Tie2-Cre transgenic mice: a new model for endothelial cell-lineage analysis in vivo.

@article{Kisanuki2001Tie2CreTM,
  title={Tie2-Cre transgenic mice: a new model for endothelial cell-lineage analysis in vivo.},
  author={Yaz Y. Kisanuki and Robert E. Hammer and Jun-ichi Miyazaki and S. C. R. Williams and James A. Richardson and Masashi Yanagisawa},
  journal={Developmental biology},
  year={2001},
  volume={230 2},
  pages={
          230-42
        }
}
Endocardial cells are thought to contribute at least in part to the formation of the endocardial cushion mesenchyme. Here, we created Tie2-Cre transgenic mice, in which expression of Cre recombinase is driven by an endothelial-specific promoter/enhancer. To analyze the lineage of Cre expressing cells, we used CAG-CAT-Z transgenic mice, in which expression of lacZ is activated only after Cre-mediated recombination. We detected pan-endothelial expression of the Cre transgene in Tie2-Cre;CAG-CAT-Z… 

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References

SHOWING 1-10 OF 54 REFERENCES

Uniform vascular-endothelial-cell-specific gene expression in both embryonic and adult transgenic mice.

This work describes the identification and characterization of an autonomous endothelial-specific enhancer in the first intron of the mouse TIE2 gene, and identifies a short region critical for enhancer function in vivo that contains putative binding sites for Ets-like transcription factors.

Vascular endothelial cell lineage-specific promoter in transgenic mice.

The first vascular endothelial cell lineage-specific (including angioblastic precursor cells) 1.2 kb promoter in transgenic mice is reported and this system will allow for the putative inducers that exist in vivo but not in vitro to be screened for.

Connexin 43 expression reflects neural crest patterns during cardiovascular development.

The similarities in location of lacZ-expressing cells in the mouse to that of cardiac neural crest cells inThe chick suggest that this mouse is a good model for studying mammalian cardiac Neural crest and that the mammalian cardiac crest performs functions similar to those shown for chick.

Ligand-activated site-specific recombination in mice.

It is reported here that conditional site-specific recombination can be achieved in mice using a new version of the Cre/lox system, and excision of a chromosomally integrated gene flanked by loxP sites can be induced by administration of tamoxifen to these transgenic mice, whereas no excision could be detected in untreated animals.

Cx43 gap junction gene expression and gap junctional communication in mouse neural crest cells.

Observations suggest that gap junctions may play a role in mouse neural crest development, given the recent finding that the Cx43 knockout mice die of defects associated with the outflow tract, a region of the heart in which neural crest cells are required for normal development.

Site-specific recombination of a transgene in fertilized eggs by transient expression of Cre recombinase.

An efficient method of transgene modulation in fertilized eggs has been developed that uses the Cre/loxP recombination system, and should be useful for breeding transgenic lines in which transGene expression leads to sterility or lethality.

Migration of cardiac neural crest cells in Splotch embryos.

Although Pax3 itself is extinguished prior to neural crest populating the heart, derivatives of these precursors contribute to the aorticopulmonary septum, indicating that contrary to prior reports, Pax3 is not required for cardiac neural crest migration.

Promoter traps in embryonic stem cells: a genetic screen to identify and mutate developmental genes in mice.

Intercrossing of heterozygotes from 24 strains that express beta-galactosidase identified 9 strains in which homozygosity leads to an embryonic lethality, suggesting that a substantial proportion of mammalian genes identified by this approach are not essential for development.

A heart segmental defect in the anterior-posterior axis of a transgenic mutant mouse.

The data show that this insertional mutation identifies a new gene locus, hdf (heart defect), on mouse chromosome 13 that may be required for mechanisms that initially establish and/or maintain continued development of the anterior limb of the developing heart.

Cis-acting regulatory sequences governing Wnt-1 expression in the developing mouse CNS.

Transgene expression provides a new tool for the analysis of neural crest development in normal and mutant mouse embryos and is a first step towards addressing how regional cell signaling is established in the mammalian CNS.
...