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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 Proteins (6) and many more products for this protein.
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Chimpanzee Polyclonal FANCC Primary Antibody for EIA, WB - ABIN401268
Zanier, Briot, Dugas du Villard, Sarasin, Rosselli: Fanconi anemia C gene product regulates expression of genes involved in differentiation and inflammation. in Oncogene 2004
Show all 7 references for ABIN401268
Human Polyclonal FANCC Primary Antibody for EIA, FACS - ABIN952264
Barroso, Pita, Arias, Menendez, Zamora, Blanco, Benitez, Ribas: The Fanconi anemia family of genes and its correlation with breast cancer susceptibility and breast cancer features. in Breast cancer research and treatment 2009
Show all 4 references for ABIN952264
Human Polyclonal FANCC Primary Antibody for FACS, IF - ABIN653475
McWilliams, Bamlet, de Andrade, Rider, Couch, Cunningham, Matsumoto, Rabe, Hammer, Petersen: Polymorphic variants in hereditary pancreatic cancer genes are not associated with pancreatic cancer risk. in Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology 2009
Show all 4 references for ABIN653475
Lung adenocarcinomas in both male and female patients were associated with (a) genotypic polymorphisms of FANCC and FANCD1 (show BRCA2 Antibodies).
Israeli ATM (show ATM Antibodies), BLM, and FANCC heterozygous mutation carriers are not at an increased risk for developing cancer.
FANCC interacts and co-localizes with STMN1 (show STMN1 Antibodies) at centrosomes during mitosis. We also showed that FANCC is required for STMN1 (show STMN1 Antibodies) 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 Antibodies).
The successful in vitro repair of the mutated Fanconi anemia (show PALB2 Antibodies) FANCC gene using the CRISPR/Cas9 system has been described.
Data indicate that TLR-indu (show IL1B Antibodies)ced IL-1beta overproduction in FANCA- and FANCC-deficie (show CRK Antibodies)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 Antibodies)-associated sonic hedgehog (show SHH Antibodies) 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 Antibodies), FANCL (show FANCL Antibodies), and FANCC, are transcriptionally upregulated differently in melanoma compared with non-melanoma skin cancer
Data show that Fanconi anemia (show PALB2 Antibodies), complementation group C protein (show HNRNPC Antibodies) 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 Antibodies) Signaling Pathway
Combined deficiency of Foxo3a (show FOXO3 Antibodies) and Fancc or Fancd2 (show FANCD2 Antibodies) 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 Antibodies) and the FA pathway protein FancC, we show both proteins cooperate in parallel pathways, as concomitant loss of FancC and Mus81 (show MUS81 Antibodies) 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 Antibodies) 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 Antibodies) V617F mutant.
Data indicate that IL-1beta (show IL1B Antibodies) overproduction from FANCC-deficient macrophages is p38 (show CRK Antibodies) dependent.
Loss of FANCC expression results in an impaired emergency granulopoiesis response in a transgenic mouse model of Fanconi anemia (show PALB2 Antibodies).
Compromised hematopoiesis in Fancc(-/-) animals is developmentally programmed and does not arise de novo in bone marrow.
Double-mutant Fancc(-/-);Fancg (show FANCG Antibodies)(-/-) mice develop spontaneous hematologic sequelae including bone marrow failure, acute myeloid leukemia (show BCL11A Antibodies), myelodysplasia and complex random chromosomal abnormalities that the single-mutant mice do not.
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