Fig. 5
From: LanCL1 promotes motor neuron survival and extends the lifespan of amyotrophic lateral sclerosis mice

LanCL1 is a positive regulator of AKT activity. a Spinal cord and cortex lysates from LanCL1 cKO mice and wild-type (WT) littermates were used in western blots to compare the levels of pAKT(T308) and pAKT(S473). b Quantifications showing a reduction in the level of pAKT (T308) in the spinal cord and cortex of LanCL1 cKO mice at P60. Data represent mean ± SEM, spinal cord n = 5 mice per genotype, cortex n = 4 mice per genotype, *p < 0.05, by two-tailed unpaired Student’s t test. c Lysates from DIV 8 and DIV 18 cortical neurons generated from wild-type or LanCL1-deficient mice were used in western blots to compare the levels of pAKT(T308) and pAKT(S473). d Quantifications showing a reduction in the level of pAKT (T308) in cultured LanCL1-deficient cortical neurons at DIV 8 and DIV 18. Data represent mean ± SEM, n = 3 mice per genotype per timepoint, **p < 0.01, by two-tailed unpaired Student’s t test. Immunoblotting (e) and quantifications (f) show increases in the levels of pAKT(T308) and pAKT(S473) in LanCL1 plasmids (WT or point mutants)-overexpressing HEK293T cells. Data represent mean ± SEM of four independent experiments, *p < 0.05, **p < 0.01, one-way ANOVA followed by Tukey’s post hoc test. Immunoblotting (g) and quantifications (h) show increases in the levels of pAKT (T308) and pAKT (S473) in the cortex of P60 LanCL1 cKI mice. Data represent mean ± SEM, n = 3 mice per genotype, *p < 0.05, **p < 0.01, by two-tailed unpaired Student’s t test. Quantifications of pAKT (S473) and pAKT (T308) normalized to total AKT