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Tumor development in the Trp53−/+ mice was delayed compared with Trp53−/− mice (Figures 4 & 5).
Correspondingly, weight loss in CD-injected Npc1−/− mice was delayed by approximately 3 weeks.
Importantly, the pathological microglial infiltration in the untreated mice was delayed in the treated mice until the terminal stage.
After a single, low dose injection of 5-FU, hematopoietic recovery in Id1−/− mice was delayed by 3 days, as compared to wild-type littermate controls (Figure 3D).
The regeneration in dy3K/dy3K mice was delayed and not as well-organized as in control and dy3K/δE3 animals, since the muscle fibers in LMα2 chain deficient mice appeared to be less packed and surrounded by connective tissue (Fig. 9A).
Correspondingly, involution in the Trp53-/ mice was delayed when examined in the early (days 2 5) weaning period [ 27].
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We now demonstrate T cell responses in plt mice are delayed but ultimately enhanced.
Onset of intestinal cancer in Kaiso-deficient mice is delayed compared to wild-type mice [16].
The histological changes described above for normal wound healing in control mice were delayed in DAPT-treated mice and accelerated in Jagged peptide-treated mice (Fig. 2; and see SI histological evaluation).
This gene has not been implicated in BL, but MDM4 inhibits P53, and in vivo development of B-cell lymphomas in Eμ-myc MDM4+/− mice is delayed compared to that occurring in Eμ-myc MDM4+/+ mice [37].
Our data indicates that skin γδ T cells in the obese db/db mice were delayed in their ability to round following wounding as compared to lean db/+ control mice (Figure 3A).
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