This BICD2 antibody will not cross-react with BICD1.
Purification
BICD2 Antibody is affinity chromatography purified via peptide column.
Immunogène
BICD2 antibody was raised against a 13 amino acid synthetic peptide from near the carboxy terminus of human BICD2. The immunogen is located within the last 50 amino acids of BICD2.
BICD2
Reactivité: Humain
IP
Hôte: Lapin
Polyclonal
unconjugated
Indications d'application
BICD2 antibody can be used for detection of BICD2 by Western blot at 1 - 2 μ,g/mL.
Antibody validated: Western Blot in human samples. All other applications and species not yet tested.
Restrictions
For Research Use only
Format
Liquid
Concentration
1 mg/mL
Buffer
BICD2 Antibody is supplied in PBS containing 0.02 % sodium azide.
Agent conservateur
Sodium azide
Précaution d'utilisation
This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Stock
-20 °C,4 °C
Stockage commentaire
BICD2 antibody can be stored at 4°C for three months and -20°C, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.
BICD2 Antibody: BICD2 is the second human homolog discovered to the Drosophila Bicaudal-D protein that forms part of the cytoskeleton and mediates the correct sorting of mRNAs for oocyte- and axis-determining factors during oogenesis. Similar to the highly homologous protein BICD1, BICD2 can bind to dynein-dynactin complex, primarily through the dynamitin subunit of dynactin. The C-terminus of BICD2 targets the protein to the Golgi complex while the N-terminal domain of BICD2 co-immunoprecipitates with cytoplasmic dynein, suggesting BICD2 plays a role in the dynein-dynactin interaction on the surface of membranous organelles. Mice engineered to overexpress the BICD2 amino terminal domain in neurons developed amyotrophic lateral sclerosis (ALS)-like features such as Golgi fragmentation, neurofilament swelling in proximal axons, etc., suggesting that impaired dynein/dynactin function may explain some of the pathological features observed in ALS patients.