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#151520

CDH5(PAC)CreERT2 Mouse

Cat. #151520

CDH5(PAC)CreERT2 Mouse

Cat. #: 151520

Sub-type: Mouse

Availability: 8-10 weeks

Disease: Cancer

Model: Conditional KO

This fee is applicable only for non-profit organisations. If you are a for-profit organisation or a researcher working on commercially-sponsored academic research, you will need to contact our licensing team for a commercial use license.

Contributor

Inventor: Ralf H. Adams

Institute: Cancer Research UK, London Research Institute: Lincoln's Inn Fields

Tool Details
Handling
Target Details
References

Tool Details

*FOR RESEARCH USE ONLY (for other uses, please contact the licensing team)

  • Tool name: CDH5(PAC)CreERT2 Mouse
  • Research fields: Cancer;Developmental biology;Genetics;Neurobiology;Tissue-specific biology
  • Tool sub type: Mouse
  • Disease: Cancer
  • Model: Conditional KO
  • Conditional: Yes
  • Conditional description: Conditional Cre-ERT2 expression under Cdh5(PAC) promoter in endothelial cells; inducible Cre activity by treatment with hormone (tamoxifen), inducing translocation of Cre-ERT2 to nucleus.
  • Description: Cdh5(PAC)-CreERT2 enable efficient inducible conditional recombinase expression in embryonic and adult endothelial cells (tissue-specific loxP knockout/knockin/transgene). The Cdh5(PAC)-CreERT2 mouse is an ideal tool in the study of gene function in angiogenesis, atherosclerosis and neovascularisation.
  • Genetic background: A Cdh5(PAC)-CreERT2 transgene vector, containing a genomic Cdh5(PAC) promoter fragment fused to a CreERT2 cDNA, was injected into fertilised embryos (C57BL/6 or FVB/N). Founder lines were back-crossed to establish mice heterozygous for the Cdh5(PAC)-CreERT2 transgene.
  • Phenotype: The Cdh5(PAC)-CreERT2 mouse exhibits tissue-specific expression of an inducible Cre-ERT2 fusion protein, enabling tamoxifen-induced Cre recombinase activity in vascular endothelial cells.
  • Zygosity: Heterozygous
  • Production details: A Cdh5(PAC)-CreERT2 transgene vector, containing a genomic Cdh5(PAC) promoter fragment fused to a CreERT2 cDNA, was injected into fertilised embryos (C57BL/6 or FVB/N). Founder lines were back-crossed to establish mice heterozygous for the Cdh5(PAC)-CreERT2 transgene.
  • Additional notes: The Cdh5(PAC)-CreERT2 mouse exhibits tissue-specific expression of an inducible Cre-ERT2 fusion protein, enabling tamoxifen-induced Cre recombinase activity in vascular endothelial cells. 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 vascular endothelial cells. Non-induced Cdh5(PAC)-CreERT2 mice demonstrate no Cre recombinase activity, while tamoxifen-induced Cdh5(PAC)-CreERT2 mice demonstrate high penetrance in vascular endothelial cells (95%+).

Handling

  • Shipping conditions: Embryo/Spermatoza- Dry Ice

Target Details

  • Target: Estrogen receptor (ERT2) under the vascular endothelial cadherin (Cdh5(PAC)) promoter.

References

  • Machi et al. 2024. Front Cell Div Biol. 12:1-15. DoI: 10.3389/fcell.2024.1407097.
  • Brart et al. 2011. J Exp Med. 208(6):1267-78. PMID: 21576386.
  • Lipid phosphate phosphatase 3 enables efficient thymic egress.
  • Luna-Zurita et al. 2010. J Clin Invest. 120(10):3493-507. PMID: 20890042.
  • Pitulescu et al. 2010. Nat Protoc. 5(9):1518-34. PMID: 20725067.
  • Robson et al. 2010. Dev Dyn. 239(9):2435-42. PMID: 20652948.
  • Integration of a Notch-dependent mesenchymal gene program and Bmp2-driven cell invasiveness regulates murine cardiac valve formation.
  • The TGF type II receptor plays a critical role in the endothelial cells during cardiac development.
  • Inducible gene targeting in the neonatal vasculature and analysis of retinal angiogenesis in mice.
  • Wang et al. 2010. Nature. 465(7297):483-6. PMID: 20445537.
  • Ephrin-B2 controls VEGF-induced angiogenesis and lymphangiogenesis.
  • Mahmoud et al. 2010. Circ Res. 106(8):1425-33. PMID: 20224041.
  • Pathogenesis of arteriovenous malformations in the absence of endoglin.
  • Bazigou et al. 2009. Dev Cell. 17(2):175-86. PMID: 19686679.
  • Integrin-alpha9 is required for fibronectin matrix assembly during lymphatic valve morphogenesis.
  • Benedito et al. 2009. Cell. 137(6):1124-35. PMID: 19524514.
  • The notch ligands Dll4 and Jagged1 have opposing effects on angiogenesis.
  • Srensen et al. 2009. Blood. 113(22):5680-8. PMID: 19144989.
  • DLL1-mediated Notch activation regulates endothelial identity in mouse fetal arteries.

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