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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, LCE, CAN
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
Molecular analysis of Fanconi anemia: the experience of the Bone Marrow Failure Study Group of the Italian Association of Pediatric Onco-Hematology.
Bone Marrow Failure Study Group of the Italian Association of Pediatric Onco-Hematology et al., Trieste, Italy. In Haematologica, Jun 2014
We identified 108 distinct variants of the FANCA, FANCG, FANCC, FANCD2, and FANCB genes in 85, 9, 3, 2, and 1 families, respectively.
Hypersensitivities for acetaldehyde and other agents among cancer cells null for clinically relevant Fanconi anemia genes.
Kern et al., Baltimore, United States. In Am J Pathol, Jan 2014
A characteristic matching of FANCC-null, FANCG-null, BRCA2/FANCD1-null, and PALB2/FANCN-null phenotypes was confirmed by uniform tumor regression on single-dose cross-linker therapy in mice and by shared chemical hypersensitivities to various inter-strand cross-linking agents and γ-radiation in vitro.
Fanconi anaemia in black South African patients heterozygous for the FANCG c.637-643delTACCGCC founder mutation.
Krause et al., Johannesburg, South Africa. In S Afr Med J, Dec 2013
A founder mutation in the FANCG gene occurs in the homozygous state in 77.5% of southern African blacks.
Mechanism of action of salvianolic acid B by module-based network analysis.
Qiao et al., Beijing, China. In Biomed Mater Eng, Dec 2013
By fast agglomerate algorithm based on the edge clustering coefficients (FAG-EC), 11 modules were detected from the network.
Massively parallel sequencing, aCGH, and RNA-Seq technologies provide a comprehensive molecular diagnosis of Fanconi anemia.
NISC Comparative Sequencing Program et al., Bethesda, United States. In Blood, Jun 2013
The combination of TruSeq-targeted capture, aCGH, and RNA-seq enabled us to identify the complementation group and biallelic germline mutations in all 27 families: FANCA (7), FANCB (3), FANCC (3), FANCD1 (1), FANCD2 (3), FANCF (2), FANCG (2), FANCI (1), FANCJ (2), and FANCL (3).
Testing the utility of an integrated analysis of copy number and transcriptomics datasets for inferring gene regulatory relationships.
Fitzgerald et al., Cambridge, United Kingdom. In Plos One, 2012
Three additional predicted ERBB2 regulated interactions were confirmed, as well as interactions regulated by ARPC1A and FANCG.
Lymphocytes of patients with Alzheimer's disease display different DNA damage repair kinetics and expression profiles of DNA repair and stress response genes.
Sakamoto-Hojo et al., Ribeirão Preto, Brazil. In Int J Mol Sci, 2012
Real-time quantitative analysis of genes associated with DNA stress response also showed that FANCG and CDKN1A are upregulated in AD, while MTH1 is downregulated, compared with the control group.
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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