Nfatc2-/ Nfatc4-/ mice also exhibit an altered adipokine profile, with reduced resistin and leptin levels.
More recently, we have shown that these mice also exhibit autism-like traits, such as deficits in sociability, social cognition, and increased repetitive behaviors (Desbonnet et al, 2014).
Further, we show that osm-3/kif17 mutant mice also exhibit a similarly delayed outer segment development, suggesting a role for osm-3/kif17 in early outer segment development that is conserved across species.
+SINE mice also exhibit behavioral differences in anxiety assays and decreased pain sensitivity.
RARγ null mice also exhibit a non-HSC-autonomous myeloproliferative syndrome (MPS) [37].
Female TIEG1 KO mice also exhibit reduced osteocyte numbers with alterations in their ultra-structure [19].
SHIP deficient mice also exhibit decreased number of platelets as previously shown [31].
In addition to loss of IPC, Cav-1 KO mice also exhibit characteristics consistent with AD.
Myo-CELFΔ transgenic mice also exhibit no obvious impairment in mobility or gait.
In this study, we report that AICD transgenic mice also exhibit impaired adult neurogenesis by reducing neuronal proliferation and survival.
VDR KO mice also exhibit progressive loss of adipose tissue stores, hypoleptinemia and increased metabolic rate with age.
