This may also explain why high TSLP levels in fetal or neonatal Notch mutant mice cause a B-LPD [13], while the effect on B cells in adult mice is less dramatic.
Consistent with the uptake defect, proteoglycan undersulfation was observed also in the growth plate of homozygous mutant mice, causing altered histomorphometric parameters, reduced chondrocyte proliferation, and altered Ihh signaling pathway [6].
Moreover, accumulation of SM and its derivative sphingosine also occurs at the presynaptic membranes of mutant mice causing alterations in synaptic vesicle docking and presynaptic plasticity events (Camoletto et al, 2009).
Similarly, the D1CT mutant mouse, caused by transgenic potentiation of D1-associated brain circuits, shows OCD-like persistence of grooming, as well as persistence of other behaviors such as digging, climbing, and tics [ 3, 53- 57].
For example, the ability to complete syntactic grooming chains is impaired in several types of mutant mouse, caused by either a knockout of D1 dopamine receptors [ 41], or by a Weaver gene mutation that alters the nigrostriatal dopamine system [ 65, 66].
Consistently, Nakanishi et al. [ 41] have reported very recently that genetic deletion of mPGES-1 in Apc-mutant mice caused marked and persistent suppression of intestinal cancer growth in association with a disorganized vascular pattern.
These results demonstrate that the decreased fibrosis seen in mutant mice is caused directly by the increase in IL-10.
The POF in these mutant mice is caused by a similar overactivation of the follicular pool, which is followed by follicular depletion.
It remains to be determined whether acetaldehyde-mediated toxicity in FA mutant mice is caused by a specific lesion that needs to be repaired by the FA pathway.
