Although ample in vitro and nude mouse model evidence exists that dysregulated MUC4 can potentially play a role in human tumors, evidence that it does so has been harder to obtain.
What is notable in RTT mouse models is evidence of construct validity beyond the genetic mutations themselves, including neurochemical abnormalities found in individuals with RTT.
Mouse models show evidence of oxidative stress, particularly in white matter (Hagemann et al., 2006), and the cell culture models display increased sensitivity to camptothecin-induced apoptosis and H2O2-induced cell death (Tang and Goldman, 2006; Cho and Messing, 2009).
Recent knockout mouse models provided evidence that TH entry into the brain is largely dependent on two TH transporters, monocarboxylate transporter 8 (MCT8) and organic anion-transporting polypeptide 1c1 (OATP1c1) [ 4– 9].
Finally, mouse models provide evidences that this region is associated with schizophrenia.
In the synapsin-Cre-based Tsc1 mouse model, no evidence of astrogliosis was observed (37).
Each of these vaccine formulations enhances immune responses and leads to protection in a mouse model without evidence of vaccine-enhanced disease.
Data obtained from this mouse model provide evidence for an association between depression and altered circadian rhythms at the genetic level and point towards a role for Cry2.
Our genetically modified (Nkx Cre Pten +/− Spry2 +/− ) mouse model showed evidence of PI3K/AKT hyper-activation, without MAPK activation, in the prostate (Fig 6C) and enhanced capability to develop metastatic nodal disease by 12 months.
We do not know whether this increased release plays a role in the cascade of events leading to CM, but recent analyses in a mouse model provided evidence for both pro-inflammatory and pro-coagulant effects of MP (Combes et al., 2005), suggesting that MP could potentially enhance the severity of intracerebral pathology.
