These Alox12 knock-out mice exhibit a hyper-responsiveness to adenosine diphosphate (ADP) -induced platelet aggregation and may be is useful in studies of thromboembolism.Read More +
Mice that are homozygous null for the Alox12 gene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No Alox12 protein product or enzyme activity is detected in platelets derived from homozygous null animals. Platelets exhibit a hyperresponsiveness to ADP-induced aggregation. Studies examining basal transepidermal water loss indicate that null animals exhibit greater water loss through the skin when compared to control animals.
A targeting vector containing a neomycin cassette was used to disrupt exon 8. The construct was electroporated into 129S2/SvPas-derived D3H embryonic stem cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts and chimeric animals were obtained.
|Allele Name||targeted mutation 1, Colin D Funk|
|Allele Type||Targeted (Null/Knockout)|
|Allele Synonym(s)||12/15LO KO; P-12LO-|
|Gene Symbol and Name||Alox12, arachidonate 12-lipoxygenase|
|Strain of Origin||129S2/SvPas|
|Molecular Note||A neomycin resistance cassette replaced exon 8. Western blot analysis did not detect the encoded protein in homozygous mutant platelets.|
This strain originated on a B6;129S2 background and has been backcrossed to C57BL/6J for eight generations before being made homozygous.Coat color expected from breeding:Black
When using the P-12LO- mouse strain in a publication, please cite the originating article(s) and include JAX stock #004042 in your Materials and Methods section.