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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. Zusätzlich bieten wir Ihnen BIN1 Proteine (14) und BIN1 Kits (12) und viele weitere Produktgruppen zu diesem Protein an.
Showing 10 out of 111 products:
Mouse (Murine) Monoclonal BIN1 Primary Antibody für FACS, IP - ABIN1043735
Nicot, Toussaint, Tosch, Kretz, Wallgren-Pettersson, Iwarsson, Kingston, Garnier, Biancalana, Oldfors, Mandel, Laporte: Mutations in amphiphysin 2 (BIN1) disrupt interaction with dynamin 2 and cause autosomal recessive centronuclear myopathy. in Nature genetics 2007
Mouse (Murine) Monoclonal BIN1 Primary Antibody für FACS, IP - ABIN1043736
Sinha-Datta, Datta, Ghorbel, Dodon, Nicot: Human T-cell lymphotrophic virus type I rex and p30 interactions govern the switch between virus latency and replication. in The Journal of biological chemistry 2007
Mouse (Murine) Monoclonal BIN1 Primary Antibody für IP, ELISA - ABIN1043738
Wechsler-Reya, Elliott, Prendergast: A role for the putative tumor suppressor Bin1 in muscle cell differentiation. in Molecular and cellular biology 1998
Human Monoclonal BIN1 Primary Antibody für ELISA, WB - ABIN1043789
Wechsler-Reya, Sakamuro, Zhang, Duhadaway, Prendergast: Structural analysis of the human BIN1 gene. Evidence for tissue-specific transcriptional regulation and alternate RNA splicing. in The Journal of biological chemistry 1998
Human Polyclonal BIN1 Primary Antibody für ICC, IF - ABIN4284657
Stadler, Rexhepaj, Singan, Murphy, Pepperkok, Uhlén, Simpson, Lundberg: Immunofluorescence and fluorescent-protein tagging show high correlation for protein localization in mammalian cells. in Nature methods 2013
bridging integrator 1 Gene rs7561528 polymorphism contributes to Alzheimer's disease susceptibility in East Asian and Caucasian populations
Findings indicated that BIN1 restoration in NSCLC could reverse PD-L1 (zeige CD274 Antikörper)-mediated immune escape by inactivating the c-MYC (zeige MYC Antikörper) and EGFR (zeige EGFR Antikörper)/mitogen-activated protein kinase (zeige MAPK1 Antikörper) 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 (zeige CHMP4A Antikörper) 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 (zeige CHMP4A Antikörper) = charged multivesicular body protein 4B (zeige CHMP4B Antikörper); cBIN1 = cardiac bridging integrator 1)
Low Bin1 expression is associated with esophageal squamous cell carcinoma.
the depletion of BIN1 increases cellular BACE1 (zeige BACE Antikörper) levels through impaired endosomal trafficking and reduces BACE1 (zeige BACE Antikörper) 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 (zeige BACE Antikörper) 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.
Data (including data from studies using transgenic mice) suggest that the process leading to microparticle release from cardiac myocytes involves recruitment of CHMP4B (zeige CHMP4B Antikörper) 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 (zeige CHMP4B Antikörper) = charged multivesicular body protein 4B (zeige CHMP4B Antikörper); cBIN1 = cardiac bridging integrator 1)
Bin1 and CD2AP (zeige Cd2ap Antikörper) keep APP (zeige APP Antikörper) and BACE1 (zeige BACE Antikörper) apart in early endosomes by distinct mechanisms in axon and dendrites. Individuals carrying variants of either factor would slowly accumulate Abeta (zeige APP Antikörper) in neurons increasing the risk for late-onset AD.
Data demonstrate that EHBP1L1 links Rab8 (zeige RAB8A Antikörper) and the Bin1-dynamin (zeige DNM1 Antikörper) 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 (zeige E2F1 Antikörper) is a mechanism by which serum starvation promotes E2F1 (zeige E2F1 Antikörper)-induced apoptosis.
BIN1 interacts with MTM1 (zeige MTM1 Antikörper) 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