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The resulting vector backbones yield sustained transgene expression from mouse liver, providing generic DNA vectors capable of sustained transgene expression without additional genes or mammalian regulatory elements.
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In mouse liver, P2-mediated integration provided therapeutic long-term levels of human factor IX that were double those generated by wild-type φC31 integrase.
A 1.8 Kb fragment of the Math6 gene upstream of the translation initiation site was amplified by PCR from mouse liver genomic DNA (oligos provided in Methods S1) and cloned upstream of the luciferase gene in the pFOXluc1 vector [35].
cDNA from mouse liver samples were kindly provided by Gwendal Le Martelot from the laboratory of U. Schibler (Department of Molecular Biology, University of Geneva, Switzerland).
Anti-PER2 used for immunoblot analysis of immunoprecipitated samples from mouse liver extracts were kindly provided by Dr Cheng Chi Lee's lab (University of Texas Health Science Center at Houston).
JL provided the mouse liver microarray data set F prior to publication.
Extensive replacement of mouse liver parenchyma by HH does not provide a secure therapeutic advantage against vTK/GCV-induced cytotoxicity targeted to residual mouse hepatocytes.
Taken together, these findings provide unprecedented insights into the diurnal regulatory landscape of the mouse liver nucleus.
Our analyses provide the first comprehensive dissection of the transcriptional landscape in aging mouse liver.
Taken together, our results provide the first evidence that ncRNAs can also shape the landscape of aging mouse liver.
These versatile results provide evidence that mesenchymal and epithelial co-expressing cells decreased with the development stages of mouse liver.
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