Western blot analysis of extracts from C2C12 cells using FXR1 (L662) Antibody.
Western blot analysis of extracts from mouse skeletal muscle using FXR1 (L662) Antibody.
|MW (kDa)||78-80, 82-84|
Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at –20°C. Do not aliquot the antibody.
For western blots, incubate membrane with diluted primary antibody in 5% w/v BSA, 1X TBS, 0.1% Tween® 20 at 4°C with gentle shaking, overnight.
NOTE: Please refer to primary antibody product webpage for recommended antibody dilution.
From sample preparation to detection, the reagents you need for your Western Blot are now in one convenient kit: #12957 Western Blotting Application Solutions Kit
NOTE: Prepare solutions with reverse osmosis deionized (RODI) or equivalent grade water.
Load 20 µl onto SDS-PAGE gel (10 cm x 10 cm).
NOTE: Volumes are for 10 cm x 10 cm (100 cm2) of membrane; for different sized membranes, adjust volumes accordingly.
* Avoid repeated exposure to skin.
posted June 2005
revised June 2020
Protocol Id: 10
FXR1 (L662) Antibody detects endogenous levels of total FXR1 protein.
Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to the sequence of mouse 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).
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