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Gene Review

Fancd2  -  Fanconi anemia, complementation group D2

Mus musculus

Synonyms: 2410150O07Rik, AU015151, BB137857, FA-D2, FA4, ...
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Disease relevance of Fancd2


High impact information on Fancd2

  • However, Fancd2 mutant mice also displayed phenotypes not observed in other mice with disruptions of proximal FA genes [2].
  • Therefore, Trp53 is required for the S phase checkpoint activation observed in Fancd2 mutant cells [1].
  • In addition, it was found that Fancd2(-/-) mouse embryonic fibroblasts but not Fancd2(-/-)/Trp53(-/-) mouse embryonic fibroblasts arrest following DNA damage [1].
  • To further investigate the role of the FA pathway in tumor prevention, Fancd2 mutant mice were crossed to mice with a null mutation in the tumor suppressor gene, Trp53 [1].
  • Homozygous germ line mutation in exon 27 of murine Brca2 disrupts the Fancd2-Brca2 pathway in the homologous recombination-mediated DNA interstrand cross-links' repair but does not affect meiosis [3].

Biological context of Fancd2

  • We show that the targeted deletion of Fanca exons 37-39 generates a null for Fanca in mice and abolishes ubiquitination of Fancd2, the downstream effector of the FA complex [4].
  • These data demonstrate not only that expression of this FAD gene causes neuronal apoptosis, but that F11/EcR/V642I cells, the first neuronal cells with inducible FAD gene expression, provide a useful model system in investigating AD disorders [5].

Anatomical context of Fancd2

  • Quantitative electron microscopic immunocytochemistry revealed that by 6 months, the proportion of postsynaptic spines with drebrin A within somatosensory cortex layer I was smaller for the FAD model mice, when compared to the corresponding region of WT mice (P < 0.0005) [6].

Other interactions of Fancd2


  1. Heterozygosity for p53 (Trp53+/-) accelerates epithelial tumor formation in fanconi anemia complementation group D2 (Fancd2) knockout mice. Houghtaling, S., Granville, L., Akkari, Y., Torimaru, Y., Olson, S., Finegold, M., Grompe, M. Cancer Res. (2005) [Pubmed]
  2. Epithelial cancer in Fanconi anemia complementation group D2 (Fancd2) knockout mice. Houghtaling, S., Timmers, C., Noll, M., Finegold, M.J., Jones, S.N., Meyn, M.S., Grompe, M. Genes Dev. (2003) [Pubmed]
  3. Homozygous germ line mutation in exon 27 of murine Brca2 disrupts the Fancd2-Brca2 pathway in the homologous recombination-mediated DNA interstrand cross-links' repair but does not affect meiosis. Atanassov, B.S., Barrett, J.C., Davis, B.J. Genes Chromosomes Cancer (2005) [Pubmed]
  4. The Fanconi anemia group A protein modulates homologous repair of DNA double-strand breaks in mammalian cells. Yang, Y.G., Herceg, Z., Nakanishi, K., Demuth, I., Piccoli, C., Michelon, J., Hildebrand, G., Jasin, M., Digweed, M., Wang, Z.Q. Carcinogenesis (2005) [Pubmed]
  5. V642I APP-inducible neuronal cells: a model system for investigating Alzheimer's disorders. Niikura, T., Murayama, N., Hashimoto, Y., Ito, Y., Yamagishi, Y., Matsuoka, M., Takeuchi, Y., Aiso, S., Nishimoto, I. Biochem. Biophys. Res. Commun. (2000) [Pubmed]
  6. Stability of the distribution of spines containing drebrin A in the sensory cortex layer I of mice expressing mutated APP and PS1 genes. Mahadomrongkul, V., Huerta, P.T., Shirao, T., Aoki, C. Brain Res. (2005) [Pubmed]
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