IMPC phenotypes (gene matching)
STOCK Nox4tm1.2Hwsc Tg(Myh11-icre/ERT2)1Soff/Orl
| Status | Available to order |
| EMMA ID | EM:11553 |
| International strain name | STOCK Nox4tm1.2Hwsc Tg(Myh11-icre/ERT2)1Soff/Orl |
| Alternative name | C57BL/6-Tg(SMMHC-iCre)(NOX4FF) |
| Strain type | Targeted Mutant Strains : Conditional mutation |
| Allele/Transgene symbol | Nox4tm1.2Hwsc, Tg(Myh11-cre/ERT2)1Soff |
| Gene/Transgene symbol | Nox4, Tg(Myh11-cre/ERT2)1Soff |
Information from provider
| Provider | Harald Schmidt |
| Provider affiliation | Department of Pharmacology & Personalised Medicine, Maastricht University |
| Genetic information | The Nox4 gene is flanked by cre-lox sites around exons 14 and 15; cre-loxP technology, type 1 mutation for conditional knock-outs. These mice were crossed with inducible Myh11-icre/ERT2 (SMMHC-CreERT2) mice to get specific Nox4 deletion in smooth muscle cells. |
| Phenotypic information | Homozygous:No spontaneous phenotype.Heterozygous:No spontaneous phenotype. |
| Breeding history | To generate smooth muscle cell-specific Nox4 knock-out (sNOX4 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 smooth muscle cell specific Myh11 (SMMHC) promotor. As the cre transgene is located on the X chromosome, all males used for this breeding were hemizygous for the cre transgene (cre+/y). During breeding, only males that bear the cre transgene were selected for future breeding rounds, while females were not allowed to bear the cre transgene. Deletion of Nox4 in smooth muscle cells needs to be induced using tamoxifen. |
| 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 | heterozygous C57BL/6, wild-type C57BL/6 |
| 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