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. 2011 Jul 25;108(33):13379–13386. doi: 10.1073/pnas.1110104108

Fig. 1.

Fig. 1.

Loss of RBP2 inhibits proliferation and induces senescence. (A and B) Proliferation rate of WT and Rbp2−/− (KO) primary MEFs in (A) early and (B) late passages. (C) Senescence-associated β-galactosidase staining of late-passage WT and Rbp2−/− MEFs. (D) Quantitation of β-galactosidase–positive cells of late-passage WT and Rbp2−/− MEFs from three independent experiments; 300 cells of each genotype were counted (*P < 0.02). (E) Proliferation rate of Rbp2f/f;Cre-ER (f/f Cre-ER) and Rbp2+/+;Cre-ER (WT Cre-ER) primary MEFs after a 6-h pulse of tamoxifen (+Tam) compared with untreated MEFs. (F) Real-time RT-PCR analysis of Rbp2 in MEFs in E. Shown are mean values with SEM. (G) Proliferation rate of Rbp2−/− K1 MEFs infected with retroviruses encoding WT RBP2 (WT), RBP2 H483A (MT), or empty vector (EV). (H) Western blot analysis of the MEFs in G.