Sentence examples for mouse model loss from inspiring English sources

In mouse model, loss of FHL2 markedly decreases intestinal polyp formation induced by activation of the Wnt/β-catenin pathway (C.L., Y.N., F.L., S. Colnot, J. Chen, C. Perret, M.A.B. and Y.W., unpublished data).

In a cardiac-specific knockout mouse model, loss of adult troponin-I was initially compensated for by the fetal isoform.

In a cardiac-specific troponin-I knockout mouse model, loss of troponin-I was compensated for by its fetal isoform up to 15 days of age.

While we did not observe changes in histopathologic pattern as the result of PPAR ligand exposure in the MMTV-neu mouse model, loss of SRC-1 produced increased expression of differentiation markers in these mammary tumors (see below).

Despite evidence of loss of BIK expression in human tumours, in the E μ- Myc transgenic mouse model, loss of BIK was insufficient to accelerate lymphoma onset or increase disease severity.

Furthermore, in a transgenic mouse model, loss of one or both bax allele(s) significantly accelerate c-Myc-dependent lyphomagenesis in a bax gene dosage-dependent manner (Eischen et al, 2001a).

In mouse models loss of PTEN function lead to elevated erbB2 protein levels [38].

In both collagen-induced arthritis and lipopolysaccharide-induced inflammatory bone resorption mouse models, loss of IFN-γ receptor leads to enhanced osteoclast formation and bone destruction [ 16, 18].

In mouse models, loss of TIGAR has been shown to result in a decreased ability to regenerate damaged intestinal epithelium and a restraint on tumour development, both situations where ROS limitation is important.

In these mouse models, loss of E-cadherin results in the translocation of p120 to the cytosol where it regulates anchorage-independent tumor growth and metastasis through p120-dependent activation of Rho-Rock signaling (Derksen et al., 2006; Schackmann et al., 2011).

However, in Huntington's disease and myotonic dystrophy mouse models, loss of MSH3 decreases somatic mutability of very long [CAG/GTC] and [CTG/GAC] alleles, but has no significant effect on germline mutability or directionality biases (van den Broek et al. 2002; Dragileva et al. 2009).