The CXXC finger 5 protein is required for DNA damage-induced p53 activation.

The tumor suppressor p53 is a critical component of the DNA damage response pathway that induces a set of genes responsible for cell cycle arrest, senescence, apoptosis, and DNA repair. The ataxia telangiectasia mutated protein kinase (ATM) responds to DNA-damage stimuli and signals p53 stabilization and activation, thereby facilitating transactivation ...
of p53 inducible genes and maintainence of genome integrity. In this study, we identified a CXXC zinc finger domain containing protein termed CF5 as a critical component in the DNA damage signaling pathway. CF5 induces p53 transcriptional activity and apoptosis in cells expressing wild type p53 but not in p53-deficient cells. Knockdown of CF5 inhibits DNA damage-induced p53 activation as well as cell cycle arrest. Furthermore, CF5 physically interacts with ATM and is required for DNA damage-induced ATM phosphorylation but not its recruitment to chromatin. These findings suggest that CF5 plays a crucial role in ATM-p53 signaling in response to DNA damage.
Mesh Terms:
Amino Acid Sequence, Animals, Antineoplastic Agents, Phytogenic, Carrier Proteins, Cell Cycle, Cell Cycle Proteins, DNA Damage, DNA-Binding Proteins, Etoposide, Gene Expression Regulation, Hela Cells, Humans, Molecular Sequence Data, Protein-Serine-Threonine Kinases, RNA Interference, Sequence Alignment, Signal Transduction, Tumor Suppressor Protein p53, Tumor Suppressor Proteins, Zinc Fingers
Sci. China, C, Life Sci.
Date: Jun. 01, 2009
Download Curated Data For This Publication
105617
Switch View:
  • Interactions 1