BIN1 Mouse Monoclonal Antibody [Clone ID: 99F]

Specifications

Product Data
Clone Name	99F
Applications	IF, IP, WB
Recommend Dilution	ELISA: 1:5000-1:50000, WB: 1:500-1:1500, IHC: 1:100-1:500, IP: 10-100 uL
Reactivity	Mouse, Human
Host	Mouse
Clonality	Monoclonal
Immunogen	Anti-BIN1 (MOUSE) Monoclonal Antibody was produced in mouse by repeated immunizations with BIN1 polypeptide followed by hybridoma development.
Formulation	0.02 M Potassium Phosphate, 0.15 M Sodium Chloride, pH 7.2
Conjugation	Unconjugated
Storage Condition	Store at -20°C as received.
Gene Name	bridging integrator 1
Database Link	NP_004296 Entrez Gene 30948 MouseEntrez Gene 274 Human UniProt ID O00499
Synonyms	AMPH2; AMPHL; SH3P9
Note	Bin1 is a conserved member of the BAR family of genes that have been implicated in diverse cellular processes including endocytosis, actin organization, programmed cell death, stress responses, and transcriptional control. The first mammalian BAR protein to be discovered, Amphiphysin I (AmphI), was identified in an immunoscreen for proteins associated with the plasma membranes of synaptic neurons, functions in the control of clathrin-dependent synaptic vesicle endocytosis. The mammalian Bin1 gene was first identified in a two hybrid screen for polypeptides that bind to the N-terminal Myc box 1 (MB1) portion of the c-Myc oncoprotein. Bin1 is similar to AmphI in overall structure, with an N-terminal BAR domain and a C-terminal SH3 domain. However, the Bin1 gene is more complex than the AmphI gene, encoding at least seven different splice variants that differ widely in subcellular localization, tissue distribution, and ascribed functions. Alternate splicing of the Bin1 gene results in ten transcript variants encoding different isoform. Bin1 is expressed ubiquitously in mammalian cells. Certain splice variants of Bin1 are expressed in the neurons, muscle cells or tumor cells and play a role in cancer suppression. Studies in muscle cells suggest that Bin1 expression, structure, and localization are tightly regulated during muscle differentiation and suggested that Bin1 plays a functional role in the differentiation process. Defects in BIN1 are the cause of centronuclear myopathy autosomal recessive; also known as autosomal recessive myotubular myopathy.
Reference Data

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