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Non-neoplastic mammary gland regions in transgenic mice were structurally similar to those of nontransgenic mice.
It is important to note that the rod outer segments in both treated and untreated mice were structurally normal; this is expected, since the gene deficiency is cone-specific.
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However fetuses of ACE knockout mice did not die in utero and at birth the kidneys from ACE knockout mice are structurally indistinguishable from those of wild-type littermate controls [3].
Protein tyrosine kinase 6 (PTK6), also known as breast tumor kinase (BRK) in humans and Src-related intestinal kinase (Sik) in the mouse, is structurally related to Src, but is a member of a distinct family [1], [2].
By contrast, many myonuclei at the myotendinous junction of lmna−/− mice were clearly structurally abnormal, with aberrant chromatin accumulations (Figure 2b and e).
In P0-Cre/DG-null mice the myelin sheaths around the nerves were structurally abnormal and extended throughout the internodal segments.
Macrophages from diseased lungs were structurally altered, larger and in Scnn1b-Tg COPD mice, fewer macrophages internalized AuNP compared to those from healthy controls.
They also suggest that although neonatal mouse intestine is structurally fully developed, with the proper crypt-villus organization similar to that in the adult mouse, the embryonic/neonatal mouse intestinal stem cells are molecularly distinct from those in the adult mouse intestine.
Hence they were structurally unemployed.
These nanoparticles were structurally and functionally characterized.
Monomeric three-domain mouse suPAR was produced in Drosophila melanogaster S2 cells and used in the study by Cathelin et al. This monomeric mouse suPAR is structurally well-characterized [ 58].
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