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RNF13 -/- mice exhibited accelerated muscle regeneration after injury.
Following acute CCl4 exposure, the FGFR4-deficient mice exhibited accelerated liver injury, a significant increase in liver mass and delayed hepatolobular repair.
First, due to the absence of naturally occurring CD4+CD25+ Tregs, these mice exhibited accelerated disease development compared to wild-type NOD mice (overt diabetes is usually observed by 8 weeks of age).
In a lysolecithin mediated demyelination, Ptprz−/− mice exhibited accelerated axon loss (Huang et al., 2012).
Indeed, Siglec-E-deficient mice exhibited accelerated signs of aging compared to littermate controls.
Here we show that GADD34−/− mice exhibited accelerated wound closure compared with WT mice.
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Accordingly, the 4E-BP1 deficient mice exhibit accelerated re-entrainment upon light/dark shift and are more resilient to constant light mediated circadian disruption (Cao et al., 2013).
In contrast, Tgfb2 heterozygous mice exhibit accelerated metanephric development, which results in augmented nephron endowment at postnatal day (PN) 30 [6].
These data demonstrate that ΔCS mice exhibit accelerated loss of both the soma and axon in response to TNFα.
Furthermore, VDR knockout (KO) mice exhibit accelerated mammary gland development during puberty and early pregnancy, and impaired apoptosis during involution, compared to wild-type (WT) mice [10], [15].
► HSLiKO mice exhibit accelerated cholesterol absorption.
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