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In situ hybridization on sections of transgenic mouse brains expressing EGFP-BC1 RNA revealed that the chimeric RNA with full length BC1 RNA was also confined to neuronal cell bodies (Figure 3A).
Similar microdeposits have been observed in aged transgenic mouse brains expressing mutant APP (Takahashi et al., 2004; Stokin et al., 2005).
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After repeated exposure to the drug, mouse brains express higher amounts of certain long-lasting proteins, called chronic FRAs.
DOI: http://dx.doi.org/10.7554/eLife.01201.007 Interestingly, heterozygous Ptbp2+/− mouse brains express the PTBP2 protein at about half normal levels.
Straightforward immunofluoresence and Western blot assays demonstrated that cultured astrocytes from mouse brain express high levels of CK-B, which corroborates findings with immunostaining and in-situ hybridization on whole mouse brain that appeared in other reports [23], [34].
Mouse brain expressed the most Dlk1 mRNA and is characterized by an additional and abundant 4.5 kb transcript that was not detected in the other investigated tissues (Figure 3B).
Our analysis revealed that the adult mouse brain expresses a distinct combination of LEF1/TCF protein isoforms compared with the embryonic brain or any other adult or developing tissue.
We found that in BNIP3 knockout cells lacked BNIP3 expression, whereas the heterozygote (BNIP3+/−) and wild-type (wt) mice brains expressed a significant amount of BNIP3.The expression levels of DR5 and TRAIL were increased, whereas there was little change in FAS receptor and caspase 8 in astrocytes lacking BNIP3 expression (KO) compared with wild type.
Not all microglia in the mouse brain express TREM2, and its levels are reduced in cultured microglia by exposure to lipopolysaccharide.
Therefore, relative kinase activity in mouse brains was expressed as fold change in the levels of pCDK5 (Tyr15).
For mouse brain tissues expressing GFP, the corresponding depth limit is about 1 mm [ 8].
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