R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.
BIN1 (E4A1P) Rabbit mAb #51844
Filter:
- WB
- IP
Supporting Data
REACTIVITY | H M |
SENSITIVITY | Endogenous |
MW (kDa) | 45-80 |
Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
Product Information
Product Usage Information
Application | Dilution |
---|---|
Western Blotting | 1:1000 |
Immunoprecipitation | 1:50 |
Storage
Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.
Protocol
Specificity / Sensitivity
BIN1 (E4A1P) Rabbit mAb recognizes endogenous levels of total BIN1 protein. The antibody recognizes multiple BIN1 isoforms.
Species Reactivity:
Human, Mouse
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Val266 of human BIN1 protein.
Background
Bridging integrator 1 (BIN1, AMPHL) is an adaptor protein and putative tumor suppressor expressed as multiple isoforms due to alternative splicing. The BIN1 protein was originally identified as a Myc box-interacting protein with structural similarity to the synaptic vesicle protein amphiphysin (1). BIN1 protein structure contains an amino-terminal amphipathic helix and a BAR domain that is involved in sensing membrane curvature. The protein also includes a Myc-binding domain and an SH3 domain, which are implicated in protein-protein interactions (1). Multiple BIN1 isoforms range in size from approximately 45 to 65 kDa, with the nuclear BIN1 isoform found mostly in skeletal muscle and the cytoplasmic IIA isoform expressed in axon initial segments and nodes of Ranvier of the brain (2,3). Corresponding BIN1 gene mutations and incorrect splicing can lead to impaired BIN1 membrane-tabulating and protein binding activities, resulting in development of autosomal recessive centronuclear myopathy and myotonic dystrophy (4,5). Genome-wide association studies link the BIN1 gene with late onset Alzheimer disease (AD) and increased BIN1 mRNA expression is seen in AD brains (6,7).
- Sakamuro, D. et al. (1996) Nat Genet 14, 69-77.
- Ge, K. and Prendergast, G.C. (2000) Genomics 67, 210-20.
- Ramjaun, A.R. et al. (1997) J Biol Chem 272, 16700-6.
- Nicot, A.S. et al. (2007) Nat Genet 39, 1134-9.
- Fugier, C. et al. (2011) Nat Med 17, 720-5.
- Seshadri, S. et al. (2010) JAMA 303, 1832-40.
- Chapuis, J. et al. (2013) Mol Psychiatry 18, 1225-34.
限制使用
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For Research Use Only. Not For Use In Diagnostic Procedures.
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