ANTI-BIN1 (SH3P9/AMPHIPHYSIN II/AMPL)

Uses

Monoclonal Anti-Bin1 antibody produced in mouse has been used in:

• western blotting
• enzyme linked immunosorbent assay (ELISA)
• immunoprecipitation
• immunocytochemistry
• immunohistochemistry
• flow cytometry

General Description

This gene encodes several isoforms of a nucleocytoplasmic adaptor protein, one of which was initially identified as a MYC-interacting protein with features of a tumor suppressor. Isoforms that are expressed in the central nervous system may be involved in synaptic vesicle endocytosis and may interact with dynanim, synaptojanin, endophilin, and clathrin. Isoforms that are expressed in muscle and ubiquitously expressed isoforms localize to the cytoplasm and nucleus and activate a caspase-independent apoptotic process. Studies in mouse suggest that this gene plays an important role in cardiac muscle development. Alternate splicing of the gene results in ten transcript variants encoding different isoforms. Aberrant splice variants expressed in tumor cell lines have also been described. (provided by RefSeq)

Biochem/physiol Actions

Box-dependent myc-interacting protein-1 (Bin1) interacts with and inhibits the oncogenic activity of the myc oncoprotein that has a major role in many human cancers. The loss of Bin1 may contribute to growth deregulation in cancer cells in carcinoma of the breast, colon, lung, cervix, prostate and liver. In bin1 locus mid-2q region that is deleted in approx. 42% of metastatic prostate cancers, and at the syntenic murine locus, in >90% of radiation-induced myeloid leukemias. In addition to the role of Bin1 in controlling neoplastic cell growth and cell cycle by the inhibition of transformation by both myc and the adenovirus E1A protein. Deficits in expression are functionally significant, because ectopic Bin1 can inhibit the growth of tumor cells that lack endogenous expression. Bin1 has also been found to be highly expressed in murine skeletal muscle; overexpression of Bin1 promotes myotube formation and upregulation of myosin heavy chain, while interference with Bin1 expression significantly impairs these processes.