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Here we present a four stage mouse model addressing copy number alterations in tumorigenesis.
The use of the mouse-to-mouse model addresses key gaps in our existing knowledge (54) that other transmission-blocking assays cannot, being the only fully in vivo model that measures the impact of an intervention on mosquito-to-vertebrate and vertebrate-to-vertebrate transmission.
Furthermore, a more global view on T2DM has been achieved by involving mouse as well as human data because the available mouse models address specific aspects of the disease and it is unclear, whether these mice have diabetes for the same reason as humans do.
The present study describes the generation of a knock-in mouse model to address the role of type II procollagen (Col2a1) alternative splicing in skeletal development and maintenance.
In this study, we have measured developmental and sex-based differences in hypothalamic kisspeptin expression and distribution in the hpg mouse model, to address questions of the programming role of the HPG axis itself on the kisspeptinergic system.
Therefore, we used tcl1tg mice as a CLL mouse model to address this question.
It is critical to use a specific mouse model to address a particular research question.
We recently generated a mouse model to address the role of Mdm4-S, a short splice variant of Mdm4.
We turned to the well-characterized tetracycline inducible rTg4510 mouse model to address the gaps in our knowledge about the role of tau in BBB damage.
We have used a well-characterized transgenic mouse model to address the relationship in vivo between human NAT1/mouse Nand and folate metabolism, and describe phenotypic effects of deleting the mouse Nat2 gene in mice.
Since many of the histological and molecular hallmarks of psoriasis are reproduced in mice with epidermal deletion of JunB and Jun, we employed this mouse model to address the role of immunocytes during disease development.
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