Product Pathways - Translational Control
FXR1 Antibody #4173
|W||H M R Mk||Endogenous||78-80, 82-84||Rabbit|
Reactivity Key: H=Human M=Mouse R=Rat Mk=Monkey
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.
Specificity / Sensitivity
FXR1 Antibody detects endogenous levels of total FXR1 protein.
Source / Purification
Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to the sequence of human FXR1 protein. Antibodies are purified by protein A and peptide affinity chromatography.
Fragile X syndrome is a genetic disorder characterized by a spectrum of physical and behavioral features and is a frequent form of inherited mental retardation (1). X-linked FMRP (FMR-1) and its two autosomal homologs, FXR1 and FXR2, are polyribosome-associated RNA-binding proteins that are involved in the pathogenesis of fragile X syndrome (1-3). Each of the fragile X proteins can self-associate, as well as form heteromers with the other two related proteins (3). FMRP can act as a translation regulator and is a component of RNAi effector complexes (RISC), suggesting a role in gene silencing (4). The Drosophila homolog of FMRP (dFMRP) associates with Argonaute 2 (Ago2) and Dicer and can coimmunoprecipitate with miRNA and siRNA (5). These results suggest that fragile X syndrome is related to abnormal translation caused by defects in RNAi-related pathways. In addition, FMRP, FXR1, and FXR2 are components of stress granules (SG) and have been implicated in the translational regulation of mRNAs (6).
- Verkerk, A.J. et al. (1991) Cell 65, 905-14.
- Siomi, M.C. et al. (1995) EMBO J 14, 2401-8.
- Zhang, Y. et al. (1995) EMBO J 14, 5358-66.
- Caudy, A.A. et al. (2002) Genes Dev 16, 2491-6.
- Siomi, H. et al. (2004) Ment Retard Dev Disabil Res Rev 10, 68-74.
- Linder, B. et al. (2008) Hum Mol Genet 17, 3236-46.
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For Research Use Only. Not For Use In Diagnostic Procedures.