- muscle weakness / MGI
- increased body weight / MGI
- female infertility / MGI
- preneoplasia / MGI
- no abnormal phenotype detected / MGI
- increased circulating testosterone level / MGI
- decreased incidence of tumors by chemical induction / MGI
- growth/size/body region phenotype / MGI
- decreased grip strength / MGI
- mortality/aging / MGI
- increased urine major urinary protein level / MGI
B6.129S2(Cg)-Artm1Fcl/Cnbc
| Status | Available to order |
| EMMA ID | EM:06160 |
| Citation information | RRID:IMSR_EM:06160 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 | B6.129S2(Cg)-Artm1Fcl/Cnbc |
| Alternative name | SPARKI (SPecificity-affecting AR KnockIn) |
| Strain type | Targeted Mutant Strains : Knock-in |
| Allele/Transgene symbol | Artm1Fcl |
| Gene/Transgene symbol | Ar |
Information from provider
| Provider | Frank Claessens |
| Provider affiliation | Molecular and Cellular Medicine, Katholieke Universiteit Leuven |
| Genetic information | Germ-line knock-in mouse model in which the second zinc-finger of the androgen receptor was replaced with that of the glucocorticoid receptor, resulting in a chimeric protein that retains its ability to bind classical androgen response elements but is unable to bind selective androgen response elements. |
| Phenotypic information | The reproductive organs of SPARKI (SPecificity-affecting AR KnockIn) males are smaller compared to wild-type animals, and they are also subfertile. The impaired fertility of the male SPARKI mice correlates with the reduced motility of the spermatozoa. |
| Breeding history | The SPARKI mice were backcrossed to a genetic background of >96% C57BL/6 (6 generations). As the mutation is located on the X-chromosome and males are subfertile, the breeding scheme consists of crossing heterozygous females with wild-type males. |
| References |
|
| Homozygous fertile | no |
| Homozygous viable | yes |
| Homozygous matings required | no |
| Immunocompromised | no |
Information from EMMA
| Archiving centre | CNB-CSIC, Centro Nacional de Biotecnologia, Madrid, Spain |
| Animals used for archiving | wild-type C57BL/6J males, heterozygous C57BL/6J females |
| Stage of embryos | 2-cell |
Disease and phenotype information
MGI phenotypes (gene matching)
Literature references
- Loss of androgen receptor binding to selective androgen response elements causes a reproductive phenotype in a knockin mouse model.;Schauwaers Kris, De Gendt Karel, Saunders Philippa T K, Atanassova Nina, Haelens Annemie, Callewaert Leen, Moehren Udo, Swinnen Johannes V, Verhoeven Guido, Verrijdt Guy, Claessens Frank, ;2007;Proceedings of the National Academy of Sciences of the United States of America;104;4961-6; 17360365
- A role for selective androgen response elements in the development of the epididymis and the androgen control of the 5α reductase II gene.;Kerkhofs Stefanie, Dubois Vanessa, De Gendt Karel, Helsen Christine, Clinckemalie Liesbeth, Spans Lien, Schuit Frans, Boonen Steven, Vanderschueren Dirk, Saunders Philippa T K, Verhoeven Guido, Claessens Frank, ;2012;FASEB journal : official publication of the Federation of American Societies for Experimental Biology;26;4360-72; 22798427
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