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Fanconi anemia, complementation group G

The Fanconi anemia complementation group (FANC) currently includes FANCA, FANCB, FANCC, FANCD1 (also called BRCA2), FANCD2, FANCE, FANCF, FANCG, FANCI, FANCJ (also called BRIP1), FANCL, FANCM and FANCN (also called PALB2). The previously defined group FANCH is the same as FANCA. Fanconi anemia is a genetically heterogeneous recessive disorder characterized by cytogenetic instability, hypersensitivity to DNA crosslinking agents, increased chromosomal breakage, and defective DNA repair. The members of the Fanconi anemia complementation group do not share sequence similarity; they are related by their assembly into a common nuclear protein complex. This gene encodes the protein for complementation group G. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: FAA, FANCC, Fam, CAN, LCE
Papers using FANCG antibodies
Defective mitochondrial peroxiredoxin-3 results in sensitivity to oxidative stress in Fanconi anemia
Plon Sharon E. et al., In The Journal of Cell Biology, 2004
... FANCG cDNA were cloned into pAS2-1 bait vector (CLONTECH Laboratories, Inc.) ...
Papers on FANCG
Clinico-biochemical investigations of aging effects on normoglycemic and hyperglycemic murine retinal tissues.
Moon et al., Seoul, South Korea. In Microsc Res Tech, 11 Oct 2014
Changes in the retinal thickness and neovascularization were evaluated with optical coherence tomography and fluorescein angiography (FAG).
K63-linked ubiquitination of FANCG is required for its association with the Rap80-BRCA1 complex to modulate homologous recombination repair of DNA interstand crosslinks.
Shao et al., Beijing, China. In Oncogene, 18 Sep 2014
Here we report that FANCG was modified by the addition of lysine63-linked polyubiquitin chains (K63Ub) in response to DNA damage.
MicroRNA regulation of DNA repair gene expression in 4-aminobiphenyl-treated HepG2 cells.
Chen et al., Taiwan. In Toxicology, Sep 2014
Among them, the expression of selected six genes (UNG, LIG1, EXO1, XRCC2, PCNA, and FANCG) from different DNA repair pathways was decreased with quantitative real-time PCR (qRT-PCR).
Assessing the function of homologous recombination DNA repair in malignant pleural effusion (MPE) samples.
Curtin et al., Newcastle upon Tyne, United Kingdom. In Br J Cancer, Aug 2014
No mutations in DNA repair genes were associated with HRR status, but there was probable loss of heterozygosity of FANCG, RPA1 and PARP1.
New parametric imaging method with fluorescein angiograms for detecting areas of capillary nonperfusion.
Kim et al., South Korea. In Healthc Inform Res, Jul 2014
OBJECTIVES: Fluorescein angiography (FAG) is currently the most useful diagnostic modality for examining retinal circulation, and it is frequently used for the evaluation of patients with diabetic retinopathy, occlusive diseases, such as retinal venous and arterial occlusions, and wet macular degeneration.
Modularized functions of the Fanconi anemia core complex.
Li et al., Houston, United States. In Cell Rep, Jul 2014
Through epistasis analyses, we identify three functional modules in the FA core complex: a catalytic module consisting of FANCL, FANCB, and FAAP100 is absolutely required for the E3 ligase function, and the FANCA-FANCG-FAAP20 and the FANCC-FANCE-FANCF modules provide nonredundant and ancillary functions that help the catalytic module bind chromatin or sites of DNA damage.
Differential radiosensitivity phenotypes of DNA-PKcs mutations affecting NHEJ and HRR systems following irradiation with gamma-rays or very low fluences of alpha particles.
Chen et al., Tottori, Japan. In Plos One, Dec 2013
We also compared sister chromatid exchanges (SCE) production by very low fluences of α-particles in DNA-PKcs mutant cells, and in homologous recombination repair (HRR) mutant cells including Rad51C, Rad51D, and Fancg/xrcc9.
Impaired functionality and homing of Fancg-deficient hematopoietic stem cells.
Fouchet et al., Fontenay-aux-Roses, France. In Hum Mol Genet, 2012
Hematopoietic stem cells of Fancg-/- mice Impaired functionality and homing.
Oxidative stress in Fanconi anaemia: from cells and molecules towards prospects in clinical management.
Degan et al., Napoli, Italy. In Biol Chem, 2012
Some FA gene products involved in redox homeostasis can be summarized as follows: (a) FANCA, FANCC, and FANCG interact with cytochrome P450-related activities and/or respond to oxidative damage; (b) FANCD2 in OS response interacts with forkhead box O3 and ataxia telangiectasia mutated protein; (c) FANCG is found in mitochondria and interacts with PRDX3, and FA-G cells display distorted mitochondria and decreased peroxidase activity; (d) FANCJ (BACH1/BRIP1) is a repressor of haeme oxygenase-1 gene and senses oxidative base damage; (e) antioxidants, such as tempol and resveratrol decrease cancer incidence and haematopoietic defects in Fancd2(-/-) mice.
Evidence for complete epistasis of null mutations in murine Fanconi anemia genes Fanca and Fancg.
Arwert et al., Amsterdam, Netherlands. In Dna Repair (amst), 2012
null mutations in Fanca or Fancg are fully epistatic
Areca nut induces miR-23a and inhibits repair of DNA double-strand breaks by targeting FANCG.
Ko et al., Kao-hsiung, Taiwan. In Toxicol Sci, 2011
Areca nut extracts-induced miR-23a was correlated with a reduced FANCG expression and DSB repair, which might contribute to ANE-associated human malignancies.
Genomic instability in mice is greater in Fanconi anemia caused by deficiency of Fancd2 than Fancg.
Schiestl et al., Albany, United States. In Cancer Res, 2011
Data show that Fancd2(-/-) mice displayed a higher magnitude of chromosomal breakage and micronucleus formation than the wild-type or Fancg(-/-) mice.
Fanconi anemia.
Soulier, Paris, France. In Hematology Am Soc Hematol Educ Program, 2010
Fifteen FANC genes have been identified to date, the most prevalent being FANCA, FANCC, FANCG, and FANCD2.
The Fanconi anemia core complex is dispensable during somatic hypermutation and class switch recombination.
Jacobs et al., Amsterdam, Netherlands. In Plos One, 2009
the FA pathway (FancG) is not involved in regulating the outcome of SHM in mammals and it appears dispensable for class switch recombination
Assembling an orchestra: Fanconi anemia pathway of DNA repair.
Zhang et al., Miami, United States. In Front Biosci, 2009
Although all thirteen FA complementation groups show similar clinical and cellular phenotypes, approximately 85% of patients presented defective FANCA, FANCC, or FANCG.
A possible approach for stem cell gene therapy of Fanconi anemia.
Song, Waterloo, Canada. In Curr Gene Ther, 2009
13 complementation groups are currently discovered, and 13 distinct genes have been cloned (FANCA, FANCB, FANCC, FANCD1, FANCD2, FANCE, FANCF, FANCG, FNACI, FANCJ, FANCL, FANCM, FANCN).
The BRCA1-interacting helicase BRIP1 is deficient in Fanconi anemia.
Auerbach et al., New York City, United States. In Nat Genet, 2005
Seven Fanconi anemia-associated proteins (FANCA, FANCB, FANCC, FANCE, FANCF, FANCG and FANCL) form a nuclear Fanconi anemia core complex that activates the monoubiquitination of FANCD2, targeting FANCD2 to BRCA1-containing nuclear foci.
[A new approach for studying the retinal and choroidal circulation].
Yoneya, Saitama, Japan. In Nihon Ganka Gakkai Zasshi, 2004
2) Measurement of OS levels in eyes with retinal circulatory disturbances: Eleven eyes of 10 patients with central retinal vein occlusion (CRVO), which showed various degrees of severity, and 4 fellow unaffected eyes of selected patients were examined by both fluorescein angiography (FAG) and the new SRI system.
Disruption of the Fanconi anemia-BRCA pathway in cisplatin-sensitive ovarian tumors.
D'Andrea et al., London, United Kingdom. In Nat Med, 2003
This pathway regulates cisplatin sensitivity and is governed by the coordinate activity of six genes associated with Fanconi anemia (FANCA, FANCC, FANCD2, FANCE, FANCF and FANCG) as well as BRCA1 and BRCA2 (FANCD1).
The Fanconi anaemia group G gene FANCG is identical with XRCC9.
Joenje et al., Amsterdam, Netherlands. In Nat Genet, 1998
Here we report the identification of the gene mutated in group G, FANCG, on the basis of complementation of an FA-G cell line and the presence of pathogenic mutations in four FA-G patients.
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