Loss of AP3 leads to hippocampal granule deficiency in mice deficient in this component [55].
Supporting this theory, mice lacking another component of the machinery, the 5HT1B receptor, also show defects in eye-specific segregation in the LGN and SC (Upton et al, 1999).
Indeed, mice lacking components of this complex or in which laminin-dystroglycan interaction is disrupted show a delayed onset of brain edema due to a redistribution of AQP4 away from astrocyte endfeet.
Mammary tumours arising in mice overexpressing components of this pathway contain cells of both basal/myoepithelial and luminal phenotypes, suggesting an origin from a common precursor [ 60].
Similarly to the reduced startle response, this phenotype was observed at reduced penetrance (15 of 58 backcross mice), and each component of the phenotype was not always observed in the same mice.
Their group found that the dysregulation of complement in mice (component 5 (C6), C6 or the complement regulatory protein (CD59a) proved to be key factors in the onset and pathogenesis of OA [ 8].
Interestingly, in the Meig1-deficient mice, the major component, α-tubulin is still present and labels the manchette structure.
A system that facilitates navigating on a display, comprising: a mouse engine component that detects a location; and an interface component that integrates the mouse engine into a handheld communication device.
Bumbaca et al. reported that a humanized mAb (hLD1.vB) directed against fibroblast growth factor receptor (FGFR) 4 exhibited specific binding to mouse complement component 3 (C3), leading to accelerated clearance and limited efficacy in mice (Bumbaca et al., 2011).
In line with the above evidence, anthracyclines and other chemotherapy agents cannot induce immunogenic cell death in mice lacking components of NLRP3 inflammasome including ASC, NLRP3, and Caspase-1 (Ghiringhelli et al., 2009).
