Although there is some variation in the counts of subpopulations of T cells in various human and mouse mutants with deficient SOCE, the overall evidence seems to suggest that the immunodeficiency caused by deficient SOCE is not a direct function of the number of T cells present.
In contrast, no in vivo studies using Irf7 deficient mouse mutants have been published so far.
Failure to degrade TAG in homozygous lipase-deficient ATGL−/− mouse mutants leads to a lack of PPAR-agonist release and impaired mitochondrial function (Haemmerle et al. 2011; Zechner et al. 2012).
The SNAP-25 deficient mouse mutant coloboma (Cm/+) is of interest to ADHD because SNAP-25 polymorphisms have been associated with the disorder [ 153, 154].
The SNAP-25 deficient mouse mutant coloboma displays spontaneous hyperactivity [ 155] but lacks impulsiveness and has not been shown to have problems with sustained attention.
Additional rodent models for ADHD have been created by genetic engineering to generate an ADHD-like phenotype, such as the SNAP-25 deficient mouse mutant coloboma [[ 21- 23], reviewed in [ 24]] and the dopamine transporter knockout mouse (DAT-KO) [e.g. [ 25, 26]].
The Tex19.1-null mouse mutant phenocopies the Ubr2-deficient mutant in three aspects: heterogeneity of spermatogenic defects, meiotic chromosomal asynapsis, and embryonic lethality preferentially affecting females.
We tested four different cerebellar mouse mutant lines, which suffer from deficient processing in their Purkinje cells, molecular layer interneurons or granule cells, on the Erasmus Ladder to study their basic walking patterns, locomotion adaptation to perturbations and interlimb coordination.
Thus, having generated a mouse mutant that expressed a phosphorylation deficient version of the M3-muscarinic receptor, the question was what impact did this mutation have on muscarinic receptor-mediated physiological responses?
As shown in Figure 1A,B, we observed markedly enhanced metastasis of B16 cells in the lungs of mutant mice deficient in the Irf5 gene (hereafter IRF5-deficient mice).
