |
Immunocompromised | no |
Information from EMMA
Archiving centre | Institut de Transgenose, INTRAGENE, Orléans, France |
Animals used for archiving | heterozygous FVB/N, wild-type FVB/N |
Stage of embryos | 2-cell |
Disease and phenotype information
MGI phenotypes (allele matching)
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