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. 2022 Jun 7;221(7):e202203095. doi: 10.1083/jcb.202203095

Figure 4.

Figure 4.

CD4+ T-cells from mice lacking Fbxo7 display metabolic reprogramming and enhanced glycolysis, alongside survival and activation defects. (A) CD4+ T cells from WT or Fbxo7LacZ/LacZ mice were activated for 48 h, then their glucose metabolism was analyzed by the Agilent Seahorse Glycolytic Rate Assay (n = 2). Basal glycolysis refers to the physiological rate, whereas compensatory glycolysis reflects the glycolytic capacity when mitochondrial respiration is inhibited. (B) Decrease in viability of CD4+ T cells over 24 h of activation in vitro (n = 3). (C) Activation of CD4+ T cells in vitro, as measured by CD69 and CD25 expression over 24 h (n ≥ 3). (D) Volcano plot of differentially expressed metabolites from untargeted metabolomics profiling of CD4+ T cells from WT or Fbxo7LacZ/LacZ mice, activated for 48 h (n = 6). (E) CD4+ T cells from WT or Fbxo7LacZ/LacZ mice were activated for 24 h in the presence of glucose-1,2-13C2, then subjected to metabolomics analysis (n = 6). m+1 and m+2 intracellular lactates are derived from radio-labeled glucose. Data are presented as mean ± SD; *, P < 0.05; **, P < 0.01; ***, P < 0.005; ****, P < 0.001.