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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). Additionally we are shipping Fanconi Anemia, Complementation Group C Antibodies (112) and Fanconi Anemia, Complementation Group C Proteins (6) and many more products for this protein.
Lung adenocarcinomas in both male and female patients were associated with (a) genotypic polymorphisms of FANCC and FANCD1 (show BRCA2 ELISA Kits).
Israeli ATM (show ATM ELISA Kits), BLM, and FANCC heterozygous mutation carriers are not at an increased risk for developing cancer.
FANCC interacts and co-localizes with STMN1 (show STMN1 ELISA Kits) at centrosomes during mitosis. We also showed that FANCC is required for STMN1 (show STMN1 ELISA Kits) phosphorylation.
FANCC interferes with UNC5A's functions in apoptosis and suggest that FANCC may participate in developmental processes through association with the dependence receptor UNC5A (show UNC5A ELISA Kits).
The successful in vitro repair of the mutated Fanconi anemia (show PALB2 ELISA Kits) FANCC gene using the CRISPR/Cas9 system has been described.
Data indicate that TLR-indu (show IL1B ELISA Kits)ced IL-1beta overproduction in FANCA- and FANCC-deficie (show CRK ELISA Kits)nt mononuclear phagocyte cell lines and primary cells requires activation of the inflammasome.
deregulations of the FANCC-mediated DNA damage repair pathway and the PTCH1 (show PTCH1 ELISA Kits)-associated sonic hedgehog (show SHH ELISA Kits) pathway are associated with the development of early dysplastic head and neck lesions.
we identified faults in two genes, Fanconi C and Bloom helicase( FANCC and BLM), in six families. Faults in these genes appear to increase the risk of developing breast cancer
FANCC polymorphisms might be associated with the obstructive symptoms in allergic diseases.
FA DNA repair genes, FANCD2 (show FANCD2 ELISA Kits), FANCL (show FANCL ELISA Kits), and FANCC, are transcriptionally upregulated differently in melanoma compared with non-melanoma skin cancer
Genetic deletion of Fancc blocks the autophagic clearance of viruses (virophagy) and increases susceptibility to lethal viral encephalitis. Fanconi anemia complementation group C (FANCC) protein interacts with Parkin (show PARK2 ELISA Kits), is required in vitro and in vivo for clearance of damaged mitochondria, and decreases mitochondrial reactive oxygen species (ROS (show ROS1 ELISA Kits)) production and inflammasome activation.
Data show that Fanconi anemia (show PALB2 ELISA Kits), complementation group C protein knockout (Fancc -/-) mice develop hematopoietic chromosomal instability followed by leukemia in an age-dependent manner.
Loss of Fancc Impairs Antibody-Secreting Cell Differentiation in Mice through Deregulating the Wnt (show WNT2 ELISA Kits) Signaling Pathway
Combined deficiency of Foxo3a (show FOXO3 ELISA Kits) and Fancc or Fancd2 (show FANCD2 ELISA Kits) not only impairs the self-renewal capacity but also markedly increases the apoptosis of neural stem and progenitor cells (NSPCs), leading to defective neurogenesis.
Using mice deficient in both Mus81 (show MUS81 ELISA Kits) and the FA pathway protein FancC, we show both proteins cooperate in parallel pathways, as concomitant loss of FancC and Mus81 (show MUS81 ELISA Kits) triggered cell-type-specific proliferation arrest, apoptosis and DNA damage accumulation in utero.
Loss of FANCC leads to a drastic increase in stalled/collapsed forks in cells carrying an Mcm4 (show MCM4 ELISA Kits) missense mutation.
FANCC is most likely to be critical for resistance to DNA cross-linking drug-induced DNA damage in cells transformed by JAK2 (show JAK2 ELISA Kits) V617F mutant.
Data indicate that IL-1beta (show IL1B ELISA Kits) overproduction from FANCC-deficient macrophages is p38 (show CRK ELISA Kits) dependent.
Loss of FANCC expression results in an impaired emergency granulopoiesis response in a transgenic mouse model of Fanconi anemia (show PALB2 ELISA Kits).
Compromised hematopoiesis in Fancc(-/-) animals is developmentally programmed and does not arise de novo in bone marrow.
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 C.
Fanconi anemia, complementation group C protein
, Fanconi anemia C
, Fanconi anemia, complementation group C
, fanconi anemia group C protein-like
, Fanconi anemia group C protein-like
, Fanconi anemia group C protein
, Fanconi anemia group C protein homolog