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. Author manuscript; available in PMC: 2015 Sep 30.
Published in final edited form as: Nat Commun. 2015 Mar 30;6:6641. doi: 10.1038/ncomms7641

Figure 4. mH2A1 deficiency rescues cell growth arrest and polyploidy upon Skp2 loss.

Figure 4

(a) Primary WT and Skp2−/− MEFs were infected with lucifcerse shRNAs (shLuc) or mH2A1 shRNAs (shmH2A1), selected and harvested for Immunoblotting. (b) Flow cytometry analysis of DNA content in WT and Skp2−/− MEFs with Luc or mH2A1 knockdown. (c) G2/M phase was determined by Flow cytometry analysis of primary WT and Skp2−/− MEFs with stably expressing shLuc or shmH2A1. (d) Polyploidy of primary WT and Skp2−/− MEFs with stably expressing shLuc or shmH2A1. (e) Cell growth assay by direct cell counting of WT and Skp2−/− MEFs with Luc or mH2A1 knockdown. (f) MDA-MB-231 cells infected with various shRNAs were subcutaneously injected into nude mice (n=5 for each group). Tumour size was monitored and calculated by caliper for up to 5 weeks (see Methods). The cell lysates from tumour cells were subjected to immunoblotting (left panel). A photo of five tumours aligned together were presented (middle panel). The results were calculated as mean values ± s.d. (g)MDA-MB-231 cells infected with various shRNAs were subcutaneously injected into nude mice, and breast tumours were harvested from nude mice at week 5 for Ki-67 staining by IHC and quantitated (Scale bars, 50µm) (Error bars indicate s.e.m. Data represent mean values of three independent experiments. Student’s t-test used; *p<0.05;**p<0.01)