Validation Data Gallery
|Positive WB detected in||HeLa cells, K-562 cells, Neuro-2a cells|
|Positive IP detected in||K-562 cells|
|Positive IF detected in||HeLa cells, HepG2 cells|
|Western Blot (WB)||WB : 1:5000-1:50000|
|Immunoprecipitation (IP)||IP : 0.5-4.0 ug for IP and 1:1000-1:4000 for WB|
|Immunofluorescence (IF)||IF : 1:500-1:2000|
|Sample-dependent, check data in validation data gallery|
10260-1-AP targets Drebrin in WB, IP, IHC, IF, ELISA applications and shows reactivity with human, mouse, rat samples.
|Tested Reactivity||human, mouse, rat|
|Cited Reactivity||human, mouse, rat|
|Host / Isotype||Rabbit / IgG|
|Immunogen||Drebrin fusion protein Ag0371|
|Full Name||drebrin 1|
|Calculated molecular weight||71 kDa|
|Observed molecular weight||100-130 kDa|
|GenBank accession number||BC000283|
|Gene ID (NCBI)||1627|
|Purification Method||Antigen affinity purification|
|Storage Buffer||PBS with 0.02% sodium azide and 50% glycerol pH 7.3.|
|Storage Conditions||Store at -20°C. Stable for one year after shipment. Aliquoting is unnecessary for -20oC storage. 20ul sizes contain 0.1% BSA.|
Drebrin (DBN1) is an actin binding and stabilizing protein with roles in endocytosis, formation of dendrite spines in neurons and coordinating cell-cell synapses in immune cells. Preferentially expressed in the brain, it is highly localized in dendritic spines and regulates spine shapes. It has two isoforms that are splice variants, with drebrin A being expressed in neural cells, and drebrin E is present in several other cell types. Recently it has been reported that circulating DBN1 levels correlated with retinal nerve fiber layer defect and may reflect the severity of retinal ganglion cells injury in glaucoma patients.
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L-3-n-Butylphthalide improves synaptic and dendritic spine plasticity and ameliorates neurite pathology in Alzheimer's disease mouse model and cultured hippocampal neurons.
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Bisphenol-A exposure induced neurotoxicity and associated with synapse and cytoskeleton in Neuro-2a cells.
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Acute lead acetate induces neurotoxicity through decreased synaptic plasticity-related protein expression and disordered dendritic formation in nerve cells.
Intron retention is a stress response in sensor genes and is restored by Japanese herbal medicines: A basis for future clinical applications.