This corroborated further that liver tumors from these mouse models are indeed molecularly similar and resemble the human HCCs.
Current transgenic or knockout mouse models might indeed provide insights into the early stages of PD (Fleming et al. 2005), allowing us to decipher pathological processes that take place in brain exposed to a PD-causing insult before degeneration of the nigrostriatal system occurs, or before the disease begins elsewhere (Litvan et al. 2007).
The fact that CBA/J x DBA/2 mice develop preeclampsia-like disease with all the accepted pathological changes (hypersensitivity to Ang II, proteinuria and renal glomeruloendotheliosis suggests that this mouse model is indeed an appropriate model of human PE.
The accumulation of β-catenin in our model found after the development of atypical EH following 8 weeks of continuous exposure to E2 alongside other mutations is consistent with previous results seen in human patients, and support the fact that our E2-induced EH mouse model is indeed a representative of human disease.
Indeed, mouse models of age-related BrM lipid deposition based on such manipulations have been reported [85], [86], [87], [88], [89].
Indeed, several mouse models of glioma have causally implicated activated HRas and KRas in glioma formation [6] [8].
This is based on paradoxical observations made in tumor patients as well as mouse models indicating that apoptosis can indeed drive tumor formation, at least under certain circumstances.
Indeed, both mouse models, which shared the same mixed genetic background, were characterized by short lifespan, reduced weight gain, severe megalencephaly and ventricular enlargement, increased cortical thickness, cortical lamination defects, hippocampal alterations, hypomyelination, and spontaneous epilepsy.
Indeed, in mouse models of amyotrophic lateral sclerosis (ALS), where mutant superoxide dismutase-1 (mSOD1) is transgenically overexpressed, both Bax translocation to mitochondria and cytochrome c release are observed as the disease progresses.
