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Mouse BIN1

$260
100 µl
APPLICATIONS
REACTIVITY
Human, Mouse, Rat

Application Methods: Immunoprecipitation, Western Blotting

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 a 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).

$260
100 µl
APPLICATIONS
REACTIVITY
Human, Mouse

Application Methods: Immunoprecipitation, Western Blotting

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 a 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).