Bmx Cre ERT2 Mouse
Invented by Prof Ralf H. Adams from Max Planck Society
Invented at Cancer Research UK London Research Institute: Lincoln's Inn Fields
- Datasheet
- References (8)
- Inventor Info
Info
| Catalogue Number | 151454 |
| Antigen/Gene or Protein Targets | BMX, CreERT2 |
| Disease Keywords | Cancer; angiogenesis; |
| Relevance |
The estragen receptor (ERT2) under the Bone marrow x (Bmx) promoter (Bmx-Cre-ERT2) mouse exhibits tissue-specific expression of an inducible Cre-ERT2 fusion protein, enabling tamoxifen-induced Cre recombinase activity in arterial endothelial cells. The Bmx-Cre-ERT2 mouse is an ideal tool in the study of gene function in angiogenesis, atherosclerosis and neovascularisation. Administration of tamoxifen induces nuclear translocation of the Cre-ERT2 fusion protein, and subsequent Cre recombinase activity, allowing knockout/knockin/transgene studies of loxP flanked genes in endothelial cells. Non-induced Bmx-Cre-ERT2 mice demonstrate no Cre recombinase activity, while tamoxifen-induced Bmx-Cre-ERT2 mice demonstrate high penetrance in endothelial cells (95%+), significantly higher than existing endothelial Cre models currently available. |
| Production Details | A Bmx-Cre-ERT2 transgene vector, containing a genomic VECad promoter fragment fused to a Cre-ERT2 cDNA, was injected into fertilised embryos (C57BL/6 or FVB/N). Founder lines were back-crossed to establish mice heterozygous for the Bmx-Cre-ERT2 transgene. |
| Conditional | Yes |
| Conditional Description | Conditional Cre-ERT2 expression under Bmx promoter enabling tissue-specific recombinase in arterial endothelial cells; inducible Cre activity by treatment with hormone (tamoxifen) enabling inducible translocation of Cre-ERT2 to nucleus. |
| Mouse Genetic Background/Cross History | C57BL/6J (n=5) |
| Zygosity | Heterozygous |
| Research Area | Cardiovascular, Developmental Biology, Genetic Studies Tools, Immunology, Neurobiology |
References: 8 entries
Murphy et al. 2014. Proc Natl Acad Sci U S A. 111(50):18007-12. PMID: 25468970.
Constitutively active Notch4 receptor elicits brain arteriovenous malformations through enlargement of capillary-like vessels.
Europe PMC ID: 25468970
Noels et al. 2014. Arterioscler Thromb Vasc Biol. 34(6):1209-20. PMID: 24723559.
Schober et al. 2014. Nat Med. 20(4):368-76. PMID: 24584117.
Deficiency of endothelial CXCR4 reduces reendothelialization and enhances neointimal hyperplasia after vascular injury in atherosclerosis-prone mice.
Europe PMC ID: 24723559
MicroRNA-126-5p promotes endothelial proliferation and limits atherosclerosis by suppressing Dlk1.
Europe PMC ID: 24584117
Ehling et al. 2013. Development. 140(14):3051-61. PMID: 23785053.
Notch controls retinal blood vessel maturation and quiescence.
Europe PMC ID: 23785053
Add a reference
References: 8 entries
Murphy et al. 2014. Proc Natl Acad Sci U S A. 111(50):18007-12. PMID: 25468970.
Constitutively active Notch4 receptor elicits brain arteriovenous malformations through enlargement of capillary-like vessels.
Noels et al. 2014. Arterioscler Thromb Vasc Biol. 34(6):1209-20. PMID: 24723559.
Schober et al. 2014. Nat Med. 20(4):368-76. PMID: 24584117.
Deficiency of endothelial CXCR4 reduces reendothelialization and enhances neointimal hyperplasia after vascular injury in atherosclerosis-prone mice.
MicroRNA-126-5p promotes endothelial proliferation and limits atherosclerosis by suppressing Dlk1.
Ehling et al. 2013. Development. 140(14):3051-61. PMID: 23785053.
Notch controls retinal blood vessel maturation and quiescence.
Add a reference
