- increased papilloma incidence / MGI
- increased carcinoma incidence / MGI
- increased incidence of tumors by chemical induction / MGI
- blindness / MGI
- abnormal sperm number / MGI
- testicular atrophy / MGI
- decreased testis weight / MGI
- abnormal retinal photoreceptor morphology / MGI
- microphthalmia / MGI
- abnormal lens morphology / MGI
- abnormal retina morphology / MGI
- increased tumor incidence / MGI
- increased T cell derived lymphoma incidence / MGI
- increased fibrohistocytoma incidence / MGI
- retinal detachment / MGI
- abnormal lens capsule morphology / MGI
- abnormal retinal inner nuclear layer morphology / MGI
- increased incidence of tumors by ionizing radiation induction / MGI
- abnormal retinal ganglion layer morphology / MGI
- vision/eye phenotype / MGI
- abnormal cell physiology / MGI
- primary vitreous hyperplasia / MGI
- increased fibrosarcoma incidence / MGI
- persistent hyperplastic primary vitreous / MGI
- increased fibroblast proliferation / MGI
- increased lymphoma incidence / MGI
- increased metastatic potential / MGI
- increased tumor growth/size / MGI
- increased squamous cell carcinoma incidence / MGI
STOCK Cdkn2atm1Cjs Tg(Cnp-TVA,-lacZ)B8Ubc/Kctt
Status | Available to order |
EMMA ID | EM:04996 |
International strain name | STOCK Cdkn2atm1Cjs Tg(Cnp-TVA,-lacZ)B8Ubc/Kctt |
Alternative name | Ctv-a Arf-/- |
Strain type | Targeted Mutant Strains : Knock-out |
Allele/Transgene symbol | Cdkn2atm1Cjs, |
Gene/Transgene symbol | Cdkn2a |
Information from provider
Provider | Lene Uhrbom |
Provider affiliation | Department of Neuroscience, Uppsala University |
Additional owner | Lene Uhrbom, Uppsala University, Department of Genetics and Pathology, Rudbeck Laboratory, Uppsala, Sweden |
Genetic information | Transgenic construct: pCNPase-TV-A-IRES-lacZ made in FVB/N. Crossed with strain containing targeted deletion p19Arf (exon 1b of the cyclin-dependent kinase inhibitor 2A gene). |
Phenotypic information | Allows for infection of 2',3'-cyclic nucleotide 3' phosphodiesterase (CNPase)-expressing cells by RCAS virus. The deletion of exon 1b in the cyclin-dependent kinase inhibitor 2a gene results in complete loss of p19Arf but not p16Ink4a. |
Breeding history | The TV-A founder mouse was crossed with FVB/N and subsequently intercrossed to establish homozygotes. The p19Arf null mice on C57BL/6 background were previously crossed with another transgenic mouse on FVB/N background. These were crossed with FVB/N for two generations to isolate the p19Arf genotype solely and then intercrossed once to generate p19Arf-/- mice. Following, TV-A transgenic mice were crossed with p19Arf null mice and subsequently F1 progeny were crossed to generate mice homozygous for TV-A and p19Arf deletion. |
References |
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Homozygous fertile | yes |
Homozygous viable | yes |
Homozygous matings required | no |
Immunocompromised | no |
Information from EMMA
Archiving centre | Karolinska Institutet, Stockholm, Sweden |
Animals used for archiving | homozygous , wild-type FVB/N |
Breeding at archiving centre | No breeding. |
Stage of embryos | 2-cell |
Disease and phenotype information
MGI phenotypes (allele matching)
Literature references
- Oligodendrocyte progenitor cells can act as cell of origin for experimental glioma.;Lindberg N, Kastemar M, Olofsson T, Smits A, Uhrbom L, ;2009;Oncogene;28;2266-75; 19421151
- Tumor suppression at the mouse INK4a locus mediated by the alternative reading frame product p19ARF.;Kamijo T, Zindy F, Roussel M F, Quelle D E, Downing J R, Ashmun R A, Grosveld G, Sherr C J, ;1997;Cell;91;649-59; 9393858
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