Fanconi anemia (FA) is an autosomal recessive disorder characterized by bone marrow failure, birth defects and chromosomal instability (1-8). 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 is thought to be important for the function of the FA pathway (2,3). FA proteins encoded by 6 cloned FA genes (FANCA, FANCC, FANCD2, FANCE, FANCF, and FANCG) cooperate in a common pathway, culminating in the monoubiquitination of FANCD2 protein and the colocalization of FANCD2 and BRCA1 proteins in nuclear foci (4-6). The human FANCE gene maps to chromosome 6p22-p21, contains 10 exons and encodes a novel 536-amino acid protein with two potential nuclear localization signals (7,8).
Key Feature
Clonality
Polyclonal
Isotype
IgG
Host Species
Rabbit
Tested Applications
WBIPIFELISA
recommended for detection of FANCE of human and, to a lesser extent, mouse and rat origin by WB, IP, IF and ELISA
Species Reactivity
HumanMouseRat
Concentration
1mg/ml
Purification
Affinity purified
Target Information
Alternative Names
epitope corresponding to amino acids 237-536 mapping at the C-terminus of FANCE of human origin
Tissue Specificity
epitope corresponding to amino acids 237-536 mapping at the C-terminus of FANCE of human origin