This was indeed achieved, BUT, this mouse did not prove to be a good model for sickle cell disease . It turns out that the human β-globin protein does not complex well with the mouse α- globin protein ( α M ) and so the cloned gene encoding the human α- globin protein ( α H ) was introduced into fertilized mouse eggs to create a new transgenic mouse line, which was then mated with the β S H transgenic mouse to produce a mouse expressing both β S H and α H human proteins. Note that the α H gene is almost certain to integrate into different location than the β S H gene did, and probably in a different chromosome. These alleles will therefore sort independently when the two transgenic mouse lines are bred together. The strong expectation was that the presence of the α H α H β S H β S H hemoglobin tetramer in mouse RBCs would lead to the precipitation of fibers and the sickling of the mouse RBCs. However, much to the disappointment of the research teams involved, this was simply not the case. It turns out that the presence of the normal mouse hemoglobin proteins is enough
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