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BIN1 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. Additionally we are shipping BIN1 Antibodies (111) and BIN1 Proteins (14) and many more products for this protein.
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Findings indicated that BIN1 restoration in NSCLC could reverse PD-L1 (show CD274 ELISA Kits)-mediated immune escape by inactivating the c-MYC (show MYC ELISA Kits) and EGFR (show EGFR ELISA Kits)/mitogen-activated protein kinase (show MAPK1 ELISA Kits) pathways.
propose that efforts to define how genetic variants in BIN1 elevate the risk for Alzheimer's disease would behoove to consider BIN1 function in the context of its main expression in mature oligodendrocytes
The results emphasize an additional level of complexity in the regulation of the interaction between BIN1 and Tau dependent on the BIN1 isoforms.
Data (including data from studies using transgenic mice) suggest that the process leading to microparticle release from cardiac myocytes involves recruitment of CHMP4B (show CHMP4A ELISA Kits) protein to the forming microparticle membrane which also contains cBIN1; plasma cBIN1 is reduced in patients with heart failure as compared to control subjects. (CHMP4B (show CHMP4A ELISA Kits) = charged multivesicular body protein 4B (show CHMP4B ELISA Kits); cBIN1 = cardiac bridging integrator 1)
Low Bin1 expression is associated with esophageal squamous cell carcinoma.
the depletion of BIN1 increases cellular BACE1 (show BACE ELISA Kits) levels through impaired endosomal trafficking and reduces BACE1 (show BACE ELISA Kits) lysosomal degradation, resulting in increased Ab production. Our findings provide a mechanistic role of BIN1 in the pathogenesis of Alzheimer disease (AD), as a novel genetic regulator of BACE1 (show BACE ELISA Kits) levels and Ab production
BIN1 protein expression in cerebral cortex was related to disease progression in Alzheimer's Disease patients.
data show that the previously described consensus sequence PXRPXR for amphiphysin SH3 ligands is inaccurate and instead define it as an extended Class II binding motif PXXPXRpXR, where additional positive charges between the two constant arginine residues can give rise to extraordinary high SH3 binding affinity.
findings support a contribution of BIN1 to individual differences in episodic memory performance among Type 2 Diabetes patients.
analysis of a novel deregulated mechanism in chronic myeloid leukemia (show BCL11A ELISA Kits) patients, indicating BIN1 and RIN1 (show RIN1 ELISA Kits) as players in the maintenance of the abnormal RTK signaling in this hematological disease
Data (including data from studies using transgenic mice) suggest that the process leading to microparticle release from cardiac myocytes involves recruitment of CHMP4B (show CHMP4B ELISA Kits) protein to the forming microparticle membrane which also contains cBIN1; plasma cBIN1 is reduced in patients with heart failure as compared to control subjects. (CHMP4B (show CHMP4B ELISA Kits) = charged multivesicular body protein 4B (show CHMP4B ELISA Kits); cBIN1 = cardiac bridging integrator 1)
Bin1 and CD2AP (show Cd2ap ELISA Kits) keep APP (show APP ELISA Kits) and BACE1 (show BACE ELISA Kits) apart in early endosomes by distinct mechanisms in axon and dendrites. Individuals carrying variants of either factor would slowly accumulate Abeta (show APP ELISA Kits) in neurons increasing the risk for late-onset AD.
Data demonstrate that EHBP1L1 links Rab8 (show RAB8A ELISA Kits) and the Bin1-dynamin (show DNM1 ELISA Kits) complex, which generates membrane curvature and excises the vesicle at the endocytic recycling compartment for apical transport.
Findings show how cardiac deficiency in Bin1 function causes age- and stress-associated heart failure suggesting that Bin1 is a positive modifier of cardiac contractility that helps sustain adult heart function under stress conditions.
Reorganization of BIN1-induced microdomains recruits phosphorylated ryanodine receptors into dyads, increasing calcium signaling.
Bin1 mAb reduced colitis morbidity in mice while unprotected mice were characterized by severe lesions throughout the mucosa, rupture of lymphoid follicle, high-level neutrophil and lymphocyte infiltration into the mucosal areas, loss of surface crypts.
The release of BIN1 from hypo-poly(ADP-ribosyl)ated E2F1 (show E2F1 ELISA Kits) is a mechanism by which serum starvation promotes E2F1 (show E2F1 ELISA Kits)-induced apoptosis.
BIN1 interacts with MTM1 (show MTM1 ELISA Kits) in skeletal muscle.
Cardiac BIN1 folds T-tubule membrane, controlling ion flux and limiting arrhythmia.
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 dynamin, 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.
bridging integrator 1
, myc box-dependent-interacting protein 1-like
, amphiphysin II
, amphiphysin-like protein
, box dependant MYC interacting protein 1
, box-dependent myc-interacting protein 1
, myc box-dependent-interacting protein 1
, SH3 domain-containing protein 9
, amphiphysin 2
, myc box dependent interacting protein 1
, amphiphysin IIamph2