Skip to main content
. 2017 Jun 13;3:17019. doi: 10.1038/celldisc.2017.19

Figure 1.

Figure 1

Loss of UHRF1 in IMR90 and HBE cells leads to a senescent phenotype. (a) Cell proliferation was measured by EdU incorporation in control (shNT) or UHRF1 knockdown IMR90 cells 6 days after virus transduction. (b, c) SA-β-gal staining of control and UHRF1 knockdown IMR90 cells (b) and quantification (c). (d, e) Whole-cell lysates from control, UHRF1 knockdown, or UHRF1 and p53 co-knockdown IMR90 cells were collected and subsequently immunoblotted with the indicated antibodies. Cells were collected 6 days after virus transduction. Note that p21 expression in UHRF1-deficient cells correlates with p53 induction. (f) Cell proliferation was measured by EdU incorporation in control (shNT) or UHRF1 knockdown HBE cells in culture 6 days after virus transduction. (g, h) Representative SA-β-gal staining is shown in g, and quantification is shown in h. (i) Whole-cell lysates from control (shNT) or the UHRF1 knockdown HBE cells (shU_1 and shU_2) from three independent donors were collected and subsequently immunoblotted with the indicated antibodies. Data are reported as mean±s.e.m. P-value was calculated based on at least three independent experiments. ***P<0.001; **P<0.01; *P<0.05.