HIPK2: A tumour suppressor that controls DNA damage-induced cell fate and cytokinesis

Bioessays. 2013 Jan;35(1):55-64. doi: 10.1002/bies.201200060. Epub 2012 Nov 21.


In response to DNA-damage, cells have to decide between different cell fate programmes. Activation of the tumour suppressor HIPK2 specifies the DNA damage response (DDR) and tips the cell fate balance towards an apoptotic response. HIPK2 is activated by the checkpoint kinase ATM, and triggers apoptosis through regulatory phosphorylation of a set of cellular key molecules including the tumour suppressor p53 and the anti-apoptotic corepressor CtBP. Recent work has identified HIPK2 as a regulator of the ultimate step in cytokinesis: the abscission of the mother and daughter cells. Since proper cytokinesis is essential for genome stability and maintenance of correct ploidy, this finding sheds new light on the tumour suppressor function of HIPK2. Here we highlight the molecular mechanisms coordinating HIPK2 function and discuss its emerging role as a tumour suppressor.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Alcohol Oxidoreductases / metabolism
  • Animals
  • Apoptosis*
  • Ataxia Telangiectasia Mutated Proteins
  • Carrier Proteins / metabolism*
  • Cell Cycle Proteins / metabolism
  • Cytokinesis* / genetics
  • DNA Damage / genetics*
  • DNA Repair* / genetics
  • DNA-Binding Proteins / metabolism
  • Humans
  • Protein-Serine-Threonine Kinases / metabolism*
  • Signal Transduction / genetics
  • Tumor Suppressor Protein p53 / metabolism
  • Tumor Suppressor Proteins / metabolism


  • Carrier Proteins
  • Cell Cycle Proteins
  • DNA-Binding Proteins
  • Tumor Suppressor Protein p53
  • Tumor Suppressor Proteins
  • Alcohol Oxidoreductases
  • C-terminal binding protein
  • HIPK2 protein, human
  • ATM protein, human
  • Ataxia Telangiectasia Mutated Proteins
  • Protein-Serine-Threonine Kinases