- abnormal retinal photoreceptor morphology / MGI
- microphthalmia / MGI
- cataract / MGI
- abnormal posterior eye segment morphology / MGI
- abnormal lens development / MGI
- abnormal retinal neuronal layer morphology / MGI
- persistent hyperplastic primary vitreous / MGI
- increased brain tumor incidence / MGI
- extramedullary hematopoiesis / MGI
- abnormal spleen morphology / MGI
- increased tumor incidence / MGI
- increased B cell derived lymphoma incidence / MGI
- increased sarcoma incidence / MGI
- abnormal spleen red pulp morphology / MGI
- abnormal cell cycle / MGI
- increased hemangiosarcoma incidence / MGI
- increased spleen white pulp amount / MGI
- increased cutaneous melanoma incidence / MGI
- increased fibrosarcoma incidence / MGI
- increased fibroblast proliferation / MGI
- abnormal keratinocyte physiology / MGI
- increased squamous cell carcinoma incidence / MGI
- abnormal skin physiology / MGI
- abnormal cell physiology / MGI
- delayed cellular replicative senescence / MGI
- premature death / MGI
- increased lymphoma incidence / MGI
STOCK Cdkn2atm1Rdp Tg(Cnp-TVA,-lacZ)B8Ubc/Kctt
Status | Available to order |
EMMA ID | EM:04997 |
International strain name | STOCK Cdkn2atm1Rdp Tg(Cnp-TVA,-lacZ)B8Ubc/Kctt |
Alternative name | Ctv-a Ink4a-Arf-/- |
Strain type | Targeted Mutant Strains : Knock-out |
Allele/Transgene symbol | Cdkn2atm1Rdp, |
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 p16Ink4a and p19Arf (exons 2 and 3 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 exons 2 and 3 in the cyclin-dependent kinase inhibitor 2a gene results in complete loss of both p16Ink4a and p19Arf. |
Breeding history | The TV-A founder mouse was crossed with FVB/N and subsequently intercrossed to establish homozygotes. The p16Ink4a-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 p16Ink4a-p19Arf genotype solely and then intercrossed once to generate p16Ink4a-p19Arf-/- mice. Following, TV-A transgenic mice were crossed with p16Ink4a-p19Arf null mice and subsequently F1 progeny were crossed to generate mice homozygous for TV-A and p16Ink4a-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 | heterozygous 0, wild-type FVB/N |
Breeding at archiving centre | no breeding at Karolinska Inst. |
Stage of embryos | 2-cell |
Disease and phenotype information
MGI phenotypes (allele matching)
Literature references
- Role of the INK4a locus in tumor suppression and cell mortality.;Serrano M, Lee H, Chin L, Cordon-Cardo C, Beach D, DePinho R A, ;1996;Cell;85;27-37; 8620534
- 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
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