Oncogenic HRasV12 interferes the proapoptotic capacity of ∆Np73-α
(A) HRasV12 (black bars) activates the basal activity of the ∆Np73 responsive element in BIK promoter, but impairs its induction by ∆Np73-α. Expression vectors for HRasV12 and ∆Np73-α were cotransfected along with the reporter construct containing the region from −72 to −38 of BIK promoter, and RLA was measured. (B) Deletion of the C-terminal region of ∆Np73 (∆505–587) impairs the inhibitory effect of HRasV12 over it. Expression vectors for the indicated constructs were cotransfected with a −56 to −38 BIK reporter construct. RLA is depicted. (C) Cotransfection of HRasV12 reverted the apoptosis induced by ∆Np73-α. When HRasV12 is cotransfected with ∆Np73-α, the percentage of Annexin V-IP positive cells is reduced to that in cells transfected with empty vectors.