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In 129 strain mice, inactivation of Dnd1, as in the 129-Ter mouse strain, causes loss of germ cells and in addition, development of testicular germ cell tumors [3].
A mutation found in the lpr (lymphoproliferation) mouse strain causes defective expression of CD95.
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However, ablation of MAPK14 in the epithelial cells of the digestive tract of another mouse strain caused development of significantly more tumours [ 16].
For example, Npc1-null mutations put into the C57BL/6 mouse strain cause a more severe early defect (leading to premature death prior to obvious neurodegeneration) than in FVB/N, Balb/c or mixed genetic backgrounds.
In wild-type mice, neither strain caused mortality or weight loss, though one mouse inoculated with WNV-MADIC showed mild signs of disease.
This mouse strain carries a mutation that causes incomplete loss of function due to the alternate gene splicing (Li et al., 2011).
In B6 and relative mouse strains M. avium causes lung granuloma with regular structure, sharing many features with human TB granuloma; thus, corresponding models of infection were used to study cellular and molecular interactions during mycobacterial granulomatosis [12], [13].
Accordingly, it seemed possible that the genetic manipulations used for preparation of either of these mouse strains might have caused a change in the expression pattern.
However, it is not clear why lack of Dnd1 causes germs cells to become transformed as in the Ter mouse strain.
The present study was designed to examine gastric lesions and immune responses caused by intragastric H. heilmannii infection of an inbred mouse strain, C57BL/6.
Of the three influenza strains used in the macaque studies, this particular strain causes a gene expression response that compares best to the common mouse response.
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