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. 1999 Jun 22;96(13):7276–7281. doi: 10.1073/pnas.96.13.7276

Figure 3.

Figure 3

Induction of growth arrest by C/EBPα and its abrogation in the absence of p21. (A) p21−/− MEFs were stably transfected with empty vector (vector control) or with the chimeric C/EBPαER construct (+ C/EPBαER). A C/EPBαER-expressing clone was infected with recombinant retroviruses encoding vector (+ vector) or HA-tagged HPV-16 E7 (+ 16E7) (infection rate, >90%). Cells were examined for growth kinetics (means of triplicates and SDs) in the presence (●) and absence (○) of estrogen (0.5 μM). (B) Immunoblot analysis of C/EBPαER-fusion protein expression in p21−/− MEF. Lysates from p21−/− parental cells (lane 1), vector control (lane 2), C/EBPαER-transfected cells (lane 3), or C/EBPαER-expressing cells infected with recombinant retroviruses encoding vector (lane 4) or HA-tagged HPV-16 E7 (lane 5) were examined. (C) Immunoblot analysis of HPV-16 E7 expression in p21−/− MEFs. Nuclear extracts from p21−/− MEF transfected with empty vector (lane 1) or C/EBPαER (lane 2) and from C/EBPαER-expressing cells infected with recombinant retroviruses encoding the empty vector (lane 3) or HA-tagged HPV-16 E7 (lane 4) were examined.