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A mouse model harboring embryonic deletion of Sav1, Mst1/2 or Lats2 in the heart revealed the importance of these Hippo components for proper organ development [60].
To directly assess the levels of different types of spontaneous mutations in organs and tissues during aging, we have used a mouse model harboring a chromosomally integrated cluster of lacZ-containing plasmids that can be recovered and analyzed in Escherichia coli.
The mouse model harboring leptin V145E mutation will serve as an excellent model for human obesity which results from leptin dysfunction.
Using a transgenic mouse model harboring chromosomally integrated lacZ mutational target genes, we previously demonstrated that mutations accumulate with age much more rapidly in the small intestine than in the brain.
A consistent mouse model harboring sound-induced (and/or age-induced) strial micro-ischemia will be advantageous for ototoxicity research, and provide opportunities to investigate any correlation between sound-induced strial micro-ischemia and enhanced drug uptake by hair cells.
The mouse model harboring leptin V145E mutation will provide new information on the current understanding of leptin biology and novel mouse model for the study of human obesity syndrome.
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Our mouse model harbors a truncation variant in A-band TTN, making it a good mouse model for a wide spectrum of human DCM.
The myodystrophy Large myd mouse model harbors a mutation in the gene Large, which encodes a glycosyltransferase that presumably alters the glycosylation of α-DG.
This mouse model harbors the human amyloid precursor protein (APP) gent containing Swedish mutant and human presenilin 1 (PS1) gene encoding the deleted exon 9 mutation under control of mouse PrP promoter which directs the transgene expression predominantly in brain neurons [ 18], and develops amyloid plaques at 6 months of age [ 17].
However, these approaches have only been demonstrated in human tumor-derived cell lines or mouse models harboring mtDNA mutations.
In this review, we provide examples of mouse models harboring modified endogenous gene(s), generated using the technique commonly referred to as the "knock-in" approach, to exemplify the important and sometimes superior role of this methodology in dermatological research.
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