IMPC phenotypes (gene matching)
STOCK Nox4tm1.2Hwsc Tg(Tek-cre)1Ywa/Orl
| Status | Available to order |
| EMMA ID | EM:11552 |
| Citation information | RRID:IMSR_EM:11552 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 Nox4tm1.2Hwsc Tg(Tek-cre)1Ywa/Orl |
| Alternative name | C57BL/6-Tg(Tie2-Cre)(Nox4-FF) |
| Strain type | Transgenic Strains |
| Allele/Transgene symbol | Tg(Tek-cre)1Ywa, Nox4tm1.2Hwsc |
| Gene/Transgene symbol | Tg(Tek-cre)1Ywa, Nox4 |
Information from provider
| Provider | Harald Schmidt |
| Provider affiliation | Department of Pharmacology & Personalised Medicine, Maastricht University |
| Genetic information | The Nox4 gene is flanked by loxP sites around exons 14 and 15; cre-loxP technology, type 1 mutation for conditional knock-outs. These mice were crossed with Tek-cre (Tie2-cre) mice to get a specific Nox4 deletion in endothelial cells. |
| Phenotypic information | Homozygous:No spontaneous phenotype. Decreased infarct size in stroke.Heterozygous:No spontaneous phenotype. |
| Breeding history | To generate endothelial cell-specific Nox4 knock-out (eNOX4 KO) mice, female mice (homozygous for the floxed Nox4 gene) were bred with male mice (C57BL/6 strain background) that express the cre recombinase gene under control of the endothelial-cell specific Tek (Tie2) promoter. As the cre gene is located on the X chromosome, all males used for this breeding were hemizygous for the cre gene (cre+/y). During breeding, only males that bear the cre gene were selected for future breeding rounds, while females were not allowed to bear the cre gene. |
| References |
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| Homozygous fertile | yes |
| Homozygous viable | yes |
| Homozygous matings required | no |
| Immunocompromised | no |
Information from EMMA
| Archiving centre | Institut de Transgenose, INTRAGENE, Orléans, France |
| Animals used for archiving | homozygous C57BL/6N males, wild-type C57BL/6N females |
| Stage of embryos | 2-cell |
Disease and phenotype information
MGI phenotypes (gene matching)
- abnormal lung morphology / MGI
- cardiac hypertrophy / MGI
- abnormal kidney physiology / MGI
- no phenotypic analysis / MGI
- abnormal redox activity / MGI
- decreased neuron apoptosis / MGI
- oxidative stress / MGI
- increased response of heart to induced stress / MGI
- dilated heart / MGI
- abnormal blood-brain barrier function / MGI
- cardiovascular system phenotype / MGI
- cardiac interstitial fibrosis / MGI
- decreased apoptosis / MGI
- decreased cerebral infarction size / MGI
- decreased susceptibility to ischemic brain injury / MGI
- decreased physiological sensitivity to xenobiotic / MGI
- decreased susceptibility to weight loss / MGI
Literature references
- NOX4-dependent neuronal autotoxicity and BBB breakdown explain the superior sensitivity of the brain to ischemic damage.;Casas Ana I, Geuss Eva, Kleikers Pamela W M, Mencl Stine, Herrmann Alexander M, Buendia Izaskun, Egea Javier, Meuth Sven G, Lopez Manuela G, Kleinschnitz Christoph, Schmidt Harald H H W, ;2017;Proceedings of the National Academy of Sciences of the United States of America;114;12315-12320; 29087944