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Fanconi anemia protein, FANCG, is a phosphoprotein and is upregulated with FANCA after TNF-alpha treatment.

Fanconi anemia (FA) is a genetic syndrome characterized by bone marrow failure, birth defects, and a predisposition to malignancy. At this time, six FA genes have been identified, and several gene products have been found to interact in a protein complex. FA cells appear to overexpress the proinflammatory cytokine, tumor necrosis factor-alpha (TNF-alpha). We therefore examined the effects of TNF-alpha on the regulation of FA complementation group proteins, FANCG and FANCA. We found that treatment with TNF-alpha induced FANCG protein expression. FANCA was induced concurrently with FANCG, and the FANCA/FANCG complex was increased in the nucleus following TNF-alpha treatment. Inactivation of inhibitory kappa B kinase-2 modulated the expression of FANCG. We also found that both nuclear and cytoplasmic FANCG fractions were phosphorylated. These results show that FANCG is a phosphoprotein and suggest that the cellular accumulation of FA proteins is subject to regulation by TNF-alpha signaling.

Pubmed ID: 11181053

Authors

  • Futaki M
  • Watanabe S
  • Kajigaya S
  • Liu JM

Journal

Biochemical and biophysical research communications

Publication Data

February 23, 2001

Associated Grants

None

Mesh Terms

  • Blotting, Western
  • Cell Line
  • Cell Nucleus
  • Cytoplasm
  • DNA, Recombinant
  • DNA-Binding Proteins
  • Fanconi Anemia Complementation Group A Protein
  • Fanconi Anemia Complementation Group G Protein
  • HeLa Cells
  • Humans
  • Phosphoproteins
  • Phosphorylation
  • Plasmids
  • Precipitin Tests
  • Proteins
  • Transfection
  • Tumor Necrosis Factor-alpha
  • Up-Regulation