STOCK Tg(tetO-AGTR1,-lacZ)1Aco/Cnbc
| Status | Available to order |
| EMMA ID | EM:04643 |
| Citation information | RRID:IMSR_EM:04643 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 | STOCK Tg(tetO-AGTR1,-lacZ)1Aco/Cnbc |
| Alternative name | ZhAT1Rwt1 |
| Strain type | Transgenic Strains |
| Allele/Transgene symbol | Tg(tetO-AGTR1,-lacZ)1Aco |
| Gene/Transgene symbol | Tg(tetO-AGTR1,-lacZ)1Aco |
Information from provider
| Provider | Justin Ainscough |
| Provider affiliation | Central Biomedical Services, University of Leeds |
| Genetic information | A lacZ reporter gene and the human angiotensin II type 1 receptor are expressed under control of a bidirectional minimal CMV promoter linked to a tet response element (TRE). Gene expression is induced in the presence of a transactivator molecule (tTA or rtTA), and can be regulated by doxycycline. |
| Phenotypic information | No phenotype in uninduced state. Induction of hAT1R expression in adult cardiomyocytes by crossing with alphaMHC tTA transactivator mice causes blood pressure-independent cardiac hypertrophy. Effects of activation in other tissues have not been tested. |
| Breeding history | The line was crossed with FVB transactivator mice and subsequently backcrossed for at least four generations onto C57BL/6. Currently maintained by inbreeding. |
| References |
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| Homozygous fertile | not known |
| Homozygous viable | not known |
| Homozygous matings required | no |
| Immunocompromised | no |
Information from EMMA
| Archiving centre | CNB-CSIC, Centro Nacional de Biotecnologia, Madrid, Spain |
| Animals used for archiving | heterozygous C57BL/6J males |
Literature references
- Angiotensin II type-1 receptor activation in the adult heart causes blood pressure-independent hypertrophy and cardiac dysfunction.;Ainscough Justin F X, Drinkhill Mark J, Sedo Alicia, Turner Neil A, Brooke David A, Balmforth Anthony J, Ball Stephen G, ;2009;Cardiovascular research;81;592-600; 18703536