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Exact(7)
Scurfy mice bear a loss-of-function mutation in the Foxp3 transcription factor (Foxp3sf/+).
The ob/ob mice bear a mutation in the ob gene that causes a deficiency in the hormone leptin and hence obesity.
These mice bear a ∼1 kb genomic deletion in the endogenous murine Cln3 gene that is analogous to the most common ∼1 kb genomic deletion in juvenile NCL patients.
The mdx mice bear a naturally occurring mutation in exon 23 of the dystrophin gene that abrogates expression of the full-length dystrophin protein, causing symptoms of muscular dystrophy [7], [8].
Twitcher mice bear a spontaneous point mutation resulting in a premature stop codon and no residual GALC activity (72).
Nupr1−/− mice bear a homozygous deletion of exon 2 of the Nupr1 gene and were reported previously.
Similar(53)
Largemyd mice bear an intragenic deletion in the Large gene [41], and exhibit neuronal migration defects in the brain and eye abnormalities similar to CMDs in humans [44].
Consequently, these mice bear an SLE-like phenotype as early as 3 to 4 months of age.
This kind of mouse bears a point mutation in the dystrophin gene.
These triple transgenic mice (=3×Tg-AD mice) finally bear a mutated knocked-in PS1 gene, as well as a mutated APP and a mutated tau gene.
It is, however, unlikely that the increase in lifespan of male RIIβ−/− mice bears any relation to their increased insulin sensitivity, as we did not find differences in insulin sensitivity between young and old WT mice, and the modestly lower blood glucose levels found in the mutants did not show gender specificity.
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