Palmdelphin, a novel target of p53 with Ser46 phosphorylation, controls cell death in response to DNA damage

Cell Death Dis. 2014 May 8;5(5):e1221. doi: 10.1038/cddis.2014.176.


The tumor suppressor gene p53 regulates apoptosis in response to DNA damage. Promoter selectivity of p53 depends on mainly its phosphorylation. Particularly, the phosphorylation at serine-46 of p53 is indispensable in promoting pro-apoptotic genes that are, however, poorly determined. In the current study, we identified palmdelphin as a pro-apoptotic gene induced by p53 in a phosphorylated serine-46-specific manner. Upregulation of palmdelphin was observed in wild-type p53-transfected cells, but not in serine-46-mutated cells. Expression of palmdelphin was induced by p53 in response to DNA damage. In turn, palmdelphin induced apoptosis. Intriguingly, downregulation of palmdelphin resulted in necroptosis-like cell death via ATP depletion. Upon DNA damage, palmdelphin dominantly accumulated in the nucleus to induce apoptosis. These findings define palmdelphin as a target of serine-46-phosphorylated p53 that controls cell death in response to DNA damage.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenosine Triphosphate / metabolism
  • Apoptosis*
  • Cell Line, Tumor
  • Cell Nucleus / metabolism*
  • Cell Nucleus / pathology
  • DNA Damage*
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Membrane Proteins / genetics
  • Membrane Proteins / metabolism*
  • Mutation
  • Necrosis
  • Phosphorylation
  • RNA Interference
  • Serine
  • Time Factors
  • Transfection
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism*


  • Membrane Proteins
  • PALMD protein, human
  • TP53 protein, human
  • Tumor Suppressor Protein p53
  • Serine
  • Adenosine Triphosphate