Fig 1: Expression and cellular localization of GAPDHS, PGK2 and LDHC in testes from young adults and elderly adults. (A-F) The testes of five samples from young adults and five from elderly men were (A) evaluated by Johnsen scoring method and analyzed by (B-E) western blotting and (F) immunohistochemistry; scale bar, 20 µm. The expression between young adult and elderly adult were compared statistically by Student's t-test; *P<0.05 and **P<0.01. ACTB, ß-actin; GAPDHS, glyceraldehyde-3-phosphate dehydrogenase, testis-specific; LDHC, lactate dehydrogenase C; PGK2, phosphoglycerate kinase 2.
Fig 2: Shikonin downregulates PFKFB2 expression levels in A549 and H446 cells. (A) A549 and H446 cells were incubated with 0, 10, 20 or 50 µM shikonin for 24 h. Expression levels of PFKFB2, PDK1, GLUT1, PGK2, LDHA, PKM2, GLUT3, PDH and p-PDH in A549 and H446 cells were analyzed using western blotting. (B) mRNA expression levels of PFKFB2 were analyzed using reverse transcription-quantitative PCR in A549 and H446 cells treated with 50 µM shikonin. *P<0.05 vs. control. PFKFB2, 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 2; PDK1, pyruvate dehydrogenase kinase 1; GLUT, glucose transporter; PGK2, phosphoglycerate kinase 2; LDHA, lactate dehydrogenase A; PKM2, pyruvate kinase M1/2; PDH, pyruvate dehydrogenase phosphatase catalytic subunit 1; p-, phosphorylated.
Fig 3: Immunohistochemical analysis of HSPA4L and PGK2 in testes from control and CP-treated mice at different time-points after CP treatment. A, Representative images of cellular localization of HSPA4L and PGK2 in the testes; B, quantitative intensity of HSPA4L and PGK2 in the testes. Quantitative evaluation was performed by ImageJ and compared by one-way ANOVA; *P < .05, **P < .01. Lu, tubule lumen. Each bar represents 10 µm
Fig 4: The effects of SBP on the expression of genes involved in sperm motility. (A) Relative PGK2 mRNA level. (B) Relative Cfap69 mRNA level. (C) The protein level of PGK2 and grayscale analysis. (D) The protein level of Cfap69 and grayscale analysis. **p< 0.01 vs. Control group; ##p< 0.01 vs. Busulfan group. Data are expressed as mean ± SDE, with n = 3 for each group.
Fig 5: P7C3 reduces the protein level of PGK1 and PGK2. (A) Representative spots of P7C3 target proteins, including the glycolytic process. (B) Western blotting for detecting protein levels of P7C3 target proteins that are related to glycolysis after U87MG and U118MG cells were treated with P7C3 at a concentration of 0 µM, 30 µM, and 50 µM for 24 h. (C) PGK1 activity levels in P7C3-treated U87MG and U118MG cells at a concentration of 0 µM, 30 µM, and 50 µM (n = 4). (D) The expression profiles of PGK1 and PGK2 mRNA levels. Data were obtained from the Human Protein Atlas database. The images are available at: https://www.proteinatlas.org/ENSG00000102144-PGK1/cell, and (https://www.proteinatlas.rg/ENSG00000170950-PGK2/cell). (E) Statistical analysis of PGK1 mRNA level among WHO grade II-IV glioma. The data were based on TCGA and CGGA and are available at: http://gliovis.bioinfo.cnio.es/. (F) Kaplan–Meier survival analysis of PGK1 mRNA level in glioma patients. The data were based on TCGA and CGGA and are available at: http://gliovis.bioinfo.cnio.es/. (The data were expressed as mean ± SD, *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001).
Supplier Page from Abcam for Anti-PGK2 antibody [EPR14909(B)]