Knockout mouse studies suggest that ablation of one of the several K6 genes can be tolerated owing to compensatory expression of the others.
Recent in vivo mouse studies suggest that WNT7A is an inducer of ovarian cancer growth [ 19].
In addition, recent data from mouse studies suggest that BPA alters gene expression in the placenta (Susiarjo et al. 2013).
Initial data from mouse studies suggest that prion protein is required for synaptic transmission and mice lacking PrPC show reduced excitatory and inhibitory synaptic currents.
On first examination, however, these mouse studies suggest that exposure to airborne mold toxins may adversely affect people's ability to smell.
(Kane, et al, unpublished data, 2014) The transgenic mouse studies suggest that APP signaling can be manipulated to inhibit AD pathophysiology.
Mouse studies suggest that one of the genes, MAP/microtubule affinity-regulating kinase 2 (MARK2), plays a role in maintenance of immune system homeostasis and prevention of autoimmunity [ 56].
Knockout mouse studies suggest that Rif plays no critical functions in platelets, likely due to functional overlap with other Rho GTPases.
While these mouse studies suggest that GLI3 negatively regulates HH signaling in the placenta and fetal growth, which contrasts with the positive regulation suggested by our findings, this may be explained by sex- or species-specific differences or compensatory mechanisms.
Intriguing data from mouse studies suggest that hepcidin might play a role in modulating clinical malaria (Wang et al., 2011, Portugal et al., 2011), but we are not aware of any previous studies that have investigated this possibility in humans.
