UC San Diego

ABL is an ubiquitously expressed non-receptor tyrosine kinase involved in multiple cellular functions including programmed cell death. Upon DNA damage, ABL has been shown to upregulate PUMA, p53 upregulated modulator of apoptosis, and causes downstream mitochondrial intrinsic apoptotic events. However, the mechanism by which ABL regulates PUMA expression remains unknown. We have shown that ABL does not change PUMA protein subcellular localization through immunofluorescence. Through protein and RNA quantification, we showed that overproduction of PUMA RNA leads to an increase in PUMA protein expression. ABL requires a functional kinase domain to stimulate PUMA protein expression. Inhibition of ABL kinase activity using Imatinib diminishes the ability of ABL to induce PUMA protein expression.