B6.129S4-Apoa2tm1Bres/Orl
| Status | Available to order |
| EMMA ID | EM:14982 |
| Citation information | RRID:IMSR_EM:14982 Research Resource Identifiers (RRID) are persistent unique ID numbers assigned to help researchers cite key resources (e.g. antibodies, model organisms and software projects) in the biomedical literature to improve transparency and reproducibility in research. See https://www.rrids.org/ for more information. |
| International strain name | B6.129S4-Apoa2tm1Bres/Orl |
| Alternative name | murine apoAII -/- |
| Strain type | Targeted Mutant Strains : Knock-out |
| Allele/Transgene symbol | Apoa2tm1Bres |
| Gene/Transgene symbol | Apoa2 |
Information from provider
| Provider | Jan L Breslow |
| Provider affiliation | Rockefeller University |
| Genetic information | Weng & Breslow studied the role of Apoa2 by deleting the gene in mice by homologous recombination (Weng W. & Breslow J.L., Proc. Natl. Acad. Sci. USA 1996, 93:14788-14794). The targeting strategy almost replaced the entire Apoa2 gene with an intact neo gene. The neo gene encodes for the neomycin resistance and allows the survival of ES cells transfected with the targeting vector in a culture medium containing neomycin. Embryonic stem cells of J1 type (agouti coat color) were microinjected into C57BL/6J and BALB/cJ host blastocysts and produced chimeric mice containing 50-100% agouti coat color contributed by the ES cell line. Professor J.L. Breslow generously gave us these mice. In our animal facility at the Centre de Recherche des Cordeliers in Paris we performed more than 10 backcrosses to the C57BL/6J background with black coat color and then crossbred each amyloidogenic transgenic line (F, K and Y), already in the C57BL/6J background, with the Apoa2-/- mice. |
| Phenotypic information | Homozygous:Homozygous knock-out mice (Apoa2-/-) displayed drastically decreased HDL levels, showing the importance of Apoa2 in the formation and metabolism of HDL.Heterozygous:Heterozygous mice (Apoa2+/-) displayed moderately decreased HDL levels. |
| Breeding history | In our animal facility at the Centre de Recherche des Cordeliers in Paris we performed more than 10 backcrosses to C57BL/6J background with black coat colour. We first obtained heterozygous Apoa2 +/- mice which were then mated to obtain homozygous Apoa2 -/- mice. Currently, male and female Apoa2 knock-out mice are mated to maintain the Apoa2 knock-out mutation on the C57BL/6J background. We have cross-bred with the Apoa2 -/- mice each of three distinct amyloidogenic transgenic lines (F, K and Y, each expressing the human STOP78SER-APOA2 mutant; Chabert M et al., 2019, PubMed ID 31200944), already backcrossed to the C57BL/6J background (EMMA strain IDs EM:14979, EM:14980, EM:14981). |
| References |
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| Homozygous fertile | yes |
| Homozygous viable | yes |
| Homozygous matings required | yes |
| Immunocompromised | not known |
Information from EMMA
| Archiving centre | CNRS-TAAM – Typing and Archiving of Animal Models, Orléans, France |
| Animals used for archiving | homozygous C57BL/6J males |
Disease and phenotype information
Orphanet associated rare diseases, based on orthologous gene matching
- AApoAII amyloidosis / Orphanet_238269
Literature references
- Dramatically decreased high density lipoprotein cholesterol, increased remnant clearance, and insulin hypersensitivity in apolipoprotein A-II knockout mice suggest a complex role for apolipoprotein A-II in atherosclerosis susceptibility.;Weng W, Breslow J L, ;1996;Proceedings of the National Academy of Sciences of the United States of America;93;14788-94; 8962133