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Previous work revealed that functional deficiency in microglia is associated with much more severe deposition of amyloid plaques in AD mouse models, indicating a protective role of microglia in AD (Zhang et al., 2007).
Loss of Sun1 rescues the phenotype in mouse models, indicating that SUN1 accumulation is a common pathogenic event in laminopathies.
This is based on paradoxical observations made in tumor patients as well as mouse models indicating that apoptosis can indeed drive tumor formation, at least under certain circumstances.
(8, 9) Further, experimentally induced thrombocytopenia and antiplatelet agents decrease the rate of lung metastasis in mouse models, indicating the requirement for platelets in the formation of hematogenous metastasis.
In combination with a Tp53 homozygous deletion, rapid development of MBs occurred in all three mouse models, indicating that both defective NHEJ and homologous recombination (HR) DNA repair pathways predispose the developing cerebellum to MB initiation.
Importantly, p53 deficiency rescues both the stem cell defects and skin hyperpigmentation, as well as mouse survival, in both mouse models, indicating that the severe skin defects associated with TRF1 and TPP1 abrogation are mediated by p53.
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However, the high degree of growth retardation and peri-natal mortality in IGF-I deficient mouse models indicates that it plays a critical role during this time.
Results from SMA mouse models indicate ISIS-SMNRx had a significant effect on functional and histological measures of neuromuscular health when delivered to the CNS.
However, recent findings in preclinical mouse models indicate that infusion of T-cells directed against tumor-associated auto-antigens can be associated with higher 'on target' toxicity than was anticipated on the basis of anti-tumor vaccination studies.
Together, our observations in these two mouse models indicate that a B cell response is required for the development of granulomas early in Schistosoma infection.
Studies conducted in mutant SOD1 transgenic mouse models indicate that loss of synaptic connections, leading to nerve retraction, are early events in development of pathological phenotypes [35] [37].
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