Molecular biology of Fanconi anaemia—an old problem, a new insight

No abstract is available for this paper.

• Publication year

  2002

• Venue

  Bioessays

• Publication date

  2002-05-01

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1002/bies.10082PMID 12001267
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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• Functional correction of FA-C cells with FANCC suppresses the expression of interferon gamma-inducible genes.

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• Functional correction of fanconi anemia group C hematopoietic cells by the use of a novel lentiviral vector.

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• Interaction of the Fanconi anemia proteins and BRCA1 in a common pathway.

  2001influential reference
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• Fanconi Anemia Proteins Localize to Chromatin and the Nuclear Matrix in a DNA Damage- and Cell Cycle-regulated Manner*

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• Positional cloning of a novel Fanconi anemia gene, FANCD2.

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

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• Deficient DNA End Joining Activity in Extracts from Fanconi Anemia Fibroblasts*

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• Direct interactions of the five known Fanconi anaemia proteins suggest a common functional pathway.

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• Hydrogen peroxide: effects on DNA, chromosomes, cell cycle and apoptosis induction in Fanconi's anemia cell lines.

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• Localization of the Fanconi anemia complementation group D gene to a 200-kb region on chromosome 3p25.3.

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• Complementation analysis in Fanconi anemia: assignment of the reference FA-H patient to group A.

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• Mice with a targeted disruption of the Fanconi anemia homolog Fanca.

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• Carboxy terminal region of the Fanconi anemia protein, FANCG/XRCC9, is required for functional activity.

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• The role of STATs in transcriptional control and their impact on cellular function

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• The Fanconi Anemia Protein FANCC Binds to and Facilitates the Activation of STAT1 by Gamma Interferon and Hematopoietic Growth Factors

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• Arrest of S-phase progression is impaired in Fanconi anemia cells.

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• Isolation of a cDNA representing the Fanconi anemia complementation group E gene.

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• Cytoskeleton alterations of erythrocytes from patients with Fanconi's anemia

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• The Fanconi anaemia gene FANCF encodes a novel protein with homology to ROM

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• The Fanconi anemia protein FANCF forms a nuclear complex with FANCA, FANCC and FANCG.

  2000influential reference
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• The IVS4 + 4 A to T mutation of the fanconi anemia gene FANCC is not associated with a severe phenotype in Japanese patients.

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• Mitomycin C and diepoxybutane action mechanisms and FANCC protein functions: further insights into the role for oxidative stress in Fanconi's anaemia phenotype.

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• Fanconi anemia, complementation group A, cells are defective in ability to produce incisions at sites of psoralen interstrand cross-links.

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• Redox-dependent toxicity of diepoxybutane and mitomycin C in sea urchin embryogenesis.

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• Interferon-gamma-induced apoptotic responses of Fanconi anemia group C hematopoietic progenitor cells involve caspase 8-dependent activation of caspase 3 family members.

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• Human α Spectrin II and the Fanconi Anemia Proteins FANCA and FANCC Interact to Form a Nuclear Complex*

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• The Fanconi anemia group E gene, FANCE, maps to chromosome 6p.

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• Drug sensitivity spectra in Fanconi anemia lymphoblastoid cell lines of defined complementation groups.

  1999cited by this paper
• Mitomycin C-induced DNA damage in Fanconi anemia: cross-linking or redox-mediated effects?

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• Molecular spectra of HPRT deletion mutations in circulating T-lymphocytes in Fanconi anemia patients.

  1999influential reference
• Nuclear localization of the Fanconi anemia protein FANCC is required for functional activity.

  1999cited by this paper
• The molecular and cellular biology of Fanconi anemia.

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• A novel BTB/POZ transcriptional repressor protein interacts with the Fanconi anemia group C protein and PLZF.

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• Regulated Binding of the Fanconi Anemia Proteins, FANCA and FANCC

  1999cited by this paper
• Expression of the Fanconi anemia group A gene (Fanca) during mouse embryogenesis.

  1999cited by this paper
• High frequency of large intragenic deletions in the Fanconi anemia group A gene.

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• Loss of FancC Function Results in Decreased Hematopoietic Stem Cell Repopulating Ability

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• The human and rat forms of multiple inositol polyphosphate phosphatase: functional homology with a histidine acid phosphatase up‐regulated during endochondral ossification

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• Fanconi Anemia Proteins FANCA, FANCC, and FANCG/XRCC9 Interact in a Functional Nuclear Complex

  1999cited by this paper
• Overexpression of thioredoxin in Fanconi anemia fibroblasts prevents the cytotoxic and DNA damaging effect of mitomycin C and diepoxybutane

  1998cited by this paper
• Fanconi's anemia cells are relatively resistant to H2O2-induced damage.

  1998cited by this paper
• The fanconi anemia pathway requires FAA phosphorylation and FAA/FAC nuclear accumulation.

  1998influential reference
• Fanconi anemia C gene product plays a role in the fidelity of blunt DNA end-joining.

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• Abnormal microsomal detoxification implicated in Fanconi anemia group C by interaction of the FAC protein with NADPH cytochrome P450 reductase.

  1998cited by this paper
• The Fanconi anaemia group G gene FANCG is identical with XRCC9

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• Localisation of a Fanconi anaemia gene to chromosome 9p

  1998cited by this paper
• Identification of Alu‐mediated deletions in the Fanconi anemia gene FAA

  1998cited by this paper
• Overexpression of the fanconi anemia group C gene (FAC) protects hematopoietic progenitors from death induced by Fas-mediated apoptosis.

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• Fanconi ’ s anemia cells are relatively resistant to H 202-induced damage

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• Fanconi's anaemia cells have normal steady-state levels and repair of oxidative DNA base modifications sensitive to Fpg protein.

  1998cited by this paper
• Abnormal rearrangements associated with V(D)J recombination in Fanconi anemia.

  1998cited by this paper
• Involvement of the Fanconi anemia protein FA‐C in repair processes of oxidative DNA damages

  1998cited by this paper
• Functional Activity of the Fanconi Anemia Protein FAA Requires FAC Binding and Nuclear Localization

  1998cited by this paper
• [Repair of oxidized guanine in mammals: OGG1 genes].

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• Inactivation of the Fanconi anemia group C gene augments interferon-gamma-induced apoptotic responses in hematopoietic cells.

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• Evidence for at least eight Fanconi anemia genes.

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• The fidelity of double strand breaks processing is impaired in complementation groups B and D of fanconi anemia, a genetic instability syndrome

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• The genomic organization of the Fanconi anemia group A (FAA) gene.

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• Mutagenic activity of ambient oxygen and mitomycin C in Fanconi's anaemia cells.

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• GSTT1-dependent induction of centromere-negative and -positive micronuclei by 1,2:3,4-diepoxybutane in cultured human lymphocytes.

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• Erratum: Expression cloning of a cDNA for the major Fanconi anaemia gene, FAA

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• A common mutation in the FACC gene causes Fanconi anaemia in Ashkenazi Jews

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