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Blood, 15 January 2005, Vol. 105, No. 2, pp. 759-766. Prepublished online as a Blood First Edition Paper on July 15, 2004; DOI 10.1182/blood-2004-01-0001. This Article Full Text Full Text (PDF) Supplemental Videos All Versions of this Article: 2004-01-0001v1 105/2/759    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Mi, J. Articles by Kupfer, G. M. Search for Related Content PubMed PubMed Citation Articles by Mi, J. Articles by Kupfer, G. M. Related Collections Hematopoiesis and Stem Cells Neoplasia Red Cells Cell Cycle Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA The Fanconi anemia core complex associates with chromatin during S phase Jun Mi, and Gary M. Kupfer From the Departments of Microbiology and Pediatrics, the University of Virginia Health System, University of Virginia, Charlottesville. Fanconi anemia (FA) is an autosomal recessive disease marked by bone marrow failure, birth defects, and cancer. The FA proteins FANCA, FANCC, FANCE, FANCF, FANCG, and FANCL participate in a core complex. We previously have shown that several members of this complex bind to chromatin until mitosis and that this binding increases after DNA damage. The purpose of the present study was to determine the dynamics of complex movement between cytoplasm and nuclear compartments. Fluorescent-tagged versions of FANCA, FANCC, and FANCG colocalize in cytoplasm and nucleus, chiefly in chromatin. At the G1-S border, the FA core complex exists as foci on chromatin, progressively diffusing and migrating to the nuclear periphery and becoming completely excluded from condensed chromosomes by mitosis. Chromatin fiber analysis shows FA proteins diffusely staining along chromatin fibers during G1-S and S phase. Treatment with the DNA cross-linker mitomycin C results in a diffusion of foci and increased binding of complex proteins to chromatin, as well as diffuse and increased complex binding to chromatin fibers. These data are consistent with the idea that the FA proteins function at the level of chromatin during S phase to regulate and maintain genomic stability. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J. Hejna, M. Holtorf, J. Hines, L. Mathewson, A. Hemphill, M. Al-Dhalimy, S. B. Olson, and R. E. Moses Tip60 Is Required for DNA Interstrand Cross-link Repair in the Fanconi Anemia Pathway J. Biol. Chem., April 11, 2008; 283(15): 9844 - 9851. [Abstract] [Full Text] [PDF] A. Alpi, F. Langevin, G. Mosedale, Y. J. Machida, A. Dutta, and K. J. Patel UBE2T, the Fanconi Anemia Core Complex, and FANCD2 Are Recruited Independently to Chromatin: a Basis for the Regulation of FANCD2 Monoubiquitination Mol. Cell. Biol., December 15, 2007; 27(24): 8421 - 8430. [Abstract] [Full Text] [PDF] A. Sobeck, S. Stone, and M. E. Hoatlin DNA Structure-Induced Recruitment and Activation of the Fanconi Anemia Pathway Protein FANCD2 Mol. Cell. Biol., June 15, 2007; 27(12): 4283 - 4292. [Abstract] [Full Text] [PDF] J. Dunn, M. Potter, A. Rees, and T. M. Runger Activation of the Fanconi Anemia/BRCA Pathway and Recombination Repair in the Cellular Response to Solar Ultraviolet Light Cancer Res., December 1, 2006; 66(23): 11140 - 11147. [Abstract] [Full Text] [PDF] S. S. Mukhopadhyay, K. S. Leung, M. J. Hicks, P. J. Hastings, H. Youssoufian, and S. E. Plon Defective mitochondrial peroxiredoxin-3 results in sensitivity to oxidative stress in Fanconi anemia J. Cell Biol., October 23, 2006; 175(2): 225 - 235. [Abstract] [Full Text] [PDF] A. L. Medhurst, E. H. Laghmani, J. Steltenpool, M. Ferrer, C. Fontaine, J. de Groot, M. A. Rooimans, R. J. Scheper, A. R. Meetei, W. Wang, et al. Evidence for subcomplexes in the Fanconi anemia pathway Blood, September 15, 2006; 108(6): 2072 - 2080. [Abstract] [Full Text] [PDF] T. Taniguchi and A. D. D'Andrea Molecular pathogenesis of Fanconi anemia: recent progress Blood, June 1, 2006; 107(11): 4223 - 4233. [Abstract] [Full Text] [PDF] A. Sobeck, S. Stone, V. Costanzo, B. de Graaf, T. Reuter, J. de Winter, M. Wallisch, Y. Akkari, S. Olson, W. Wang, et al. Fanconi Anemia Proteins Are Required To Prevent Accumulation of Replication-Associated DNA Double-Strand Breaks Mol. Cell. Biol., January 15, 2006; 26(2): 425 - 437. [Abstract] [Full Text] [PDF] R. D. Kennedy and A. D. D'Andrea The Fanconi Anemia/BRCA pathway: new faces in the crowd Genes & Dev., December 15, 2005; 19(24): 2925 - 2940. [Abstract] [Full Text] [PDF] M. Ferrer, J. A. Rodriguez, E. A. Spierings, J. P. de Winter, G. Giaccone, and F. A.E. Kruyt Identification of multiple nuclear export sequences in Fanconi anemia group A protein that contribute to CRM1-dependent nuclear export Hum. Mol. Genet., May 15, 2005; 14(10): 1271 - 1281. [Abstract] [Full Text] [PDF]

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