When the researchers knocked out the gene for Npas4, they found that mice could not remember their fearful conditioning.
Supplementary Figure 3 Fear memory deficits of ZI TetTox-injected mice could not be explained by reduced foot shock responses or freezing expression.
Thus, although physiological estrogen levels in young ROP Os/+ mice could not prevent the development of glomerulosclerosis, estrogen deficiency accelerated the progression of glomerular scarring in this mouse strain.
Stopping the gene from producing the particular molecule after neural development resulted in mice that, unlike normal mice, could not learn how to get out of a maze after being placed in it day after day.
The approach used in the mice could not be readily applied to humans as it would require embryos to be genetically manipulated, but the Salk team believe the same genes could be targeted with drugs.
Similarly, Sesn2−/− mice could not downregulate hepatic protein synthesis upon 24 h of Tm treatment or 2 months of HFD feeding (Fig. 2o r and Supplementary Fig. 3d g) in contrast to wild-type (WT) mice8,15.
The mice could not only sense the presence of light, but they also responded to a moving black-and-white pattern, suggesting that they could distinguish objects of a certain size.
Defective mucosal priming in male mice could not be overcome by multiple mucosal immunizations.
After iohexol injection (II), the vascular system of the experimental mice could not be imaged.
Given the multiple differences between mice and men, it was once thought that mice could not be used to model atherosclerosis, principally a human disease.
Spleen cells from PG490-88-treated mice could not respond to the host antigens measured by a popliteal lymph node weight gain assay.
