p63 is a homologue of the tumor-suppressor p53 and can exist as one of at least six different isoforms. p53-/- mice develop normally but are particularly susceptible to tumor growth. p63-/- mice experience severe developmental problems and lack stratified epithelia and all of its derivatives. Both microarray and Chromatin Immunoprecipitation (ChIP) have been used to determine possible genes regulated by p63. AMPK-Related Kinase-5 (ARK5) has been identified as one of the possible target genes. During nutrient starvation, it has been observed that ARK5 promotes cell survival. It has also been discovered that ARK5 transcript levels increase following application of DNA-damaging agents. We hypothesized that ARK5 may cause an increase in survival when cells were subjected to DNA-damaging agents. Experiments show that over-expression of ARK5 does not alter the sensitivity of HEK293 cells to DNA-damage-induced apoptosis. Other cell lines may however be susceptible to ARK5 apoptosis influence following DNA-damage. ChIP analyses have shown that p63 is bound to a specific sequence within the ARK5 gene. A luciferase reporter assay indicates that TAp63g is able to activate transcription from this site. Studies are currently underway to establish a link between p63 and ARK5 signaling.

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