Here we use chromosome engineering to generate mouse models with gain and loss of a region corresponding to human 1p36.
Over the last few decades, study of cancer in mouse models has gained popularity. Sophisticated genetic manipulation technologies and commercialization of these murine systems have made it possible to generate mice to study human disease.
In recent times, genetically modified mouse models have gained popularity in the study of clinical SAN dysfunction (39, 42).
Mouse models harboring both gain and loss of function in Tcf7l2 do not readily reconcile these differences.
For example, Merchan et al. generated mouse models that allow gain-of-function of Ezh2 in the haematopoietic system [ 17], and we identified a 2.2-fold decrease of Sema3a expression in Ezh2 + mice compared with wild-types (Q-value = 0.05, the limma test [ 25]).
Clinical issue In humans, the protein kinase Cdk5 plays a central role in the progression of many forms of neurodegenerative disease, including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis and others, and this is reflected in mouse models of Cdk5 gain- and loss-of-function.
Given the increasing interest in mouse models of TDP-43 gain or loss of function as models of neurodegenerative diseases, such as ALS animal models [ 70, 71], we believe that the elucidation of the physiological role of TDP-43 in the SC would provide an important contribution.
Mouse models are often used to gain further insight into the pathological mechanisms of joint inflammation as well as for preclinical evaluation of therapeutic agents.
Using the well-established SCID mouse model we could gain a good quality of RNA from the primary tumour, the tumour invasion site and the liver metastases.
In this article, insights gained from mouse models towards the understanding of HD and the design of new therapeutic strategies are discussed.
