TDP-43 controlsled neuronal glycolysis possibly by directly regulating the transcription of PFKP through BMAL1 (Related to Fig. 8 ). (A) M17 cells were transfected with PX458 (NC) or PX458/TDP-43_KO (TKD) for 48 h. The cell lysates were analyzed using western blotting with glycolytic kinase antibodies and quantitated. (B) M17 cells were transfected with PX458 (NC) or gene editor vector target BMAL1 designed as BMAL1_KO (BKD) for 48 h. The cell lysates were analyzed using western blotting and quantitated. (C) Chromatin from M17 cells was immunoprecipitated with normal mouse IgG (IgG) or anti-BMAL1 (BMAL1). Quantitative PCR was used to detect IgG and BMAL1 antibody-enriched DNA fragments containing indicated four BMAL1 binding consensuses (site1, site2, site3, and site4) in the PFKP promoter and quantitated. Data are presented as mean ± S.D. (n = 3) and compared with unpaired t test. **P < 0.01; ***P < 0.001. Source data are available for this figure: SourceData FS5.