IMPC phenotypes (gene matching)
STOCK Nox4tm1.2Hwsc Tg(Tek-cre)1Ywa/Orl
| Status | Available to order |
| EMMA ID | EM:11552 |
| 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, wild-type C57BL/6N |
| 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