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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].
Both resin-fed and FXR-null mouse models indicate that BAs regulate their own biosynthesis through the FXR-regulated ileal fibroblast growth factor 15. BA flux also influences the daily mRNA levels of multiple BA transporters.
In various other tumor cells, however, checkpoint strength was found to be diminished [5], and recent evidence from mouse models indicate that in cases where such weakening occurs, it can contribute to carcinogenesis ([23] [25] and references in [2]).
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Short telomeres, a hallmark of dyskeratosis congenita, impair tissue stem cell function in mouse models, indicating that a tissue stem cell defect may underlie the pathophysiology of dyskeratosis congenita.
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.
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).
A wealth of evidence obtained using mouse models indicates that CD4+CD25+FOXP3+ regulatory T cells (Treg) maintain peripheral tolerance to self-antigens and also inhibit anti-tumor immune responses.
Transcription analyses of in vitro stress, macrophage infection, and mouse models indicated that virB positively regulates vjbR, a quorum sensing (QS) regulator that functions in a cell-dependent manner.
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