raised against amino acids 1172-1471 mapping at the C-terminus of FANCD2 of human origin
Modification Notes
Fanconi anemia (FA) is an autosomal recessive disorder character-ized by bone marrow failure, birth defects and chromosomal instability (1-7). At the cellular level, FA is characterized by spontaneous chromosomal breakage and a unique hypersensitivity to DNA cross-linking agents (1). At least 8 complementation groups (A-G) have been identified and 6 FA genes (for subtypes A, C, D2, E, F and G) have been cloned (2). The FA proteins lack sequence homologies or motifs that could point to a molecular function (1). Phosphorylation of FANC (Fanconi anemia complementation group) proteins are thought to be important for the function of the FA pathway (2,3). Several FA proteins, including FANCA, FANCC, FANCF, and FANCG, interact in a nuclear complex, and this complex is required for the activation (monoubiquitination) of the downstream FANCD2 protein (4,5). When monoubiquitinated, the FANCD2 protein co-localizes with the breast cancer susceptibility protein BRCA1 in DNA damage induced foci (4,5). In male meiosis, FANCD2 also co-localizes with BRCA1 at synaptonemal complexes (6). The human FANCD2 gene maps to chromosome 3p25.3, contains 44 exons and encodes a 1,451-amino acid nuclear protein that exists as 2 protein isoforms (7).
Key Feature
Clonality
Polyclonal
Isotype
IgG
Host Species
Rabbit
Tested Applications
WBIPIFIHCELISA
recommended for detection of FANCD2 of mouse, rat and human origin by WB, IP, IF, IHC(P) and ELISA:
Species Reactivity
HumanMouseRat
Concentration
1mg/ml
Purification
Affinity purified
Target Information
Alternative Names
raised against amino acids 1172-1471 mapping at the C-terminus of FANCD2 of human origin
Tissue Specificity
raised against amino acids 1172-1471 mapping at the C-terminus of FANCD2 of human origin