Pcna Promoter Studies in Radiation-Sensitive Mice

摘要

Since the C_4TAC_(11) sequence strongly binds some protein(s) in all cell extracts that we tested so far, we propose that the C_4TAC_(11) element is a positive regulatory element that acts in combination with T-cell-specific negative regulatory elements crucial for T-cell-specific Pcna gene expression; it can be "bypassed" in other cell types due to a redundancy of positive regulatory elements. Our model is as follows: Absence of Pcna expression in the thymuses (and motor neurons) of "wasted" mice causes cellular apoptosis; this absence of expression is mediated by a positive transfactor(s) that can bind to the wild-type but not the "wasted" mutant Pcna promoter; the bound protein induces late expression of Pcna in T-lymphocyte subsets and prevents onset of radiation sensitivity in the cells.