Recombinant Mouse Fanconi anemia group C protein homolog (Fancc)

1. 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, is required in vitro and in vivo for clearance of damaged mitochondria, and decreases mitochondrial reactive oxygen species (ROS) production and inflammasome activation. PMID: 27133164
2. Data show that Fanconi anemia, complementation group C protein knockout (Fancc -/-) mice develop hematopoietic chromosomal instability followed by leukemia in an age-dependent manner. PMID: 26860989
3. Loss of Fancc Impairs Antibody-Secreting Cell Differentiation in Mice through Deregulating the Wnt Signaling Pathway PMID: 26895835
4. Combined deficiency of Foxo3a and Fancc or Fancd2 not only impairs the self-renewal capacity but also markedly increases the apoptosis of neural stem and progenitor cells (NSPCs), leading to defective neurogenesis. PMID: 24483844
5. Using mice deficient in both Mus81 and the FA pathway protein FancC, we show both proteins cooperate in parallel pathways, as concomitant loss of FancC and Mus81 triggered cell-type-specific proliferation arrest, apoptosis and DNA damage accumulation in utero. PMID: 25056314
6. Loss of FANCC leads to a drastic increase in stalled/collapsed forks in cells carrying an Mcm4 missense mutation. PMID: 24589582
7. FANCC is most likely to be critical for resistance to DNA cross-linking drug-induced DNA damage in cells transformed by JAK2 V617F mutant. PMID: 23838005
8. Data indicate that IL-1beta overproduction from FANCC-deficient macrophages is p38 dependent. PMID: 24046015
9. Loss of FANCC expression results in an impaired emergency granulopoiesis response in a transgenic mouse model of Fanconi anemia. PMID: 23925293
10. Compromised hematopoiesis in Fancc(-/-) animals is developmentally programmed and does not arise de novo in bone marrow. PMID: 23315168
11. Double-mutant Fancc(-/-);Fancg(-/-) mice develop spontaneous hematologic sequelae including bone marrow failure, acute myeloid leukemia, myelodysplasia and complex random chromosomal abnormalities that the single-mutant mice do not. PMID: 20606166
12. Fancc deficiency accelerates telomere shortening during high turnover of hematopoietic cells and promotes telomere recombination initiated by short telomeres. PMID: 20022886
13. whereas Fancc-/- mice failed to form hematopoietic or solid malignancies, mice mutant at both Fancc and Trp53 developed tumors more rapidly than mice mutant at Trp53 alone. PMID: 12855557
14. Fancc mutations result in a subtle immunological defect owing to the failure of FANCC to normally support Janus kinase/STAT signaling, such that differentiation of Fancc-/- CD4+ T cells into the Th1 subset is impaired in Fancc-deficient mice. PMID: 15356134
15. the intrinsic defects in the genomic stability of Fancc(-/-) stem/progenitor cells provide a selective pressure for cells that are resistant to apoptosis and have a propensity for the evolution to clonal hematopoiesis and malignancy PMID: 15644418
16. predisposition of Fancc-/- hematopoietic progenitors to apoptosis is mediated in part through altered redox regulation and apoptosis signal-regulating kinase 1 hyperactivation PMID: 16109778
17. Data suggest that TNF-alpha exposure creates an environment in which somatically mutated preleukemic stem cell clones are selected and from which unaltered TNF-alpha-hypersensitive Fancc-/- stem cells are purged. PMID: 17960249
18. Short-term transduction of c-kit(+) cells with a foamyviral vector is sufficient for functional correction of a stem cell phenotype in a murine Fanconi anemia model. PMID: 18684868

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KEGG: mmu:14088

UniGene: Mm.126106