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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
Diadenosine 5', 5'''-P(1),P(4)-tetraphosphate (Ap4A) is synthesized in response to DNA damage and inhibits the initiation of DNA replication.
Jones et al., Liverpool, United Kingdom. In Dna Repair (amst), Sep 2015
The level of intracellular diadenosine 5', 5'''-P(1),P(4)-tetraphosphate (Ap4A) increases several fold in mammalian cells treated with non-cytotoxic doses of interstrand DNA-crosslinking agents such as mitomycin C. It is also increased in cells lacking DNA repair proteins including XRCC1, PARP1, APTX and FANCG, while >50-fold increases (up to around 25 μM) are achieved in repair mutants exposed to mitomycin C. Part of this induced Ap4A is converted into novel derivatives, identified as mono- and di-ADP-ribosylated Ap4A.
(1)H, (13)C and (15)N resonance assignments and second structure information of Fag s 1: Fagales allergen from Fagus sylvatica.
Valente et al., Rio de Janeiro, Brazil. In Biomol Nmr Assign, Sep 2015
Among them, Fag s 1 from beech pollen is an important trigger of Fagales pollen associated allergic reactions.
ClusterViz: A Cytoscape APP for Cluster Analysis of Biological Network.
Yi Pan et al., In Ieee/acm Trans Comput Biol Bioinform, Jul 2015
Three commonly used clustering algorithms, FAG-EC, EAGLE and MCODE, are included in the current version.
Clinical aspects of Fanconi anemia individuals with the same mutation of FANCF identified by next generation sequencing.
Savoia et al., Trieste, Italy. In Birth Defects Res A Clin Mol Teratol, Jul 2015
Among these, FANCA, FANCC, and FANCG account for approximately 85% of the patients whereas the remaining genes are mutated in only a small percentage of cases.
Founder haplotype analysis of Fanconi anemia in the Korean population finds common ancestral haplotypes for a FANCG variant.
Park et al., Seoul, South Korea. In Ann Hum Genet, May 2015
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.
Candidate gene analysis of BRCA1/2 mutation-negative high-risk Russian breast cancer patients.
Imyanitov et al., Saint Petersburg, Russia. In Cancer Lett, 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.
Uncoupling of transcription and translation of Fanconi anemia (FANC) complex proteins during spermatogenesis.
O'Bryan et al., Australia. In Spermatogenesis, Jan 2015
Spermatogonia and pre-leptotene spermatocytes contained the majority of the FANC components examined i.e. complex I members FANCB, FANCG and FANCM, complex II members FANCD2 and FANCI, and complex III member FANCJ.
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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