These Arnt knock-out mice exhibit failure in response to hypoxia and to hypoglycaemia. They are suitable for use in applications related to the study of angiogenesis and vasoformation during mammalian embryonic development.
M. Celeste Simon, University of Pennsylvania
Arnt-/- embryonic stem cells fail to activate genes that normally respond to low oxygen tension. They also fail to respond to a decrease in glucose concentration, indicating that ARNT is crucial in the response to hypoxia and to hypoglycaemia. Arnt-/- embryos were not viable past embryonic day 10.5 and showed defective angiogenesis of the yolk sac and branchial arches, stunted development and embryo wasting. The defect in blood vessel formation in Arnt-/- yolk sacs is similar to the angiogenic abnormalities reported for mice deficient in vascular endothelial growth factor or tissue factor.
The exon encoding the basic-helix-loop-helis (bHLH) domain of the murine Arnt gene was disrupted by insertion of the phosphoglycerate kinase (PGK) promoter/neomycin-resistance cDNA.
|Allele Name||targeted mutation 1, M Celeste Simon|
|Allele Type||Targeted (Null/Knockout)|
|Allele Synonym(s)||Arnt-; Arnt(-)|
|Gene Symbol and Name||Arnt, aryl hydrocarbon receptor nuclear translocator|
|Strain of Origin||(129X1/SvJ x 129S1/Sv)F1-Kitl+|
|Molecular Note||A PGK-neomycin resistance cassette was inserted into the exon that encodes the basic-helix-loop-helix domain.|
|Mutations Made By|| |
M. Celeste Simon, University of Pennsylvania
Homozygous mutants are not viable past embryonic day 10.5. The expected coat color is black.
When using the Arnt- mouse strain in a publication, please cite the originating article(s) and include JAX stock #003178 in your Materials and Methods section.
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