Numbers of long-term hematopoietic stem cells from bone marrow of fanca and fancc knockout mice can be greatly enhanced by their collection and processing in physioxia conditions. | Numbers of long-term hematopoietic stem cells from bone marrow of fanca and fancc knockout mice can be greatly enhanced by their collection and processing in physioxia conditions. Broxmeyer HE, Capitano ML, Cooper S, Potchanant ES, Clapp DW., Free PMC Article | 07/3/2021 |
Zika virus depletes neural stem cells and evades selective autophagy by suppressing the Fanconi anemia protein FANCC. | Zika virus depletes neural stem cells and evades selective autophagy by suppressing the Fanconi anemia protein FANCC. Tiwari SK, Dang JW, Lin N, Qin Y, Wang S, Rana TM., Free PMC Article | 05/1/2021 |
FancA(-/-) and FancC(-/-) embryos have abnormal skeletal development shown by skeletal malformations, growth delay, and reduced bone mineralization. | Deletion of the Fanconi Anemia C Gene in Mice Leads to Skeletal Anomalies and Defective Bone Mineralization and Microarchitecture. Mazon M, Julien J, Ung RV, Picard S, Hamoudi D, Tam R, Filiatrault J, Frenette J, Mac-Way F, Carreau M. | 10/26/2019 |
TP53 haploinsufficiency completely rescues emergency granulopoiesis in FANCC(-/-) mice. | TP53 Haploinsufficiency Rescues Emergency Granulopoiesis in FANCC(-/-) Mice. Hu L, Huang W, Bei L, Broglie L, Eklund EA., Free PMC Article | 02/23/2019 |
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. | Fanconi Anemia Proteins Function in Mitophagy and Immunity. Sumpter R Jr, Sirasanagandla S, Fernández ÁF, Wei Y, Dong X, Franco L, Zou Z, Marchal C, Lee MY, Clapp DW, Hanenberg H, Levine B., Free PMC Article | 01/14/2017 |
Data show that Fanconi anemia, complementation group C protein knockout (Fancc -/-) mice develop hematopoietic chromosomal instability followed by leukemia in an age-dependent manner. | Leukemia and chromosomal instability in aged Fancc-/- mice. Cerabona D, Sun Z, Nalepa G., Free PMC Article | 09/10/2016 |
Loss of Fancc Impairs Antibody-Secreting Cell Differentiation in Mice through Deregulating the Wnt Signaling Pathway | Loss of Fancc Impairs Antibody-Secreting Cell Differentiation in Mice through Deregulating the Wnt Signaling Pathway. Sertorio M, Amarachintha S, Wilson A, Pang Q., Free PMC Article | 08/6/2016 |
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. | Concomitant inactivation of foxo3a and fancc or fancd2 reveals a two-tier protection from oxidative stress-induced hydrocephalus. Li X, Li L, Li J, Sipple J, Schick J, Mehta PA, Davies SM, Dasgupta B, Waclaw RR, Pang Q., Free PMC Article | 10/31/2015 |
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. | Fanconi anemia signaling and Mus81 cooperate to safeguard development and crosslink repair. Larin M, Gallo D, Tamblyn L, Yang J, Liao H, Sabat N, Brown GW, McPherson JP., Free PMC Article | 12/6/2014 |
Loss of FANCC leads to a drastic increase in stalled/collapsed forks in cells carrying an Mcm4 missense mutation. | A concomitant loss of dormant origins and FANCC exacerbates genome instability by impairing DNA replication fork progression. Luebben SW, Kawabata T, Johnson CS, O'Sullivan MG, Shima N., Free PMC Article | 07/19/2014 |
FANCC is most likely to be critical for resistance to DNA cross-linking drug-induced DNA damage in cells transformed by JAK2 V617F mutant. | Critical role of FANCC in JAK2 V617F mutant-induced resistance to DNA cross-linking drugs. Ueda F, Sumi K, Tago K, Kasahara T, Funakoshi-Tago M. | 03/22/2014 |
Data indicate that IL-1beta overproduction from FANCC-deficient macrophages is p38 dependent. | FANCA and FANCC modulate TLR and p38 MAPK-dependent expression of IL-1β in macrophages. Garbati MR, Hays LE, Keeble W, Yates JE, Rathbun RK, Bagby GC., Free PMC Article | 12/28/2013 |
Loss of FANCC expression results in an impaired emergency granulopoiesis response in a transgenic mouse model of Fanconi anemia. | Increased Fanconi C expression contributes to the emergency granulopoiesis response. Hu L, Huang W, Hjort E, Eklund EA., Free PMC Article | 11/30/2013 |
Compromised hematopoiesis in Fancc(-/-) animals is developmentally programmed and does not arise de novo in bone marrow. | Fetal origins of hematopoietic failure in a murine model of Fanconi anemia. Kamimae-Lanning AN, Goloviznina NA, Kurre P., Free PMC Article | 05/18/2013 |
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. | Genetic disruption of both Fancc and Fancg in mice recapitulates the hematopoietic manifestations of Fanconi anemia. Pulliam-Leath AC, Ciccone SL, Nalepa G, Li X, Si Y, Miravalle L, Smith D, Yuan J, Li J, Anur P, Orazi A, Vance GH, Yang FC, Hanenberg H, Bagby GC, Clapp DW., Free PMC Article | 12/4/2010 |
Fancc deficiency accelerates telomere shortening during high turnover of hematopoietic cells and promotes telomere recombination initiated by short telomeres. | FANCC suppresses short telomere-initiated telomere sister chromatid exchange. Rhee DB, Wang Y, Mizesko M, Zhou F, Haneline L, Liu Y., Free PMC Article | 07/5/2010 |
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. | Overnight transduction with foamyviral vectors restores the long-term repopulating activity of Fancc-/- stem cells. Si Y, Pulliam AC, Linka Y, Ciccone S, Leurs C, Yuan J, Eckermann O, Fruehauf S, Mooney S, Hanenberg H, Clapp DW., Free PMC Article | 01/21/2010 |
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. | TNF-alpha induces leukemic clonal evolution ex vivo in Fanconi anemia group C murine stem cells. Li J, Sejas DP, Zhang X, Qiu Y, Nattamai KJ, Rani R, Rathbun KR, Geiger H, Williams DA, Bagby GC, Pang Q., Free PMC Article | 01/21/2010 |
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. | Impaired type I IFN-induced Jak/STAT signaling in FA-C cells and abnormal CD4+ Th cell subsets in Fancc-/- mice. Fagerlie SR, Koretsky T, Torok-Storb B, Bagby GC. | 01/21/2010 |
predisposition of Fancc-/- hematopoietic progenitors to apoptosis is mediated in part through altered redox regulation and apoptosis signal-regulating kinase 1 hyperactivation | Enhanced TNF-alpha-induced apoptosis in Fanconi anemia type C-deficient cells is dependent on apoptosis signal-regulating kinase 1. Bijangi-Vishehsaraei K, Saadatzadeh MR, Werne A, McKenzie KA, Kapur R, Ichijo H, Haneline LS., Free PMC Article | 01/21/2010 |
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 | Ex vivo culture of Fancc-/- stem/progenitor cells predisposes cells to undergo apoptosis, and surviving stem/progenitor cells display cytogenetic abnormalities and an increased risk of malignancy. Li X, Le Beau MM, Ciccone S, Yang FC, Freie B, Chen S, Yuan J, Hong P, Orazi A, Haneline LS, Clapp DW., Free PMC Article | 01/21/2010 |
The results support a model where both FANCA and FANCC are part of a multi-protein nuclear FA complex with identical function in cellular responses to DNA damage and germ cell survival. | Fanconi anemia group A and C double-mutant mice: functional evidence for a multi-protein Fanconi anemia complex. Noll M, Battaile KP, Bateman R, Lax TP, Rathbun K, Reifsteck C, Bagby G, Finegold M, Olson S, Grompe M. | 01/21/2010 |
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. | Fanconi anemia type C and p53 cooperate in apoptosis and tumorigenesis. Freie B, Li X, Ciccone SL, Nawa K, Cooper S, Vogelweid C, Schantz L, Haneline LS, Orazi A, Broxmeyer HE, Lee SH, Clapp DW. | 01/21/2010 |