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Convergence of the fanconi anemia and ataxia telangiectasia signaling pathways.

Cell | May 17, 2002

http://www.ncbi.nlm.nih.gov/pubmed/12086603

Fanconi anemia (FA) and ataxia telangiectasia (AT) are clinically distinct autosomal recessive disorders characterized by spontaneous chromosome breakage and hematological cancers. FA cells are hypersensitive to mitomycin C (MMC), while AT cells are hypersensitive to ionizing radiation (IR). Here, we identify the Fanconi anemia protein, FANCD2, as a link between the FA and ATM damage response pathways. ATM phosphorylates FANCD2 on serine 222 in vitro. This site is also phosphorylated in vivo in an ATM-dependent manner following IR. Phosphorylation of FANCD2 is required for activation of an S phase checkpoint. The ATM-dependent phosphorylation of FANCD2 on S222 and the FA pathway-dependent monoubiquitination of FANCD2 on K561 are independent posttranslational modifications regulating discrete cellular signaling pathways. Biallelic disruption of FANCD2 results in both MMC and IR hypersensitivity.

Pubmed ID: 12086603 RIS Download

Mesh terms: Ataxia Telangiectasia | Ataxia Telangiectasia Mutated Proteins | Cell Cycle Proteins | Cell Line, Transformed | Cell Nucleus | DNA-Binding Proteins | Fanconi Anemia | Fanconi Anemia Complementation Group D2 Protein | G1 Phase | G2 Phase | Genes, cdc | HeLa Cells | Humans | Mitomycin | Mutation | Nuclear Proteins | Nucleic Acid Synthesis Inhibitors | Phosphorylation | Phosphoserine | Protein-Serine-Threonine Kinases | Radiation, Ionizing | S Phase | Signal Transduction | Tumor Suppressor Proteins | Ubiquitin

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Associated grants

  • Agency: NCI NIH HHS, Id: CA21765
  • Agency: NCI NIH HHS, Id: CA71387
  • Agency: NHLBI NIH HHS, Id: P01HL54785
  • Agency: NIDDK NIH HHS, Id: R01DK43889
  • Agency: NHLBI NIH HHS, Id: R01HL52725

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