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Figure 5. E1A-mediated bypass of ras-induced premature senescence requires the Rb-binding and p300/CBP-binding activities, but not the p400-binding activity. A, growth curves of BJ cells (PD28) cotransduced with E1A1-143 containing the  26 to 35 mutation or its vector (BP) and Ha-RasV12 or its vector (WH) were followed over a period of 16 days. Points, mean PDs for duplicates; bars, SD. B, growth curves of BJ cells (PD27) cotransduced with E1A1-143, E1A1-143 containing the 27/124 or RG2 mutation or their vector (BP), and Ha-RasV12 or its vector (WH) were followed over a period of 14 days. Points, mean PDs for duplicates; bars, SD. C, percentage of cells positive for senescence-associated ß-galactosidase were determined in BJ cell populations cotransduced with E1A1-143, E1A1-143 containing the 27/124 or RG2 mutation or their vector (BP), and Ha-RasV12 or its vector (WH) on day 14 postinfection. *P < 0.001 versus BP + BH; **P < 0.0001 versus BP + BH, #P < 0.05 versus BP + BH. D, Rb-binding defective and the p300/CBP-binding defective mutants of E1A complemented each other to rescue ras-induced senescence. Growth curves of BJ cells (PD27) transduced first with the E1A1-143-RG2 mutant or its vector (WN), and then cotransduced with the E1A1-143-27/124 mutant or its vector (BP) and Ha-RasV12 or its vector (WH) were followed over a period of 14 days. Points, mean PDs for duplicates; bars, SD. ##P < 0.005 versus BP-WN-Ras. E, Western blot analysis of BJ cells transduced with wild-type or indicated mutants of E1A1-143 or BP vector and Ha-RasV12 or WH vector, showing protein levels of Ras and E1A.
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His should have read Tyr47
His, Cys124
