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Indeed, 5fC and 5caC are substrates for TDG, and the embryonic lethal phenotype of Tdg null mice was explained in part by aberrant methylation during early development.
This paradoxical effect reduction of muscarinic and enhancement of β-adrenergic responses in BKCa knock-out mice was explained by a compensatory upregulation of the cGMP pathway.
However, although brown adipose tissue was not elevated, the explanation for the increased energy expenditure in the C/EBP- β knockout mice was explained by elevated gene expression in brown adipose tissue β-oxidation (LCAD and AOX).
This wholesale hypomethylator phenotype in mice was explained by Zhu and colleagues with the finding that Lsh and the de novo methyltransferases (Dnmt3a and Dnmt3b) can interact and contribute to the silencing of an episomal transgene independent of DNA replication [ 28].
The paired-pulse depression seen in the R26CT x Thy1.2-CRE mice was explained as a change in vesicular trafficking due to sequestration of F-actin in model Hirano bodies [ 28, 75], decreasing the amount of cellular actin available for cytoskeletal functions.
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How can the abnormal CS patterns during locomotion in tg/tg mice be explained?
Therefore, we suggest that social recognition deficit observed in APP mice is explained rather by diminished levels of nuclear pCREB.
The shortening of appendicular bones in PTHrP gene null mice is explained by an effect of PTHrP on endochondral bone growth.
Thus, we concluded that the ALK-1 receptor is involved in the control of AP, and the high AP of Alk1 +/− mice is explained mainly by the sympathetic overactivation shown by these animals, which is probably related to the decreased number of cholinergic neurons.
The higher percentage of normal-specific AS events in mouse is explained by the limited cancer transcripts available for this species (Table 1).
Further the lethal concentration of brine shrimp can be correlated with the lethal dose in mice and was explained using medicinal plants earlier [ 63].
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