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The COET transgenic mouse line has been described previously [23].
The OPN KO mouse line has been backcrossed into the C57Bl/6J background >10 generations.
Cell death in the hippocampus from single systemic injections of KA in this mouse line has been previously described [2].
Generation of the 5 kb rat Gata4 promoter 1a-GFP transgenic mouse line has been described previously [29].
Cre expression in this mouse line has previously been demonstrated to be specific for vascular and visceral SMCs [28].
A Plxdc1 knockout mouse line has also been analysed and showed no obvious phenotype in the central nervous system (data not shown).
Similar(40)
Studies on the R6/1 model so far have employed mice of either sex, and sex differences in the severity of HD-like symptoms in this mouse line have not been systematically investigated.
Problems with the osterix-cre mouse line have been described.
In preclinical literature, the use of inbred mouse lines has allowed for the examination of ethanol effects across vulnerable and resistant phenotypes.
This phenomenon of failed beta-galactosidase activity in the ZEG mouse lines has been previously described: beta-galactosidase activity was absent in the liver and lungs of ZEG lines, but robust GFP fluorescence was observed following cre-mediated recombination[5].
Specifically, neither of the two independent DUSP6-deficient mouse lines has shown any thymic phenotypes [ 60, 61].
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