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.

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.

Typically mice are recovered in 12-16 weeks. Contact Customer Service to place an order or for more information.

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