“…However, stabilization is not solely a property of mutant p53 protein, since it can also occur with wild-type p53 following a variety of stimuli, and these can result in either a decrease or an increase in function (Table 1). Thus, p53 elevation following transformation by DNA tumor viruses [SV40 large Tantigen (Oren et al, 1981;Sarnow et al, 1982;Deppert and Haug, 1986), E1B and E1A oncoproteins (Braithwaite and Jenkins, 1989;Yew and Berk, 1992;Steegenga et al, 1996)] results in a loss of p53 function. In contrast, stabilization following pharmacological stimuli, including DNA damage, hypoxia, depletion of ribonucleotide pools, and microtubule disruption, result in a higher level of a functional p53 (Maltzman and Czyzyk, 1984;Kastan et al, 1991Kastan et al, , 1992Fritsche et al, 1993;Graeber et al, 1994;Blagosklonny et al, 1995a;Chernova et al, 1995;Tishler et al, 1995;Wahl et al, 1996;Linke et al, 1996).…”