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Fanconi anemia, complementation group G

FANCG, FAG, XRCC9
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
Supplier
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
Candidate gene analysis of BRCA1/2 mutation-negative high-risk Russian breast cancer patients.
New
Imyanitov et al., Saint Petersburg, Russia. In Cancer Lett, 10 May 2015
The analysis of genes with yet unproven BC-predisposing significance (BARD1, BRD7, CHEK1, DDB2, ERCC1, EXO1, FANCG, PARP1, PARP2, RAD51, RNF8, WRN) identified single women carrying a protein-truncating allele, WRN R1406X.
Hematological consequences of a FANCG founder mutation in Black South African patients with Fanconi anemia.
New
Krause et al., Johannesburg, South Africa. In Blood Cells Mol Dis, 31 Mar 2015
In South Africa, FA in the Black population is caused by a homozygous deletion mutation in the FANCG gene in more than 80% of cases.
Founder Haplotype Analysis of Fanconi Anemia in the Korean Population Finds Common Ancestral Haplotypes for a FANCG Variant.
New
Park et al., Seoul, South Korea. In Ann Hum Genet, 20 Mar 2015
UNASSIGNED: A common ancestral haplotype is strongly suggested in the Korean and Japanese patients with Fanconi anemia (FA), because common mutations have been frequently found: c.2546delC and c.3720_3724delAAACA of FANCA; c.307+1G>C, c.1066C>T, and c.1589_1591delATA of FANCG.
[Buckwheat allergy can cause live-threatening anaphylaxia.]
New
Kristensen et al., In Ugeskr Laeger, Jan 2015
Reliable serological tests showing specific IgE to buckwheat protein 2S albumin (Fag e2) are available in most countries.
Clinico-biochemical investigations of aging effects on normoglycemic and hyperglycemic murine retinal tissues.
New
Moon et al., Seoul, South Korea. In Microsc Res Tech, Dec 2014
Changes in the retinal thickness and neovascularization were evaluated with optical coherence tomography and fluorescein angiography (FAG).
New parametric imaging method with fluorescein angiograms for detecting areas of capillary nonperfusion.
New
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.
RNA-seq profiling of a radiation resistant and radiation sensitive prostate cancer cell line highlights opposing regulation of DNA repair and targets for radiosensitization.
Brettingham-Moore et al., Hobart, Australia. In Bmc Cancer, 2013
Candidate genes BRCA1, RAD51, FANCG, MCM7, CDC6 and ORC1 were identified as being significantly differentially regulated post-irradiation.
Impaired functionality and homing of Fancg-deficient hematopoietic stem cells.
GeneRIF
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.
Review
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.
GeneRIF
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.
GeneRIF
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.
GeneRIF
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.
Review
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.
GeneRIF
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.
Review
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.
Review
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.
Impact
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].
Review
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.
Impact
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.
Impact
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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