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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). Zusätzlich bieten wir Ihnen Fanconi Anemia Group A Protein Proteine (4) und Fanconi Anemia Group A Protein Kits (2) und viele weitere Produktgruppen zu diesem Protein an.
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Human Polyclonal FANCA Primary Antibody für IP, WB - ABIN5665644
Hicks, Chute, Paulsen, Ragland, Howlett, Guéranger, Glover, Canman: Differential roles for DNA polymerases eta, zeta, and REV1 in lesion bypass of intrastrand versus interstrand DNA cross-links. in Molecular and cellular biology 2010
Show all 3 Pubmed References
Human Polyclonal FANCA Primary Antibody für WB - ABIN251002
Park, Ciccone, Beck, Hwang, Freie, Clapp, Lee: Oxidative stress/damage induces multimerization and interaction of Fanconi anemia proteins. in The Journal of biological chemistry 2004
Human Polyclonal FANCA Primary Antibody für ELISA, ICC - ABIN4309986
Huard, Tremblay, Magron, Lévesque, Carreau: The Fanconi anemia pathway has a dual function in Dickkopf-1 transcriptional repression. in Proceedings of the National Academy of Sciences of the United States of America 2014
we show that although FANCA S1088F protein properly localizes to the nucleus, it alters FANC complex function, enhances sensitivity to DNA damaging agents, and sensitizes cells to PARP (zeige COL11A2 Antikörper) inhibitors in vitro and in vivo.
FancA amplification and overexpression appear to be crucial for radiotherapeutic failure in head and neck squamous cell carcinomas.
High resolution melting curve analysis was used to screen FANCA, and LinReg software version 1.7 was utilized for analysis of expression. RESULTS: In total, six sequence alterations were identified, which included two stop codons, two frames-shift mutations, one large deletion and one amino acid exchange. FANCA expression was downregulated in patients who had sequence alterations.
Results identified homozygous mutations in FANCA and FANCP/SLX4 (zeige BTBD12 Antikörper) genes, both located on chromosome 16, were the affected recessive FA genes in three and one family respectively. Genotyping with short tandem repeat markers and SNP arrays revealed uniparental disomy of the entire mutation-carrying chromosome 16 in all four patients.
Using human and murine cells defective in FANCD2 (zeige FANCD2 Antikörper) or FANCA and primary bone marrow cells derived from FANCD2 (zeige FANCD2 Antikörper) deficient mice, we show that the FA pathway removes R loops and that many DNA breaks accumulated in FA cells are R loop-dependent.
FANCA safeguards interphase and mitosis during hematopoiesis
The I939S point mutation prevented binding to the FAAP20 subunit of the FA core complex, caused SUMOylation at K921, RNF4 (zeige RNF4 Antikörper)-mediated polyubiquitination and degradation.
A frameshifting mutation and a truncating mutation of FANCA are associated with Fanconi anemia (zeige PALB2 Antikörper).
Proliferation is compromised in FANCA-deficient pluripotent embryonic stem cells.
FANCA-modulated neddylation pathway involved in CXCR5 (zeige CXCR5 Antikörper) membrane targeting and cell mobility.
study indicates that Fanca expression during endomitosis is crucial for normal megakaryopoiesis and platelet production.
Data show that Fanconi anemia complementation group A Fanca is required for the induction of transition mutations at A/T residues during somatic hypermutation (SHM (zeige CNTNAP1 Antikörper)) and immunoglobulin (Ig) class switch recombination (CSR (zeige SCARA3 Antikörper)).
CD25 (zeige IL2RA Antikörper)(+)Foxp3 (zeige FOXP3 Antikörper)(+) Tregs of Fanca(-/-) or Fancd2 (zeige FANCD2 Antikörper)(-/-) mice were less efficient in suppressing the production of GVHD-associated inflammatory cytokines.
null mutations in Fanca or Fancg (zeige FANCG Antikörper) are fully epistatic
genetic diversity in FANCA, FANCC (zeige FANCC Antikörper) and FANCL (zeige FANCL Antikörper) does not support an association of these genes with cervical cancer susceptibility in the Swedish population.
The results support a model where both FANCA and FANCC (zeige FANCC Antikörper) are part of a multi-protein nuclear FA complex with identical function in cellular responses to DNA damage and germ cell survival.
To study the in vivo role of the FA group A gene (Fanca), gene-targeting techniques were used to generate Fanca(tm1Hsc) mice in which Fanca exons 1-6 were replaced by a beta (zeige SUCLA2 Antikörper)-galactosidase (zeige GLB1 Antikörper) reporter construct.
GnRH (zeige GNRH1 Antikörper) induced a rapid, transient increase in Fanca mRNA.
Fanca protein as an integral component in the early step of homologous repair of DNA double-strand brearks thereby minimizing the genomic instability.
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 A. Alternative splicing results in multiple transcript variants encoding different isoforms. Mutations in this gene are the most common cause of Fanconi anemia.
Fanconi anemia group A protein
, Fanconi anemia, complementation group H
, Fanconi anemia, type 1
, Fanconi anemia group A protein homolog