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Subsequently, these mice develop a lymphoproliferative syndrome that culminates with the development of lymphomas displaying features typical of human DLBCL.
Mice deficient in Hspb5 (αB-crystallin) develop normally and are viable [57]; however, these mice develop a skeleton muscle myopathy late in life.
GM-CSF-deficient mice develop a similar pathology to human pulmonary alveolar proteinosis (PAP) [25].
Nf1 heterozygous (Nf1+/-) mice develop a robust neointima that mimics human disease.
The researchers found that the mice develop a hypersensitivity to insulin.
Surprisingly, although the VLCAD−/− mice develop a marked steatosis after 24 h of fasting, the kidneys were fully unaffected as shown by the strong downregulation of lipogenic genes.
Infected mice develop a reliable inflammatory arthritis of the ankle joint with severity that typically peaks around two to three weeks post-infection and then undergoes spontaneous resolution.
Significant amounts of ferritin and iron accumulate in white matter tracts and nuclei, and adult IRP2-deficient mice develop a movement disorder consisting of ataxia, bradykinesia, and tremor.
If the mice develop a tolerance to NY-ESO-1 over time, the therapy may only be a temporary fix, she says.
These mice develop a disease with remarkable similarities to human CLL.
Thus, it is interesting to note that adult Notch mutant mice develop a severe MPD.
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