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Rabbit Anti-FANCD2 Recombinant Antibody (1290D) (CBMAB-F0054-CQ)

This product is a rabbit antibody that recognizes FANCD2. The antibody 1290D can be used for immunoassay techniques such as: WB, FC, IHC, IHC-P, Knockout.
See all FANCD2 antibodies

Summary

Host Animal
Rabbit
Specificity
Human
Clone
1290D
Antibody Isotype
IgG
Application
WB, FC, IHC, IHC-P, Knockout

Basic Information

Immunogen
Human FANCD2 fusion protein (N-terminal fragment)
Specificity
Human
Antibody Isotype
IgG
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
Concentration
1 mg/mL
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
Fanconi Anemia Complementation Group D2
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 D2. This protein is monoubiquinated in response to DNA damage, resulting in its localization to nuclear foci with other proteins (BRCA1 AND BRCA2) involved in homology-directed DNA repair. Alternative splicing results in multiple transcript variants.
Entrez Gene ID
2177
UniProt ID
Q9BXW9
Alternative Names
Fanconi Anemia Complementation Group D2; FACD; Fanconi Anemia Group D2 Protein; Protein FACD2; FANCD; FA-D2; FAD2; FAD; FA4;
Research Area
Required for maintenance of chromosomal stability. Promotes accurate and efficient pairing of homologs during meiosis. Involved in the repair of DNA double-strand breaks, both by homologous recombination and single-strand annealing. May participate in S phase and G2 phase checkpoint activation upon DNA damage. Plays a role in preventing breakage and loss of missegregating chromatin at the end of cell division, particularly after replication stress. Required for the targeting, or stabilization, of BLM to non-centromeric abnormal structures induced by replicative stress. Promotes BRCA2/FANCD1 loading onto damaged chromatin. May also be involved in B-cell immunoglobulin isotype switching.
Biological Process
Double-strand break repair involved in meiotic recombination Source: GO_Central
Homologous chromosome pairing at meiosis Source: GO_Central
Interstrand cross-link repair Source: GO_Central
Mitotic intra-S DNA damage checkpoint signaling Source: GO_Central
Response to gamma radiation Source: UniProtKB
Cellular Location
Nucleus. Concentrates in nuclear foci during S phase and upon genotoxic stress. At the onset of mitosis, excluded from chromosomes and diffuses into the cytoplasm, returning to the nucleus at the end of cell division. Observed in a few spots localized in pairs on the sister chromatids of mitotic chromosome arms and not centromeres, one on each chromatids. These foci coincide with common fragile sites and could be sites of replication fork stalling. The foci are frequently interlinked through BLM-associated ultra-fine DNA bridges. Following aphidicolin treatment, targets chromatid gaps and breaks.
Involvement in disease
Fanconi anemia complementation group D2 (FANCD2):
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.
PTM
Monoubiquitinated on Lys-561 during S phase and upon genotoxic stress by FANCL in complex with E2 ligases UBE2T or UBE2W (isoform 1 and isoform 2). Deubiquitinated by USP1 as cells enter G2/M, or once DNA repair is completed. Monoubiquitination requires the joint intervention of the FANC core complex, including FANCA, FANCB, FANCC, FANCE, FANCF, FANCG, and FANCM, and proteins involved in cell cycle checkpoints and DNA repair, including RPA1, ATR, CHEK1 and BRCA1, and is mediated by FANCL/PHF9. Ubiquitination is required for binding to chromatin, interaction with BRCA1, BRCA2 and MTMR15/FAN1, DNA repair, and normal cell cycle progression, but not for phosphorylation on Ser-222 or interaction with MEN1.
Phosphorylated in response to various genotoxic stresses by ATM and/or ATR. Upon ionizing radiation, phosphorylated by ATM on Ser-222 and Ser-1404. Phosphorylation on Ser-222 is required for S-phase checkpoint activation, but not for ubiquitination, foci formation, or DNA repair. In contrast, phosphorylation by ATR on other sites may be required for ubiquitination and foci formation.

Lemonidis, K., Arkinson, C., Rennie, M. L., & Walden, H. (2022). Mechanism, specificity, and function of FANCD2‐FANCI ubiquitination and deubiquitination. The FEBS Journal, 289(16), 4811-4829.

Sijacki, T., Alcón, P., Chen, Z. A., McLaughlin, S. H., Shakeel, S., Rappsilber, J., & Passmore, L. A. (2022). The DNA-damage kinase ATR activates the FANCD2-FANCI clamp by priming it for ubiquitination. Nature Structural & Molecular Biology, 29(9), 881-890.

Rennie, M. L., Arkinson, C., Chaugule, V. K., Toth, R., & Walden, H. (2021). Structural basis of FANCD2 deubiquitination by USP1− UAF1. Nature Structural & Molecular Biology, 28(4), 356-364.

Alcón, P., Shakeel, S., Chen, Z. A., Rappsilber, J., Patel, K. J., & Passmore, L. A. (2020). FANCD2–FANCI is a clamp stabilized on DNA by monoubiquitination of FANCD2 during DNA repair. Nature structural & molecular biology, 27(3), 240-248.

Li, L., Tan, W., & Deans, A. J. (2020). Structural insight into FANCI–FANCD2 monoubiquitination. Essays in biochemistry, 64(5), 807-817.

Tan, W., van Twest, S., Leis, A., Bythell-Douglas, R., Murphy, V. J., Sharp, M., ... & Deans, A. J. (2020). Monoubiquitination by the human Fanconi anemia core complex clamps FANCI: FANCD2 on DNA in filamentous arrays. elife, 9, e54128.

Liang, Z., Liang, F., Teng, Y., Chen, X., Liu, J., Longerich, S., ... & Kupfer, G. M. (2019). Binding of FANCI-FANCD2 complex to RNA and R-loops stimulates robust FANCD2 monoubiquitination. Cell reports, 26(3), 564-572.

Dubois, E. L., Guitton-Sert, L., Béliveau, M., Parmar, K., Chagraoui, J., Vignard, J., ... & Masson, J. Y. (2019). A Fanci knockout mouse model reveals common and distinct functions for FANCI and FANCD2. Nucleic acids research, 47(14), 7532-7547.

Liang, F., Miller, A. S., Longerich, S., Tang, C., Maranon, D., Williamson, E. A., ... & Sung, P. (2019). DNA requirement in FANCD2 deubiquitination by USP1-UAF1-RAD51AP1 in the Fanconi anemia DNA damage response. Nature communications, 10(1), 1-8.

Lopez-Martinez, D., Kupculak, M., Yang, D., Yoshikawa, Y., Liang, C. C., Wu, R., ... & Cohn, M. A. (2019). Phosphorylation of FANCD2 inhibits the FANCD2/FANCI complex and suppresses the Fanconi anemia pathway in the absence of DNA damage. Cell reports, 27(10), 2990-3005.

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

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