Figure 2. Myc^HEA and Myc^RA are defective in sustaining cell proliferation.

1. Colony formation for cb9^Δmyc cells infected with retroviral vectors expressing the indicated Myc proteins; all cells were expanded with doxycycline prior to the final plating step, upon which the compound was either maintained (+dox) or removed (−dox) to switch off the tet‐Myc transgene. One representative experiment out of 3 is shown.
2. Cumulative cell counts for cb9^Δmyc cells upon serial passaging with or without dox (removed at day 2). The data are presented as mean ± SD; n = 3 (biological replicates).
3. Percentage of BrdU‐positive cb9^Δmyc cells, in the presence or absence (24h after removal) of doxycycline. Data are presented as mean ± SD; n = 3. Two‐tailed Student’s t‐test was used to compare between two groups and expressed as P‐values.
4. Immunoblot analysis of c‐myc ^−/− HO15.19 rat fibroblasts infected with retroviral vectors expressing the indicated Myc proteins. Parental TGR1 cells serve as control for endogenous levels of the Myc^WT protein.
5. Colony formation for the same cells as in (D). One representative experiment out of 3 is shown.
6. Cumulative cell counts for the same cells as in (D). Data are presented as mean ± SD; n = 3 (biological replicates). Two‐tailed Student’s t‐test was used to compare between two groups and expressed as P‐values.

Source data are available online for this figure.