Research Paper Volume 17, Issue 7 pp 1746—1761

Figure 1. AUF1 deficiency accelerates senescence by targeting glycolytic enzymes. (A) Western blot analysis of Auf1, p16, p21, and Tubulin from primary lung fibroblasts of Auf1^+/+ and Auf1^−/− mice. (B, C) Serum levels of IL-6 (B) and TNF-α (C) isolated from Auf1^+/+ and ^−/− mice (n = 4, 23-week-old mice). The results shown in (A) represent data from four independent experiments. The graph in (B) and (C) is an average ± standard deviation (S.D.) of four mice (^*p < 0.05). (D) Western blot analysis of AUF1, p16, p21, and Tubulin in lysates from proliferating HDFs transfected with control or AUF1 siRNA for 72 hours. (E) The pipeline for identifying mRNAs targeted by AUF1 for the regulation of mRNA and protein abundance in replicative senescence via direct binding of AUF1 with target mRNAs. (F) Western blot analysis of PGAM1, PDP2, and Tubulin from proliferating HDFs transfected with control or AUF1 siRNA. The data shown in (F) represent three independent experiments. (G, H) Number of β-GAL-positive fibroblasts in the presence or absence of a chemical inhibitor against PGAM1, PGMI-004A (20 μM), in proliferating or senescent fibroblasts (G) transfected with control or AUF1 siRNA (H). The graphs in (G) and (H) are an average ± S.D. of three independent experiments (^*p < 0.001).