Synonyms: Anti-Amphiphysin II antibody produced in rabbit; Anti-Amphiphysin-like protein antibody produced in rabbit; Anti-Box-dependent myc-interacting protein 1 antibody produced in rabbit; Anti-Bridging integrator 1 antibody produced in rabbit; Anti-Myc box-dependent-interacting protein 1 antibody produced in rabbit
MDL Number: MFCD01633055
Storage: -20C
Application: All Prestige Antibodies Powered by Atlas Antibodies are developed and validated by the Human Protein Atlas (HPA) project (www.proteinatlas.org)and as a result, are supported by the most extensive characterization in the industry. The Human Protein Atlas project can be subdivided into three efforts: Human Tissue Atlas, Cancer Atlas, and Human Cell Atlas. The antibodies that have been generated in support of the Tissue and Cancer Atlas projects have been tested by immunohistochemistry against hundreds of normal and disease tissues and through the recent efforts of the Human Cell Atlas project, many have been characterized by immunofluorescence to map the human proteome not only at the tissue level but now at the subcellular level. These images and the collection of this vast data set can be viewed on the Human Protein Atlas (HPA) site by clicking on the Image Gallery link. To view these protocols and other useful information about Prestige Antibodies and the HPA, visit sigma.com/prestige.
Biochem Physiol Actions: Bridging integrator 1 is a protein encoded by the BIN1 gene in humans and is mapped to chromosome 2q14. It consists of an N-BAR domain that is essential for biogenesis of plasma membrane invaginations (T-tubules) in muscle tissues. The protein is a key player involved in membrane remodeling during endocytosis, cell migration and endosomal sorting. The novel protein interacts with the functionally critical Myc box regions at the N terminus of the MYC oncoprotein. It may have a role in malignancy and cell cycle control. It also plays a crucial role in the biogenesis of T-tubules. Mutation in this gene causes centronuclear myopathy by interfering with remodeling of T tubules and/or endocytic membranes.
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