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Mouse Anti-FANCC (AA 1-101) Recombinant Antibody (CBXF-0283) (CBMAB-F2188-CQ)

This product is a mouse antibody that recognizes FANCC (AA 1-101). The antibody CBXF-0283 can be used for immunoassay techniques such as: ELISA, WB.
See all FANCC antibodies

Summary

Host Animal
Mouse
Specificity
Human
Clone
CBXF-0283
Antibody Isotype
IgG2b, κ
Application
ELISA, WB

Basic Information

Specificity
Human
Antibody Isotype
IgG2b, κ
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Buffer
PBS, pH 7.2
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.
Epitope
AA 1-101

Target

Full Name
Fanconi anemia, complementation group C
Introduction
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.
Entrez Gene ID
2176
UniProt ID
Q00597
Alternative Names
Fanconi Anemia Complementation Group C; FACC; FAC; Fanconi Anemia Group C Protein; Protein FACC; FA3;
Research Area
DNA repair protein that may operate in a postreplication repair or a cell cycle checkpoint function. May be implicated in interstrand DNA cross-link repair and in the maintenance of normal chromosome stability. Upon IFNG induction, may facilitate STAT1 activation by recruiting STAT1 to IFNGR1.
Biological Process
Brain morphogenesis Source: Ensembl
Cellular response to oxidative stress Source: GO_Central
DNA repair Source: ProtInc
Germ cell development Source: Ensembl
Interstrand cross-link repair Source: InterPro
Myeloid cell homeostasis Source: Ensembl
Neuronal stem cell population maintenance Source: Ensembl
Nucleotide-excision repair Source: GO_Central
Protein-containing complex assembly Source: ProtInc
Removal of superoxide radicals Source: Ensembl
Cellular Location
Nucleus; Cytoplasm. The major form is nuclear. The minor form is cytoplasmic.
Involvement in disease
Fanconi anemia complementation group C (FANCC):
A disorder affecting all bone marrow elements and resulting in anemia, leukopenia and thrombopenia. It is associated with cardiac, renal and limb malformations, dermal pigmentary changes, and a predisposition to the development of malignancies. At the cellular level it is associated with hypersensitivity to DNA-damaging agents, chromosomal instability (increased chromosome breakage) and defective DNA repair.

Xia, M., Li, X., Ye, S., Zhang, Q., Zhao, T., Li, R., ... & Yang, L. (2022). FANCC deficiency mediates microglial pyroptosis and secondary neuronal apoptosis in spinal cord contusion. Cell & Bioscience, 12(1), 1-15.

Shahid, M., Azfaralariff, A., Zubair, M., Najm, A. A., Khalili, N., Law, D., ... & Fazry, S. (2022). In silico study of missense variants of FANCA, FANCC and FANCG genes reveals high risk deleterious alleles predisposing to Fanconi anemia pathogenesis. Gene, 812, 146104.

Plimack, E. R., Tangen, C., Plets, M., Kokate, R., Xiu, J., Nabhan, C., ... & McConkey, D. J. (2022). S1314 correlative analysis of ATM, RB1, ERCC2, and FANCC mutations and pathologic complete response (pT0) at cystectomy after neoadjuvant chemotherapy (NAC) in patients with muscle invasive bladder cancer (MIBC): Implications for bladder preservation.

Singh, D. K., Salinas-Gamboa, R., Singh, A. K., Walkemeir, B., Van Leene, J., De Jaeger, G., ... & Mercier, R. (2022). The FANCC-FANCE-FANCF complex is evolutionarily conserved and regulates meiotic recombination. bioRxiv.

Tiwari, S. K., Dang, J. W., Lin, N., Qin, Y., Wang, S., & Rana, T. M. (2020). Zika virus depletes neural stem cells and evades selective autophagy by suppressing the Fanconi anemia protein FANCC. EMBO reports, 21(12), e49183.

Negahdari, S., Zamani, M., Seifi, T., Sedighzadeh, S., Mazaheri, N., Zeighami, J., ... & Galehdari, H. (2020). Identification of three novel mutations in the FANCA, FANCC, and ITGA2B genes by whole exome sequencing. International journal of preventive medicine, 11.

Pan, Z. W., Wang, X. J., Chen, T., Ding, X. W., Jiang, X., Gao, Y., ... & Cao, W. M. (2019). Deleterious mutations in DNA repair gene FANCC exist in BRCA1/2-Negative Chinese familial breast and/or Ovarian Cancer patients. Frontiers in Oncology, 9, 169.

Zha, J., Kunselman, L., Fan, J. M., & Olson, T. S. (2019). Bone marrow niches of germline FANCC/FANCG deficient mice enable efficient and durable engraftment of hematopoietic stem cells after transplantation. haematologica, 104(7), e284.

García‐de Teresa, B., Frias, S., Molina, B., Villarreal, M. T., Rodriguez, A., Carnevale, A., ... & Torres, L. (2019). FANCC Dutch founder mutation in a Mennonite family from Tamaulipas, México. Molecular genetics & genomic medicine, 7(6), e710.

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For research use only. Not intended for any clinical use.

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