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. 2020 Sep 16;39(21):e103420. doi: 10.15252/embj.2019103420

Figure 1. DC patient fibroblasts exhibit defects in NAD metabolism and NAD‐dependent PARylation and SIRT1 deacetylation activity.

Figure 1

  • A, B
    Intracellular NAD levels and NAD/NADH ratio in DC and age‐matched healthy control fibroblasts. All values are presented as mean ± SD of four and eight replicates in (A) and (B), respectively. Student's t‐test was performed on DC cells vs controls.
  • C
    An overview of NAD metabolism. The activity of NAD‐consuming enzymes, such as PARPs, SIRTs, or CD38 consumes NAD and results in NAM production. The NAD biosynthesizing enzymes NMNATs and NAMPT recycle NAM back to NMN and then NMN to NAD, respectively. NR is converted to NMN, followed by conversion of NMN to NAD.
  • D, E
    Immunoblots of the expression of NAD synthesis and consuming proteins, and their activities in DC and control cells. Protein levels are normalized to GAPDH. Quantification values are presented as mean ± SD of four controls vs five DC samples as shown in (D). Student's t‐test was performed on DC cells vs controls. Con: control fibroblasts. Irrelevant intervening lanes in (D) have been removed for clarity (full blots are available online as Source Data).
  • F
    Effects of NR and NAM supplementation (24 h) on the NAD levels in DC fibroblasts. All values are presented as mean ± SD of four replicates. One‐way ANOVA was performed on DC cells in indicated conditions.

Source data are available online for this figure.