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Additional genetic studies, such as the chromosomal deletion of the complete stefin gene cluster mapped on mouse chromosome 16 or the cystatin gene cluster mapped on chromosome 2, would be required to potentially uncover and dissect compensation mechanisms that might be occurring in the mutant mouse model presented here.
Concluding, the human melanoma xenograft scid mouse model presented in this study (i) closely reflects the clinical situation and (ii) underlines the complexity of metastasis formation.
Thus, the mouse model presented here has advantages in respect to investigate the multiplicity and tissue sampling for gene expression analysis.
Interestingly, in the mouse model presented here, we observe slowed pacemaking, yet with little variation between the WT and mutant mice across age.
In conclusion, we have shown that the mouse model presented here can be used to detect activation of ERs by maternally applied BPA and that other estrogens can be detected in living embryos in utero.
The Int6sh transgenic mouse model presented here provides the first and to date only in vivo evidence that the expression of truncated Int6 leads to persistent mammary hyperplasia and increased predisposition to mammary tumors.
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The adenomatous polyposis coli multiple intestinal neoplasia (ApcMin/+) mouse model presents phenotypes reminiscent of Familial Adenomatous Polyposis (FAP) in humans [18], [19].
In both cases, the mouse model presents problems specific to a therapy depending on immune effector cells and their products.
The Cln1 ko mouse model presents with a severe neurodegenerative disease, whereas Cln5 ko mice have a much milder phenotype that progresses more slowly.
In addition, original data from a recently published LQT3 mouse model presenting with atrial fibrillation and increased late Na current showed early afterdepolarizations in the presence of long atrial action potentials.
This mouse model presents progressive tau pathology with the first tau deposits in homozygous mice appearing at 2 months of age and developing until the age of 5 6 months when the mice have to be culled due to their motor phenotype (Allen et al., 2002; Delobel et al., 2008).
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