Research Paper Volume 14, Issue 18 pp 7527—7546

Figure 2. FAT10 is required for CHK-1-mediated G2/M arrest in RTECs under hypoxia treatment. (A) Western blotting showing the protein expression of CHK1, CDKN1A, TGF-β and CTGF in CHK1-silencing HK-2 cells following hypoxia injury. Tubulin was used as a loading control. (B) TGF-β and CTGF in the culture supernatants was measured in culture supernatants by ELISA assay. ^**P < 0.01. (C) Detection for cell cycle of CHK1-silencing HK-2 cells following hypoxia injury. Results are expressed as peak diagram (left) and calculated distribution for cells in G0/G1, S and G2/M phases (right). ^*P < 0.05. (D) Upon hypoxia treatment, western blotting of FAT10, CHK1, CDKN1A, TGF-β and CTGF in HK-2 cells stably transfected with shFAT10 in the presence or absence of Flag-CHK1. (E) Detection for cell cycle of FAT10-silencing HK-2 cells in the presence or absence of Flag-CHK1 following hypoxia injury. Results are expressed as peak diagram (left) and calculated distribution for cells in G0/G1, S and G2/M phases (right). ^*P < 0.05. (F) Western blotting showing the protein expression of FAT10, CHK1, CDKN1A, TGF-β and CTGF in FAT10^+/+ RTECs and FAT10^−/− RTECs following treatment with hypoxia or without hypoxia. (G) Detection for cell cycle of FAT10^+/+ RTECs and FAT10^−/− RTECs following treatment with hypoxia or without hypoxia. Results are expressed as peak diagram (left) and calculated distribution for cells in G0/G1, S and G2/M phases (right). ^*P < 0.05.