| 1996 |
BIN1 physically interacts with the N-terminal Myc box regions of the MYC oncoprotein and inhibits malignant cell transformation by MYC. |
Genetic screen/protein interaction assay; ectopic expression growth suppression assay |
Nature genetics |
High |
8782822
|
| 1997 |
BIN1 (Amphiphysin II) localizes to the cortical cytomatrix of axon initial segments and nodes of Ranvier in brain, and concentrates around T tubules in skeletal muscle, co-localizing with ankyrin3 splice variants. |
Immunofluorescence, subcellular fractionation, direct localization experiments in tissue sections |
The Journal of cell biology |
High |
9182667
|
| 1997 |
BIN1 is a short-lived nuclear phosphoprotein (half-life ~2 h) with altered subcellular localization in tumor cells versus normal cells: predominantly nucleoplasmic in normal cells but shifted to a subnuclear compartment in tumor cells. |
Pulse-chase experiments, immunoprecipitation, immunofluorescence with monoclonal antibodies |
Cancer research |
Medium |
9242458
|
| 1997 |
Alternative splicing of BIN1 controls its MYC-binding capacity; one alternatively spliced exon encodes part of the MYC-binding domain, and MyoD transactivates the BIN1 promoter accounting for high muscle expression. |
Gene cloning, exon mapping, promoter reporter assays, cell-type-specific RT-PCR |
The Journal of biological chemistry |
Medium |
9395479
|
| 1998 |
BIN1 promotes skeletal muscle differentiation; overexpression accelerates differentiation while antisense BIN1 impairs differentiation of C2C12 myoblasts; during differentiation BIN1 protein relocates from nucleus to cytoplasm via isoform switching. |
Stable antisense/sense overexpression in C2C12 cells, morphological and marker analysis of differentiation, immunolocalization |
Molecular and cellular biology |
Medium |
9418903
|
| 1999 |
BIN1 interacts with and inhibits c-Myc transactivation through its Myc-binding domain (MBD), and inhibits cell proliferation via both MYC-dependent and MYC-independent mechanisms involving the BAR, U1, and SH3 domains. |
Co-immunoprecipitation, transcriptional reporter assays, Ras cotransformation assay, growth inhibition assays |
Oncogene |
High |
10380878
|
| 1999 |
Aberrant inclusion of brain-specific exon 12A in BIN1 abrogates its ability to inhibit malignant transformation by c-Myc or adenovirus E1A and eliminates its ability to induce programmed cell death in melanoma cells. |
RT-PCR isoform analysis, ectopic expression of exon 12A-containing vs. non-containing BIN1 in transformation and apoptosis assays |
Proceedings of the National Academy of Sciences of the United States of America |
Medium |
10449755
|
| 2000 |
BIN1 engages a caspase-independent cell death program characterized by cell shrinkage, vacuolated cytoplasm, and DNA degradation; this is abrogated by BAR domain mutation or the melanoma-associated exon 12A missplicing event, and is not blocked by Bcl-2 or caspase inhibitor ZVAD.fmk. |
Ectopic expression, domain mutagenesis, pharmacological inhibitors, cell death assays |
Oncogene |
Medium |
11032017
|
| 2001 |
BIN1 mediates c-Myc-induced apoptosis in transformed primary cells via protein-protein interaction; antisense or dominant-inhibitory BIN1 reduced susceptibility to c-Myc-induced apoptosis without affecting proliferation or transformation. |
Antisense/dominant-negative expression, apoptosis assays in chick and rat primary transformed cells |
Cancer research |
Medium |
11306501
|
| 2003 |
Constitutive knockout of murine Bin1 causes perinatal lethality with severe ventricular cardiomyopathy and disorganized myofibrils, but does not impair endocytosis, phagocytosis, actin organization, proliferation, or apoptosis in fibroblasts/macrophages. |
Homologous recombination knockout mouse, histology, electron microscopy, endocytosis/phagocytosis assays |
Molecular and cellular biology |
High |
12773571
|
| 2004 |
The Exon10 (polybasic) sequence of BIN1 binds PI(4,5)P2 and also intramolecularly binds the BIN1 SH3 domain, blocking SH3-mediated binding to PxxP ligands (including dynamin); this blockage is released by PI(4,5)P2, providing a phosphoinositide-regulated SH3 domain mechanism. |
In vitro binding assays, PI(4,5)P2 addition/depletion experiments, cell overexpression with PI4P5-kinase, T-tubule formation assay |
The EMBO journal |
High |
15483625
|
| 2005 |
The BIN1 SH3 domain binds a class II SH3-binding motif in c-Myc; tumor-specific BIN1 isoforms are prevented from binding c-Myc via an intramolecular polyproline-SH3 interaction; phosphorylation of c-Myc at Ser62 inhibits BIN1 binding. |
NMR structure, surface plasmon resonance, biochemical binding assays, structure-based modeling |
Journal of molecular biology |
High |
15992821
|
| 2006 |
Crystal structure of the BIN1 BAR domain at 2.0 Å resolution reveals a homodimeric crescent-shaped architecture with knobs-into-holes coiled-coil packing governing membrane-engaging concave face curvature, and identifies two potential protein-protein interaction sites on the convex face. |
X-ray crystallography |
Biochemistry |
High |
17059209
|
| 2006 |
HCV NS5A protein interacts with BIN1 via NS5A's SH3-binding motif (PxxP) and BIN1's SH3 domain; this interaction inhibits BIN1-induced apoptosis and is required for productive HCV infection. |
Yeast two-hybrid, in vitro binding, co-immunoprecipitation, confocal microscopy, deletion/mutation analysis, HCV infectivity in chimpanzees |
Gastroenterology |
Medium |
16530520
|
| 2008 |
BIN1's membrane-tubulating activity depends on CLIP-170; BIN1 interacts with CLIP-170 via its BAR domain and CLIP-170's coiled-coil region; depletion of CLIP-170 reduces BIN1-induced tubule formation, and BIN1 tubules align with microtubules. |
Yeast two-hybrid, GST pulldown, co-immunoprecipitation, RNAi knockdown, confocal microscopy, nocodazole depolymerization |
European journal of cell biology |
Medium |
19004523
|
| 2009 |
BIN1 (AMPH-1 in C. elegans) colocalizes with RME-1/EHD1 on recycling endosomes; BIN1/AMPH-1 deletion impairs recycling endosome function; purified AMPH-1 and RME-1 together form coated membrane tubules distinct from those produced by either alone, and BIN1 is required for EHD1-regulated endocytic recycling in human cells. |
In vivo co-localization, deletion mutant analysis, in vitro reconstitution of membrane tubules, siRNA knockdown in human cells |
Nature cell biology |
High |
19915558
|
| 2009 |
BIN1's SH3 domain acts as a scaffold for sarcomere assembly; it forms transient complexes with actin, myosin filaments, and the pro-myogenic kinase Cdk5, and associates with a Cdk5 phosphorylation domain of titin; expression of isolated SH3 domain causes myofiber disorganization. |
Dominant-negative expression in mouse, co-immunoprecipitation, pull-down assays |
The Journal of biological chemistry |
Medium |
19633357
|
| 2009 |
BIN1 is a transcriptional target of E2F1 (via canonical E2F sites in the BIN1 promoter) and mediates E2F1-induced apoptosis in response to DNA damage; BIN1 suppression attenuates E2F1/etoposide-induced cell death independently of p53, p73, and caspases. |
Promoter reporter assay, ChIP, siRNA knockdown, antisense suppression, DNA damage apoptosis assays |
Cell death and differentiation |
Medium |
19629135
|
| 2010 |
BIN1 localizes to cardiac T-tubules and clusters there with L-type calcium channel Cav1.2; dynamic microtubules tethered to BIN1-scaffolded membrane enable targeted delivery of Cav1.2; BIN1 knockdown reduces surface Cav1.2 and delays calcium transient development. |
Immunocytochemistry, electron microscopy with dual immunogold labeling, co-immunoprecipitation, surface biotinylation, live-cell confocal/TIRF microscopy, shRNA knockdown |
PLoS biology |
High |
20169111
|
| 2011 |
BIN1 is required for skeletal muscle T-tubule biogenesis and excitation-contraction coupling; Bin1 knockdown in adult mouse skeletal muscle disrupts T-tubule structure, reduces DHPR-RyR1 coupling, and impairs SR Ca2+ release. |
In vivo electroporation shRNA delivery, confocal imaging of T-tubules, patch-clamp, Ca2+ spark and transient measurements |
PloS one |
Medium |
21984944
|
| 2011 |
BIN1 is significantly reduced (~36% protein) in failing human cardiomyocytes, and this reduction impairs Cav1.2 trafficking to T-tubules, reduces calcium transients, and causes contractile dysfunction (75% reduction in calcium transients in BIN1-knockdown zebrafish hearts). |
Human failing heart tissue analysis, immunostaining, biochemical fractionation, patch-clamp in cell lines, mouse cardiomyocyte shRNA knockdown, zebrafish morpholino knockdown |
Heart rhythm |
High |
22138472
|
| 2011 |
MBNL1 binds the BIN1 pre-mRNA and regulates its alternative splicing; in myotonic dystrophy, BIN1 missplicing produces an inactive BIN1 form lacking PI(5)P-binding and membrane-tubulating activities, causing T-tubule alterations; reproducing this splicing alteration in mice is sufficient to cause T-tubule defects and muscle weakness. |
RNA binding assay (MBNL1-BIN1 pre-mRNA), functional splicing assays, rescue experiments in patient muscle cells, transgenic mouse model |
Nature medicine |
High |
21623381
|
| 2011 |
BIN1 binds the automodification domain of PARP1 and suppresses its catalytic activity; c-MYC represses BIN1 expression (by blocking MIZ1-mediated activation) thereby releasing PARP1 activity and increasing cisplatin resistance. |
Co-immunoprecipitation, PARP1 activity assay, siRNA knockdown, promoter analysis, cisplatin resistance assays |
Science signaling |
High |
21447800
|
| 2012 |
BIN1 interacts with Tau and they co-localize in human neuroblastoma cells and mouse brain; decreased expression of the Drosophila BIN1 ortholog Amph suppresses Tau-mediated neurotoxicity in three assays. |
Co-immunoprecipitation, co-localization confocal microscopy, Drosophila genetic suppressor assay |
Molecular psychiatry |
Medium |
23399914
|
| 2012 |
Transient structure in the intrinsically disordered c-Myc transactivation domain (residues 22-33 and MB1) mediates binding to BIN1 SH3 domain; Bin1 binds primarily to the Ser62 region of c-Myc in a dynamically disordered, multivalent complex; binding causes population shifts in Myc conformational dynamics. |
NMR chemical shift analysis, relaxation measurements, NOE analysis, surface plasmon resonance |
Nucleic acids research |
High |
22457068
|
| 2013 |
BIN1 directly interacts with Tau through its SH3 domain binding Tau's proline-rich domain; BIN1-Tau complexes co-localize with the actin cytoskeleton in primary neurons; phosphorylation of Tau at Thr231 weakens the SH3-PRD interaction. |
GST pulldown, NMR, co-localization in primary neurons, phospho-specific analysis |
Acta neuropathologica communications |
High |
26395440
|
| 2014 |
A cardiac-specific isoform of BIN1 (BIN1+13+17) promotes N-WASP-dependent actin polymerization to fold T-tubule inner membranes at Z-discs, creating a 'fuzzy space' that restricts local ion diffusion; cardiac Bin1 deletion decreases T-tubule folding, allowing free diffusion of Ca2+ and K+, prolonging action potential duration and increasing arrhythmia susceptibility. |
Cardiac-specific Bin1 knockout mouse, electrophysiology, superresolution microscopy, BIN1 isoform re-expression, N-WASP interaction assay |
Nature medicine |
High |
24836577
|
| 2014 |
BIN1/M-Amphiphysin2 clusters PtdIns(4,5)P2 on membranes to recruit dynamin; the N-BAR domain controls kinetics and accumulation of dynamin while the SH3 domain controls its accumulation on membranes; CNM-associated BIN1 mutants show defects in this process. |
In vitro membrane binding assays, fluorescence microscopy, CNM mutant analysis, numerical simulations |
Nature communications |
High |
25487648
|
| 2014 |
BIN1 knockdown by siRNA reduces t-tubule density, calcium transient amplitude, and synchrony of systolic calcium transient in rat cardiac cells; AmpII protein levels correlate with t-tubule density across cardiac chambers and heart failure models. |
siRNA knockdown, di-4-ANEPPS/FM4-64 t-tubule staining, calcium transient measurements, Western blot across species/chamber comparisons |
Circulation research |
Medium |
25332206
|
| 2014 |
BIN1 membrane curvature sensing and generation is autoinhibited by intramolecular exon10-SH3 interaction on membranes lacking PI(4,5)P2; addition of PI(4,5)P2 or SH3 domain ligands (PRD peptides) relieves autoinhibition and activates BIN1 membrane deformation. |
In vitro membrane deformation assays, SH3-exon10 binding assays, PI(4,5)P2 titration, CNM mutant analysis |
Biochemistry |
High |
25350771
|
| 2014 |
CNM-associated BIN1 mutants R154Q and D151N disrupt membrane tubulation through distinct mechanisms: R154Q reduces membrane-bound protein density while D151N impairs protein oligomerization upon membrane binding. |
In vitro liposome tubulation assays, protein density quantification, chemical crosslinking, live-cell depolymerization assays |
PloS one |
Medium |
24755653
|
| 2015 |
Cryo-EM reveals that BIN1 N-BAR domains self-assemble cooperatively on membrane tubes; the N-terminal amphipathic helix H0 initiates tube assembly and organizes BAR-mediated polymerization by locking adjacent N-BAR domains; loss of H0 or BAR tip disrupts polymer organization. |
Cryo-EM, 3D reconstruction, biochemical tubulation assays with mutants |
Scientific reports |
High |
26487375
|
| 2016 |
Isoproterenol (β-adrenergic activation) promotes BIN1 redistribution to T-tubules and recruits phosphorylated RyR2 (P-RyR) into BIN1+13+17-organized dyads via coimmunoprecipitation; in cardiac-specific Bin1 heterozygous mice, isoproterenol fails to concentrate BIN1 and recruit P-RyRs, resulting in uncoupled P-RyRs and spontaneous calcium release. |
Co-immunoprecipitation, superresolution fluorescent imaging, cardiac-specific Bin1 heterozygous mice, calcium imaging |
Circulation |
Medium |
26733606
|
| 2016 |
EHBP1L1 directly binds GTP-loaded Rab8 and BIN1, forming a complex with dynamin at the endocytic recycling compartment; this complex is required for apical-directed vesicular transport in polarized epithelial cells. |
Co-immunoprecipitation, biochemical binding assays, overexpression/knockdown in organoids and cells, EHBP1L1-KO mouse |
The Journal of cell biology |
Medium |
26833786
|
| 2017 |
BIN1 acts as a negative regulator of Dynamin 2 (DNM2) during muscle maturation; Bin1-/- Dnm2+/- double-null mice survive (unlike Bin1-/- alone) with normal muscle; BIN1 colocalized with and partially inhibited DNM2 activity in vitro during muscle maturation but not for the adult muscle DNM2 isoform. |
Genetic epistasis (Bin1-/- Dnm2+/- mice), in vitro DNM2 GTPase activity assay, co-localization |
The Journal of clinical investigation |
High |
29130937
|
| 2017 |
Bin1 BAR domain directly binds actin filaments, has moderate actin bundling activity, stabilizes actin filaments against depolymerization, and stabilizes tau-induced actin bundles; knockdown of Bin1 in a Drosophila tauopathy model reduces tau-induced actin inclusions. |
In vitro actin binding/bundling assays, F-actin co-sedimentation, Drosophila genetic KD with actin inclusion quantification |
EMBO reports |
Medium |
28893863
|
| 2018 |
NMR structural model of BIN1 SH3 domain binding to Tau peptide (213-229) shows P216 and P219 contact BIN1 SH3 aromatic residues F588 and W562, while R221 and K224 of Tau form electrostatic contacts with E556/E557 of BIN1; phosphorylation of Tau at T212, T217, T231, and S235 reduces interaction with BIN1 SH3 five-fold (Kd 44 to 256 μM) and prevents Tau from competing with BIN1's intramolecular SH3-CLAP interaction. |
NMR spectroscopy, SPR, competition binding assays |
Frontiers in molecular neuroscience |
High |
30487734
|
| 2018 |
BIN1 expression in hESC-derived cardiomyocytes induces T-tubule development, promotes Cav1.2 clustering along T-tubules, increases coupled Cav1.2 gating probability, anchors sarcoplasmic reticulum, and increases Cav1.2-RyR junctions. |
BIN1 transfection in hESC-CMs, electrophysiology, superresolution microscopy, Ca2+ imaging |
Stem cells |
Medium |
30353632
|
| 2019 |
BIN1 interacts with Tau via SH3-PRD interaction; calcineurin dephosphorylates BIN1 at Thr348 (a CDK phosphorylation site), promoting open BIN1 conformation and increasing availability of SH3 domain for Tau binding as demonstrated by NMR; phospho-BIN1(T348):BIN1 ratio is increased in AD brains. |
NMR spectroscopy, high-content screening (1126 compounds), calcineurin inhibitor pharmacology, primary neuron experiments, AD brain biochemistry |
Acta neuropathologica |
High |
31065832
|
| 2019 |
BIN1 loss in microglia reduces Tau secretion via extracellular vesicles in vitro and decreases Tau spreading in vivo in male PS19 mice; microglial Bin1 deletion reduces heat-shock protein expression previously linked to Tau proteostasis. |
Cre-lox microglia-specific Bin1 conditional knockout, extracellular vesicle Tau quantification, in vivo tau spreading assay in PS19 mice |
Scientific reports |
Medium |
31263146
|
| 2019 |
BIN1 interacts with L-type voltage-gated calcium channels (LVGCCs) in rat hippocampal neurons and mouse brain; BIN1-LVGCC interactions are modulated by Tau; increasing neuronal BIN1 expression induces network hyperexcitability and increased calcium transients; Tau reduction prevents BIN1-induced hyperexcitability. |
Co-immunoprecipitation, multielectrode array recordings, calcium imaging, Tau reduction genetic experiments in hippocampal neurons |
eLife |
Medium |
32657270
|
| 2019 |
Neuronal BIN1 loss-of-function impairs spatial learning and memory, reduces presynaptic release probability, alters synaptic vesicle dynamics (increases docked and reserve vesicle pools), reduces synapse density, and alters presynaptic active zone protein clustering; BIN1 localizes to presynaptic sites by superresolution and immunoelectron microscopy. |
Conditional neuronal Bin1 KO, fear conditioning/Morris water maze, electrophysiology, superresolution microscopy, immunoelectron microscopy, 3D-EM reconstruction |
Cell reports |
High |
32160554
|
| 2019 |
BIN1 loss-of-function in neurons does not regulate Aβ generation in vivo: 50% global BIN1 reduction or conditional neuronal BIN1 KO does not alter BACE1 levels, localization, APP processing, or Aβ deposition in the 5XFAD mouse model. |
Bin1 heterozygous KO mice, conditional neuronal KO, 5XFAD amyloidosis model, biochemistry, immunohistochemistry |
The Journal of biological chemistry |
Medium |
30692199
|
| 2019 |
BIN1 loss enables ATM activation via E2F1: BIN1 inactivates ATM kinase particularly when bound to E2F1; BIN1 prevents E2F1 from transcriptionally activating the ATM promoter; BIN1 loss increases MRE11A/RAD50/NBS1 complex formation and promotes ATM autophosphorylation and γH2AX, driving cisplatin resistance. |
Co-immunoprecipitation, promoter reporter assays, siRNA knockdown, ATM kinase assays, cisplatin sensitivity assays |
The Journal of biological chemistry |
Medium |
30733337
|
| 2020 |
BIN1 localizes to postsynaptic compartments (dendritic spines); participates in protein complexes with Arf6 and GluA1; manipulations of BIN1 alter AMPA receptor surface expression, trafficking, spine morphology, and AMPA receptor-mediated synaptic transmission. |
Superresolution SIM microscopy, co-immunoprecipitation, AMPA receptor surface biotinylation, electrophysiology, BIN1 knockdown/overexpression |
Molecular psychiatry |
Medium |
30967682
|
| 2020 |
Neuronal Bin1 conditional KO reduces neuronal excitability in vitro and alters microglial transcriptome in vivo; in PS19 Tau transgenic background, neuronal Bin1 loss increases mortality without worsening neuropathology. |
Conditional KO (Thy1-Cre x Bin1flox/flox x PS19), electrophysiology in primary neurons, c-fos immunostaining, microglial transcriptomics |
PloS one |
Medium |
31408457
|
| 2020 |
Dynamin 2 GTPase activity is suppressed through interaction with BIN1; CNM disease-associated mutant dynamin 2 retains active GTPase due to lack of BIN1-mediated regulation, causing aberrant membrane fission and remodeling in T-tubule equivalent structures. |
In cellulo reconstitution assay, GTPase activity measurements, BIN1-DNM2 interaction assays, CNM mutant analysis |
The Journal of biological chemistry |
High |
33187981
|
| 2021 |
Muscle-specific Bin1 knockout (Bin1mck-/-) mice recapitulate centronuclear myopathy with T-tubule and mitochondria network defects and impaired calcium homeostasis; DNM2 antisense oligonucleotides rescue force and histology, confirming BIN1-DNM2 functional pathway in vivo. |
Muscle-specific conditional KO, force measurements, histology, electron microscopy, Ca2+ homeostasis, ASO treatment |
Molecular therapy |
High |
34371181
|
| 2021 |
Cavin4 directly interacts with Bin1 (Cavin4b in zebrafish) and localizes to T-tubules; loss of Cavin4 causes aberrant T-tubule maturation and accumulation of interconnected caveolae within T-tubules, impairing Ca2+ response; Cavin4 is proposed to remodel T-tubule membrane by recycling caveolar components. |
Direct interaction assay (Cavin4b-Bin1), Cavin4 KO mouse and zebrafish, confocal microscopy, Ca2+ imaging |
The Journal of cell biology |
Medium |
34633413
|
| 2021 |
LOAD-associated BIN1 coding variants (rs754834233, rs138047593) reduce BIN1 interaction with BACE1 and fail to rescue BACE1 recycling impaired by Bin1 knockdown; BIN1 normally promotes BACE1 recycling from early endosomes, and its loss increases intracellular Aβ42 by enabling BACE1 cleavage of APP in enlarged early endosomes. |
Co-immunoprecipitation of BIN1-BACE1, early endosome morphology assay, Aβ ELISA, BACE1 recycling assay, BIN1 variant overexpression/knockdown rescue |
The Journal of biological chemistry |
Medium |
34375641
|
| 2022 |
BIN1 isoform 1 (neuronal) overexpression causes early endosome accumulation and neurodegeneration in Drosophila and human induced neurons; BIN1 KO narrows early endosomes; isoform 1 rescues BIN1-KO early endosome phenotype but isoform 9 does not, identifying isoform-specific control of early endosome size. |
Drosophila overexpression, hiN and cerebral organoid BIN1 KO, endosome morphometry, isoform rescue experiments |
Acta neuropathologica communications |
Medium |
34998435
|
| 2022 |
Neuronal BIN1 isoform 1 (BIN1V1) but not isoform 9 (BIN1V9) downregulates BACE1-mediated APP processing and Aβ generation in a RIN3-dependent manner; BIN1V1 delays APP (but not BACE1) endocytosis into early endosomes, spatially separating APP from BACE1; RIN3 sequesters BIN1V1 via CLAP domain into RAB5+ endosomes. |
Confocal microscopy, Western blot, Aβ ELISA, surface biotinylation APP internalization assay, FACS-enriched cell populations, isoform transfection |
Scientific reports |
Medium |
35241726
|
| 2022 |
Microglial BIN1 regulates proinflammatory and disease-associated microglial activation; BIN1 loss impairs type 1 interferon responses in microglia, particularly upregulation of Ifitm3; Bin1 regulates transcription factors PU.1 and IRF1, and loss of microglial Bin1 in vivo alters disease-associated gene expression and CX3CR1 signaling. |
siRNA Bin1 knockdown in primary microglia, Cre-lox microglia-specific conditional KO, NanoString transcriptomics, flow cytometry, cytokine measurement |
Molecular neurodegeneration |
Medium |
35526014
|
| 2023 |
BIN1, MTM1, and DNM2 have balanced roles in T-tubule growth in cardiomyocytes: all four cardiac BIN1 isoforms induce tubulation but with different geometries; high MTM1 (phosphoinositide phosphatase) levels are necessary for BIN1-induced tubulation (without direct binding to cardiac BIN1 isoforms lacking exon 11); high DNM2 levels are inhibitory for T-tubule formation despite DNM2 binding all four BIN1 isoforms and co-localizing at Z-lines. |
Developing mouse cardiomyocytes, gene-modified HL-1 and hiPSC-derived cardiomyocytes, confocal/Airyscan microscopy, RT-qPCR, Western blot, Ca2+ recording, co-IP |
Circulation research |
Medium |
37139790
|
| 2005 |
Bin1 loss elevates STAT1- and NF-κB-dependent expression of IDO in tumor cells, promoting immune escape from T cell-dependent antitumor immunity; Bin1 knockout studies establish that Bin1 loss upregulates IDO expression. |
Mouse knockout studies, STAT1/NF-κB pathway analysis, IDO expression measurement, immune escape assays in MMTV-Neu mice |
Nature medicine |
Medium |
15711557
|