BIN1
BIN1 (bridging integrator 1, also known as SH3P9, AMPH2 or AMPHL) is a nucleocytoplasmic adaptor protein that shapes and remodels the plasma membrane. It was first identified as a MYC-interacting protein with features of a tumour suppressor. Browse Assay Genie's current range of BIN1 research reagents below, or read on for the biology behind the target.
BIN1 is a key player in the control of plasma membrane curvature, membrane shaping and membrane remodelling. In muscle cells it is required for the formation of T-tubules, tubular invaginations of the plasma membrane that function in depolarisation-contraction coupling. It is also a negative regulator of endocytosis and is involved in the regulation of intracellular vesicle sorting. In vitro, the protein has actin bundling activity and stabilises actin filaments against depolymerisation.
The BIN1 gene encodes several isoforms of a nucleocytoplasmic adaptor protein, and alternate splicing gives rise to different transcript variants. Isoforms expressed in the central nervous system may be involved in synaptic vesicle endocytosis and may interact with dynamin, synaptojanin, endophilin and clathrin. Isoforms expressed in muscle, together with ubiquitously expressed isoforms, localise to the cytoplasm and nucleus and activate a caspase-independent apoptotic process. Aberrant splice variants have also been described in tumour cell lines. HGNC places BIN1 in the N-BAR domain containing and SH3 domain containing gene groups.
The protein is linked to several cellular pathways. It modulates BACE1 trafficking and the control of amyloid-beta production, and in neuronal circuits its regulation of endocytosis may influence the internalisation of PHF-tau aggregates. It may also regulate MYC activity and cell proliferation. Studies in mouse suggest an important role for the gene in cardiac muscle development. The related protein BIN2 is a useful comparator in studies of this family.
BIN1 controls plasma membrane curvature and remodelling, and negatively regulates endocytosis and intracellular vesicle sorting.
BIN1 is required for T-tubule formation in muscle cells, and mouse studies point to a role in cardiac muscle development.
BIN1 modulates BACE1 trafficking and amyloid-beta production, and may influence the internalisation of PHF-tau aggregates in neuronal circuits.
BIN1 was identified as a MYC-interacting protein with tumour suppressor features and may regulate MYC activity and cell proliferation.
BIN1 controls plasma membrane curvature, membrane shaping and remodelling. It is required for T-tubule formation in muscle cells, negatively regulates endocytosis, helps sort intracellular vesicles and bundles actin filaments in vitro. It may also regulate MYC activity and cell proliferation.
BIN1 is also known as SH3P9, AMPH2 and AMPHL, and UniProt names the protein Myc box-dependent-interacting protein 1. Alternate splicing yields several isoforms, with distinct forms expressed in the central nervous system, in muscle and ubiquitously across tissues.
Yes, mouse and rat both have a Bin1 ortholog. Mouse studies suggest the gene plays an important role in cardiac muscle development. Check the datasheet of any product for its validated reactivity.
BIN2, a related bridging integrator, and other targets in membrane remodelling and endocytosis research.
Gene and protein annotations from HGNC, NCBI Gene and UniProt O00499; product specifications from Assay Genie datasheets.