Figure 8.

A working model that demonstrates control of apoptosis and tumorigenesis by UGT1A proteins through regulation of p53. In this model, we are showing that p53 when activated can induce apoptosis and repress tumor formation. After p53 activation by cellular or chemical stress the presence of UGT1A proteins in the endoplasmic reticulum (ER) is required to sustain and maintain p53 levels. Knockdown of the UGT1 locus and the resulting UGT1A proteins increases ER stress leading to inhibition of p53 activation/elevation and subsequent reduction in apoptosis and tumor suppression.