Cited by 1,198DNA Repair MechanismsBlood disorders and treatmentsPARP inhibition in cancer therapy

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Interaction of the Fanconi Anemia Proteins and BRCA1 in a Common Pathway

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Garcia-Higuera, Irene, Taniguchi, Toshiyasu, Ganesan, Shridar, Meyn, M.Stephen, Timmers, Cynthia, Hejna, James, Grompe, Markus, D'Andrea, Alan D·2001·Molecular Cell

DOI 10.1016/s1097-2765(01)00173-3

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Abstract

Fanconi anemia (FA) is a human autosomal recessive cancer susceptibility disorder characterized by cellular sensitivity to mitomycin C and ionizing radiation. Although six FA genes (for subtypes A, C, D2, E, F, and G) have been cloned, their relationship to DNA repair remains unknown. In the current study, we show that a nuclear complex containing the FANCA, FANCC, FANCF, and FANCG proteins is required for the activation of the FANCD2 protein to a monoubiquitinated isoform. In normal (non-FA) cells, FANCD2 is monoubiquitinated in response to DNA damage and is targeted to nuclear foci (dots). Activated FANCD2 protein colocalizes with the breast cancer susceptibility protein, BRCA1, in ionizing radiation-induced foci and in synaptonemal complexes of meiotic chromosomes. The FANCD2 protein, therefore, provides the missing link between the FA protein complex and the cellular BRCA1 repair machinery. Disruption of this pathway results in the cellular and clinical phenotype common to all FA subtypes.

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Authors: Garcia-Higuera, I., Taniguchi, T., Ganesan, S., Meyn, M. S., Timmers, C., Hejna, J., Grompe, M., & D'Andrea, A. D.
Affiliations: Harvard University (US)
Dana-Farber Cancer Institute (US)
Hospital for Sick Children (CA)
Oregon Health & Science University (US)
ORCID: Taniguchi, Toshiyasu
Ganesan, Shridar
Meyn, M.Stephen
Timmers, Cynthia
Hejna, James
Grompe, Markus
Venue: Molecular Cell
Publisher: Elsevier BV
Published: 2001-02
Volume: 7
Issue: 2
Pages: 249-262
ISSN: 1097-2765 (ISSN-L)
DOI: 10.1016/s1097-2765(01)00173-3
OpenAlex: W1991841649
Cited by: 1,198
References: 71
Citations by year: 2026: 14 · 2025: 13 · 2024: 14 · 2023: 20 · 2022: 15 · 2021: 24 · 2020: 25 · 2019: 41 · 2018: 28 · 2017: 20 · 2016: 54 · 2015: 49 · 2014: 51 · 2013: 44 · 2012: 66
FWCI: 31.72
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 4549 d)
Locations: Molecular Cell (publishedVersion)
PubMed (publishedVersion)
Funders: National Heart, Lung, and Blood Institute (P01HL54785-04, R01HL52725-04, R01HL052725)
National Institute of Diabetes and Digestive and Kidney Diseases (R01DK043889, R01DK43889-09)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
Health Sciences › Medicine › Hematology › Blood disorders and treatments
Health Sciences › Medicine › Oncology › PARP inhibition in cancer therapy
Keywords: Fanconi anemia, BRCA1, FANCD2 monoubiquitination, FANCA, FANCC, FANCF, FANCG, DNA repair, radiosensitivity, mitomycin C sensitivity, synaptonemal complex, meiotic chromosomes, nuclear foci, cancer susceptibility
MeSH terms: Animals, Cell Line, Cell Survival, DNA Damage, DNA-Binding Proteins, Fanconi Anemia, Fluorescent Antibody Technique, Genetic Complementation Test, Humans, Male, Meiosis, Nuclear Proteins, Protein Binding, Proteins, Radiation, Ionizing, Spermatocytes, Synaptonemal Complex, Ubiquitins, Ultraviolet Rays, Mitomycin, Cell Cycle Proteins, BRCA1 Protein, Active Transport, Cell Nucleus, Macromolecular Substances, Mice, Fanconi Anemia Complementation Group Proteins, Fanconi Anemia Complementation Group C Protein

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Interaction of the Fanconi Anemia Proteins and BRCA1 in a Common Pathway

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