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ATM-deficient (ATM−/−) mice show progressive bone marrow failure and impaired HSC self-renewal due to an elevated level of reactive oxygen species (ROS) (Ito et al., 2004).
The Naglu deficient mice show progressive deterioration of motor, vision, and hearing functions [8].
Our analyses revealed that mutant mice show progressive muscle weakness starting at approximately 6 months of age.
Supporting a role of Hsc70, CSP and SGT in protein refolding in vivo, CSP deficient mice show progressive degeneration of neuromuscular junctions, Calyx synapses [27] and photoreceptor terminals [28] in early adulthood.
These transgenic mice show progressive tau pathology in both central and peripheral nervous systems (Allen et al., 2002; Delobel et al., 2008; Mellone et al., 2013).
Tsp4 −/− mice show progressive weight loss, atrophy of muscle mass and disrupted packing of collagen fibrils, but they are viable and fertile (Frolova et al., 2010, 2014).
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Although myelination of Schwann cells in the sciatic nerve was normal for two weeks after birth, subsequently, Ndrg1-deficient mice showed progressive muscle weakness, especially in the hind limbs.
Importantly, the engineered mice showed progressive fibrosis in multiple organs including the skeletal muscle.
Furthermore, the ROP- Os/+ mice showed progressive increase in sclerosis score over time (Additional file 1).
In contrast to other reports that several JAK2V617F transgenic mice tend to show polycythemia, our transgenic mice showed progressive anemia.
B−/− mice showed progressive increases in latency to cross the beams and also in hind-limb slips on 5 and 12 mm square beams.
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