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. 2010 Jan 14;29(4):830–842. doi: 10.1038/emboj.2009.395

Figure 3.

Figure 3

SMAR1 induces an anti-apoptotic signal in response to low-dose DNA damage. (A) HCT116 p53+/+ cells were UV irradiated with 5 J/m2 UV and cells collected at different time points as indicated. Immunoblot analysis was carried out as shown. (B) Expression levels of Bax, Puma, p53, acetylated p53 and PARP cleavage on shRNA (sh1077)-mediated knockdown of SMAR1 in HCT116 p53+/+ cells. (C) Propidium iodide staining in control HCT116 p53+/+ cells (48 h), cells treated with UV (5 J/m2, 48 h) and SMAR1 knockdown UV-treated cells (5 J/m2, 48 h) showing percentage apoptosis represented by sub-G1 population. (D) Statistical representation of percentage sub-G1 population on low-dose UV treatment and SMAR1 knockdown from three independent experiments. Error bars represent standard deviation. (E) Propidium iodide staining in MEFs transduced with control and SMAR1 lentivirus (F) Knockdown of SMAR1 by transient transfection in HCT116 p53+/+ and HCT116 p53−/− cells showing differential sub-G1 population.