In contrast, B62M mice displayed small decreases in body weights and growth (male 9WK was significant, female 6WK and 9WK were suggestive at P < 0.05) and significant decreases in NA (male P = 0.0152) and tail length (Additional File 3 and Table 2).
Since Pofut1/Tgfb3-Cre mice displayed smaller hair follicles than those of control mice at P30 (Figure 4G, H), back skin sections from control and mutant mice were immunostained for Ki67, a proliferating nuclear antigen, to examine the hair bulb (Figure 8A).
Aortic root sections of anti-CXCL1 treated mice displayed smaller lesions (Fig 2H) characterized by lower numbers of lesional classical monocytes and macrophages (Fig 2I).
Indeed, KO mice displayed smaller white adipocytes (Fig 3I) and ∼2.5-fold increase in adβ3 expression (Fig 3J) in a compensatory response to maintain adrenergic signaling.
Previous studies have shown that Id1 and Id3 are important for retinal development: double-knockout mice display smaller retinas compared with WT at E13.5 (Du and Yip, 2011), and overexpression of Id1 and Id3 in the retina starting at P0 increases the number of cells that resemble retinal progenitors or Müller glia in the mature retina (after P14) (Mizeracka et al., 2013).
These mice display a small size phenotype and are insulin resistant (Bayascas et al., 2008).
As shown, treated PS1xAPP mice displayed a small, but significant, increase in the proportion of plaques without associated NPY dystrophies.
Bcl2−/− mice display runting, small ear pinnae, craniofacial abnormalities, premature greying, lymphopenia, polycystic kidney disease and premature death.
Lmna-/ mice also display smaller spleens and thymuses.
Accordingly, Cnr2 −/− mice also displayed smaller adiposity index and adipocyte size compared to WT animals (Table 1), and reduced circulating leptin levels, whereas serum adiponectin levels were unchanged (Table 1).
