Consistent with this evidence, we have found that fibroblasts isolated from aged iLID mice show increased sensitivity to peroxide, as reflected by increased levels of cleaved PARP.
Grx1 knockout mice show increased cellular protein S-glutathionylation42, and Grx2 knockout increases sensitivity to oxidative stress in mouse lens epithelial cells43.
Indeed, A2A receptor knockout mice show increased D2R levels in striatum;48 though we cannot necessarily equate the chronic state of a knockout with the effects from acute caffeine exposure.
RGS9 knockout (KO) mice show increased psychostimulant-induced behavioral sensitization, as well as exhibit higher body weights and greater fat accumulation compared to wild-type (WT) littermates.
Here we show that pFn-deficient mice show increased neuronal apoptosis and larger infarction areas following transient focal cerebral ischemia.
The phenotypes of heterozygous CBP-deficient mice show increased insulin sensitivity and glucose tolerance despite prominent lipodystrophy of white adipose tissue (Yamauchi et al., 2002).
Additionally, and consistent with a calorie restricted metabolism, Eps8 knockout mice show increased lifespan.
The FXR-knockout mice show increased bile acids and liver injury [24].
Thus, it appears as if antigen-sensitized mice show increased CD4 T-lymphocyte infiltration into antigen-containing mesenteric adipose tissues.
We previously observed that female, but not male, California mice show increased glucocorticoid secretion following aggressive interactions [18].
MyD88-deficient mice show increased proliferation in the intestinal epithelium [6], which is similar to our TNFR1KO/TAK1IEKO mice.
