Those studies used a mouse model, whereas we investigated primary human tendon tissues and tenocytes, thus our results are more likely to be relevant to human health.
The expression of a CAG repeat transcript from the antisense strand produces a toxic polyQ protein in a mouse model, whereas in HDL2 patients, polyQ proteins could not be detected despite the expression of CAG repeat RNA.
Zhao et al (2007) have shown the necessity of β-catenin for self-renewal of both normal hematopoietic stem cells and CSCs in chronic myeloid leukaemia in a mouse model, whereas more recently, Wang et al (2010) showed that β-catenin activation is necessary for myeloid precursor transformation in a HoxA9/Meis1-transduced model of AML.
In this study, Erb-hRNase and Erb-hcAb did not show toxic effects both in vitro on rat cardiomyocytes and in vivo on a mouse model, whereas trastuzumab was strongly toxic, thus suggesting that EDIA could be safely used for therapeutic applications.
Interestingly, hyperlocomotion is typically associated with positive symptoms in a mouse model of schizophrenia whereas reduced social activity is implicated as a negative symptom of this illness [31] [33].
Interestingly, the Wnt pathway is induced in ASMCs in a mouse model for asthma [ 139], whereas epithelial Fgf10, as well as downstream Notch signaling, has been shown to be implicated in mucous/goblet cell hyperplasia [ 37, 119].
Tian et al. (2004) identified the α1, α2, β1, β2, γ3 and δ subunits in CD4+ T cells from NOD (non-obese diabetic) mice, a mouse model for type 1 diabetes, whereas Bhat et al. (2010) did not identify any of the four subunits (α1, β1, ε, γ2) they examined in CD4+ T cells from EAE mice, the animal model for multiple sclerosis (MS).
More recently, it has been shown that Erb-hcAb does not display the cardiotoxic effects of Trastuzumab in vitro on rat cardiomyocytes and in vivo on a mouse model (Riccio et al, 2009), whereas Trastuzumab was found to be strongly toxic.
S. cerevisiae cells lacking RACK1 are viable whereas in a mouse model RACK1 depletion causes lethality at gastrulation [ 22].
In one in vitro study VEGF receptor-1 Fc suppressed RA synovial endothelial cell proliferation [ 6], whereas in a mouse model of collagen-induced arthritis anti-VEGF antibody reduced the onset of angiogenesis as well as onset and severity of arthritis [ 7, 8].
This may explain why treatment with 22 nt-long cholesterol- or (fluoro) O-methoxyethylphosphorothioate (F/MOE -based antagomirs against miR-21 was successF/MOE -basednt pressure-overloantagomirs cagainstfibrosis in a mouse model (Thum et al, 2011, 2008b), wasreasuccessfultoon of LNA-based 8 nt-long antimiRs did not (prevent et al, 2010).
