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Convergence of the fanconi anemia and ataxia telangiectasia signaling pathways.

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


  • Taniguchi T
  • Garcia-Higuera I
  • Xu B
  • Andreassen PR
  • Gregory RC
  • Kim ST
  • Lane WS
  • Kastan MB
  • D'Andrea AD



Publication Data

May 17, 2002

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

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