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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 FANCD2 Kits (10) and and many more products for this protein.
Showing 10 out of 122 products:
Dog (Canine) Polyclonal FANCD2 Primary Antibody for FACS, ICC - ABIN151329
Bekker-Jensen, Lukas, Kitagawa, Melander, Kastan, Bartek, Lukas: Spatial organization of the mammalian genome surveillance machinery in response to DNA strand breaks. in The Journal of cell biology 2006
Show all 113 references for ABIN151329
Dog (Canine) Polyclonal FANCD2 Primary Antibody for ICC, IF - ABIN250520
Garcia-Higuera, Taniguchi, Ganesan, Meyn, Timmers, Hejna, Grompe, DAndrea: Interaction of the Fanconi anemia proteins and BRCA1 in a common pathway. in Molecular cell 2001
Show all 15 references for ABIN250520
Dog (Canine) Polyclonal FANCD2 Primary Antibody for ICC, IF - ABIN250521
Rothfuss, Grompe: Repair kinetics of genomic interstrand DNA cross-links: evidence for DNA double-strand break-dependent activation of the Fanconi anemia/BRCA pathway. in Molecular and cellular biology 2003
Show all 15 references for ABIN250521
Human Monoclonal FANCD2 Primary Antibody for ChIP, IP - ABIN151782
Nomura, Adachi, Koyama: Human Mus81 and FANCB independently contribute to repair of DNA damage during replication. in Genes to cells : devoted to molecular & cellular mechanisms 2007
Show all 10 references for ABIN151782
Fancd2 has a role in DNA repair.
study showed that FANCI (show FANCI Antibodies)-FANCD2 is required for replication-coupled DNA interstrand cross-link (ICL) repair in S phase; results show that multiple steps of the essential S-phase ICL repair mechanism fail when the Fanconi anemia (show PALB2 Antibodies) pathway is compromised
The Fanconi anemia protein (show FANCF Antibodies) FANCM (show FANCM Antibodies) is controlled by FANCD2 and the ATR (show ATR Antibodies)/ATM (show ATM Antibodies) pathways.
silkworm cells deficient for FA proteins FancD2 and FancM (show FANCM Antibodies) exhibit normal sensitivities to hydroxyurea (HU) and camptothecin (CPT (show DHDDS Antibodies))
It was shown that silkworm FancD2 is monoubiquitinated depending on FancI (show FANCI Antibodies) and FancL (show FANCL Antibodies), and stabilized on chromatin, following mitomycin C. Depletion of FancD2, FancI (show FANCI Antibodies) or FancL (show FANCL Antibodies) effected cell proliferation in the presence of mitomycin C.
Alpha-spectrin (show SPTAN1 Antibodies) is critical for recruitment of non-ubiquitinated FANCD2 to sites of damage, which has an important role in the repair response and interstrand cross-link repair.
FANCJ (show BRIP1 Antibodies) protein is important for the stability of FANCD2/FANCI (show FANCI Antibodies) proteins and protects them from proteasome and caspase-3 (show CASP3 Antibodies) dependent degradation.
Using small interfering RNA (siRNA), knockdown of FANCF (show FANCF Antibodies), FANCL (show FANCL Antibodies), or FANCD2 inhibited function of the FA/BRCA pathway in A549, A549/DDP (show TIMM8A Antibodies) and SK-MES (show ME1 Antibodies)-1 cells, and potentiated sensitivity of the three cells to cisplatin.
Using human and murine cells defective in FANCD2 or FANCA (show FANCA Antibodies) and primary bone marrow cells derived from FANCD2 deficient mice, we show that the FA pathway removes R loops and that many DNA breaks accumulated in FA cells are R loop-dependent.
while dispensable for cell survival, FANCD2 selectively safeguards chromosomal stability after UV-triggered replication stress
These findings indicate that FANCI (show FANCI Antibodies) functions upstream of FA core complex recruitment independently of FANCD2, and alter the current view of the FA-BRCA pathway.
FANCD2 is a key factor in genome stability maintenance in response to high-LET radiation
describe a mechanism of interstrand crosslink (ICL) sensing and propose that UHRF1 (show UHRF1 Antibodies) is a critical factor that binds to ICLs. In turn, this binding is necessary for the subsequent recruitment of FANCD2, which allows the DNA repair process to initiate
Defective FANCI (show FANCI Antibodies) binding is associated with fanconi anemia (show PALB2 Antibodies)-related FANCD2 mutant.
FANCD2 expression levels are strongly associated with tumour grade, revealing a potential exploitable therapeutic window to allow inhibition of the FA pathway in tumour cells, whilst sparing normal brain tissue.
Data that suggest Usp1 (ubiquitin specific peptidase 1 (show USP1 Antibodies)) down-regulation by autocleavage is critical for Usp1 (show USP1 Antibodies) to exert role in DNA interstrand crosslink repair; Usp1 (show USP1 Antibodies) role is de-ubiquitination of Fancd2 and Pcna (proliferating cell nuclear antigen (show PCNA Antibodies)).
recruitment of Fan1 (show FAN1 Antibodies) by ubiquitinated-Fancd2 is dispensable for DNA interstrand cross-links repair
Results show that FANCD2 and ADH5 (show ADH5 Antibodies) protect hematopoietic stem cells, hepatocytes, and nephrons from endogenous DNA damage resulting from accumulation of endogenous formaldehyde.
Combined deficiency of Foxo3a (show FOXO3 Antibodies) and Fancc (show FANCC Antibodies) 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.
Data demonstrated that Fancd2 was required for nuclear retention of CA-FOXO3a (show FOXO3 Antibodies) and for maintaining hematopoietic repopulation of the HSCs.
CD25 (show IL2RA Antibodies)(+)Foxp3 (show FOXP3 Antibodies)(+) Tregs of Fanca (show FANCA Antibodies)(-/-) or Fancd2(-/-) mice were less efficient in suppressing the production of GVHD-associated inflammatory cytokines.
Fancd2-Ub activates the transcription of the tumor suppressor TAp63, thereby promoting cellular senescence and blocking skin tumorigenesis.
Studies indicate that in Fancd2-Knockout mice, the formation of sex-cords and intraovarian tubules lead to the formation of tumours with multiple phenotypes including luteomas, papillary cysts and malignant carcinomas.
the Fanconi anaemia DNA repair pathway counteracts acetaldehyde-induced genotoxicity in mice; Aldh2 (show ALDH2 Antibodies)(-/-)Fancd2(-/-) mice spontaneously develop acute leukaemia
crystal structure of FANCI (show FANCI Antibodies)-FANCD2(ID) complex; crystallographic electron-density map of FANCI (show FANCI Antibodies) protein bound to splayed Y DNA; data suggest ID complex recognizes DNA structures resulting from encounter of replication forks with an interstrand cross-link
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 two transcript variants encoding different isoforms.
Fanconi anemia, complementation group D2
, Fanconi anemia group D2 protein-like
, fanconi anemia protein FANCD2
, Fanconi anemia complementation group D2
, Fanconi anemia group D2 protein
, Fanconi anemia group D2 protein homolog
, Fanconi anemia D2 protein