Research Article

CD38 Deficiency Promotes Inflammatory Response through Activating Sirt1/NF-κB-Mediated Inhibition of TLR2 Expression in Macrophages

Figure 6

CD38-mediated Sirt1/NF-κB/TLR2 signaling is NAD-dependent. The expressions of TLR2, NF-κB p65, and acetyl-p65 (Ac-p65) proteins were detected by Western blot (a) and quantitatively determined for TLR2 (b), NF-κB p65 (c) and NF-κB Ac-p65 (d) in control and CD38-overexpressed RAW264.7 cells in the absence or presence of NAD. GAPDH was used as an internal control. The data represent the . from three independent experiments. and compared with the dCas9 group; and compared with the CD38 group.
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