| 2007 |
BAI1 functions as a phosphatidylserine recognition receptor on apoptotic cells: its thrombospondin type 1 repeats in the extracellular region directly bind phosphatidylserine, and BAI1 forms a trimeric complex with ELMO and Dock180 to activate Rac GTPase and promote apoptotic cell engulfment. |
Co-immunoprecipitation, pulldown assays, phosphatidylserine-binding assays, loss-of-function (knockdown/interference), in vivo engulfment assays |
Nature |
High |
17960134
|
| 1997 |
BAI1 is a p53-target gene; its extracellular thrombospondin type 1 repeats mediate inhibition of angiogenesis, as demonstrated by a recombinant TSP-repeat protein inhibiting bFGF-induced neovascularization in the rat cornea. |
Recombinant protein in vivo angiogenesis assay (rat cornea model), gene cloning and characterization |
Oncogene |
Medium |
9393972
|
| 1998 |
BAI1 interacts with BAP1 (a MAGUK family PDZ domain-containing protein) via a QTEV motif in the C-terminal region of BAI1 and PDZ domains of BAP1; both proteins co-localize at the cytoplasmic membrane and cell-cell junctions, and BAI1 expression induces filopodia-like extensions. |
Yeast two-hybrid, co-immunoprecipitation, immunocytochemistry in COS-7 cells |
Biochemical and biophysical research communications |
Medium |
9647739
|
| 1999 |
BAI1 interacts via its proline-rich cytoplasmic region with the SH3 domain of BAIAP2 (IRSp53 homologue); BAIAP2 localizes to the plasma membrane only when co-expressed with BAI1, and BAI1 protein is predominantly found in growth cone-enriched fractions. |
Yeast two-hybrid, in vitro binding assay, double-color immunofluorescence, subcellular fractionation |
Cytogenetics and cell genetics |
Medium |
10343108
|
| 1998 |
BAI1 interacts with BAP3, a C2 domain-containing protein homologous to Munc13, through a region distinct from the C2 domains; interaction was mapped by deletion-mutant analysis in the yeast two-hybrid system. |
Yeast two-hybrid, deletion-mutant analysis |
Biochemical and biophysical research communications |
Low |
9790924
|
| 2001 |
BAI1 interacts with PAHX-AP1 (BAP4) via its cytoplasmic region, confirmed by GST-pulldown and co-immunoprecipitation from brain lysate; BAI1 is predominantly expressed in neurons of cortex and hippocampus and its expression is decreased in the ischemic hemisphere after focal cerebral ischemia. |
GST-pulldown, co-immunoprecipitation from brain lysate, in situ hybridization, Western blot |
Brain research. Molecular brain research |
Medium |
11245925
|
| 2011 |
BAI1 acts as a pattern recognition receptor on macrophages that recognizes Gram-negative bacterial lipopolysaccharide via its thrombospondin repeats, and promotes non-opsonic phagocytosis through ELMO/Dock-dependent Rac1 activation; inhibition of the BAI1/ELMO1 interaction prevents Rac activation and bacterial uptake. BAI1 does not recognize Gram-positive bacteria. |
Recombinant ectodomain competition, BAI1 knockdown and overexpression in macrophages and non-phagocytic cells, Rac activation assay, peritoneal infection model |
Proceedings of the National Academy of Sciences of the United States of America |
High |
21245295
|
| 2012 |
The N terminus of BAI1 is proteolytically cleaved extracellularly by a two-step cascade: proprotein convertases (primarily furin) activate latent MMP-14, which then directly cleaves BAI1 to release a bioactive 40 kDa fragment (Vasculostatin-40) that inhibits angiogenesis. |
Biochemical proteolysis assays, protease inhibition, cell-based cleavage assays, in vitro angiogenesis assay |
Oncogene |
High |
22330140
|
| 2013 |
BAI1 interacts with the Par3/Tiam1 polarity complex and recruits these proteins to dendritic spines to promote spinogenesis and synaptogenesis via local Rac1 activation; a BAI1 mutant that cannot interact with ELMO/DOCK180 still rescues spine defects (ELMO interaction is dispensable for this function), while a mutant lacking Par3/Tiam1 interaction fails to rescue spine or Par3 localization defects. |
Co-immunoprecipitation, BAI1 knockdown in hippocampal neurons, rescue experiments with BAI1 mutants, immunofluorescence of Rac1 and F-actin |
The Journal of neuroscience |
High |
23595754
|
| 2013 |
BAI1 acts as a phosphatidylserine receptor on myoblasts that promotes myoblast fusion through the ELMO/Dock180/Rac1 signaling axis; apoptotic myoblasts expose phosphatidylserine and signal in a contact-dependent manner through BAI1 on neighboring healthy myoblasts to promote fusion. In vivo, Bai1−/− mice have smaller myofibers and impaired muscle regeneration after injury. |
BAI1 overexpression and knockout, apoptosis blockade, addition of exogenous apoptotic myoblasts, in vivo muscle injury model (Bai1−/− mice) |
Nature |
High |
23615608
|
| 2014 |
In zebrafish microglia, BAI1 specifically controls phagosome formation around dying neurons and intracellular cargo transport during neuronal engulfment, whereas TIM-4 is required for phagosome stabilization; combined activity of both receptors is needed for complete clearance of dying neurons. |
Live imaging in zebrafish, genetic knockdown of BAI1 and TIM-4, quantitative phagocytosis assays |
Nature communications |
High |
24898390
|
| 2015 |
BAI1 prevents MDM2-mediated polyubiquitination and proteasomal degradation of PSD-95 through a direct interaction with MDM2; loss of BAI1 in mice leads to reduced PSD-95 protein levels, thinning of the postsynaptic density, enhanced LTP, impaired LTD, and hippocampus-dependent spatial learning deficits that are rescued by viral restoration of PSD-95. |
BAI1 knockout mice, co-immunoprecipitation of BAI1-MDM2 complex, ubiquitination assay, viral gene delivery rescue, electrophysiology (LTP/LTD) |
The Journal of clinical investigation |
High |
25751059
|
| 2015 |
BAI1 constitutive signaling activity does not require the membrane-proximal stalk peptide revealed by GAIN domain cleavage; a stalkless BAI1 mutant (B1-SL) retains robust signaling activity across multiple assays, supporting stalk-independent activation of BAI1. |
Engineered stalkless mutant receptors, battery of signaling assays (TGFα shedding, NFAT-luciferase, β-arrestin recruitment, SRF-luciferase) |
The Journal of biological chemistry |
Medium |
26710850
|
| 2016 |
BAI1 mediates phagosomal ROS production in macrophages challenged with Gram-negative bacteria by activating Rac1 GTPase, which stimulates NADPH oxidase; BAI1-deficient macrophages show attenuated Rac activity, reduced ROS, and impaired bacterial killing, and BAI1-deficient mice show increased susceptibility to Gram-negative peritoneal infection. |
Primary BAI1-deficient macrophages, Rac GTPase activation assay, ROS measurement, bacterial killing assays, in vivo peritoneal infection model |
Science signaling |
High |
26838550
|
| 2018 |
BAI1 prevents MDM2-mediated p53 polyubiquitination and degradation; loss of BAI1 (ADGRB1) in mice increases proliferation of cerebellar granule neuron precursors and accelerates tumor growth in the Ptch1+/− medulloblastoma model; ADGRB1 is epigenetically silenced in medulloblastomas by MBD2 binding to the hypermethylated promoter. |
Adgrb1 knockout mice crossed with Ptch1+/− tumor model, p53 ubiquitination assay, chromatin immunoprecipitation for MBD2, in vivo tumor growth assays, MBD2 pathway inhibitor treatment |
Cancer cell |
High |
29894688
|
| 2018 |
BAI1 promotes excitatory synaptogenesis via three distinct mechanisms: (1) Stachel peptide-dependent activation drives synaptic Rac1 activation and spinogenesis; (2) BAI1 acts trans-synaptically to induce clustering of presynaptic vGluT1 in contacting axons; (3) BAI1 forms a receptor complex with Neuroligin-1 (NRLN1) to mediate NRLN1-dependent spine growth and synapse development. The N-terminal extracellular segment is required for both prospinogenic and prosynaptogenic functions. |
In utero electroporation knockdown, Stachel peptide activation, mixed-culture trans-synaptic assay, co-immunoprecipitation of BAI1-NRLN1, in vivo hippocampal spine analysis |
The Journal of neuroscience |
High |
30120207
|
| 2019 |
Crystal structure of the ELMO2 RAE supramodule (RBD-ARR-ELMO) in complex with a conserved fragment of the BAI1 C-terminal cytoplasmic tail reveals the molecular basis of BAI/ELMO interaction; disease-causing mutations in BAI and ELMO map to this interface and disrupt complex formation. |
X-ray crystallography, co-immunoprecipitation, mutagenesis of interface residues |
Nature communications |
High |
30604775
|
| 2019 |
BAI1 regulates dendritic arbor growth arrest by coupling to the RhoA pathway: BAI1 associates with Bcr late in development and stimulates its cryptic RhoA-GEF activity (together with Bcr's Rac1-GAP activity) to terminate arborization; BAI1 loss lowers RhoA activation and causes dendritic hypertrophy. This function is independent of BAI1's Rac1-dependent synaptogenic pathway. |
BAI1 loss-of-function and overexpression in hippocampal neurons, RhoA activation assay, co-immunoprecipitation of BAI1-Bcr, domain mutant rescue experiments |
eLife |
High |
31461398
|
| 2022 |
Extracellular phosphatidylserine (PS) exposure modulates BAI1 G protein-dependent signaling: reducing PS in the outer leaflet (via co-expression of the PS flippase ATP11A or deletion of the scramblase ANO6) markedly reduces BAI1 signaling activity; ATP11A also forms a protein complex with BAI1 detected by co-immunoprecipitation. A truncated BAI1 lacking the TSP repeats is insensitive to PS reduction, demonstrating the TSP repeats mediate PS-dependent signaling. |
Co-expression of PS flippase ATP11A, ANO6 knockout cells, co-immunoprecipitation, G protein signaling assays, truncation mutants |
The Journal of biological chemistry |
High |
36370845
|
| 2024 |
BAI1 is required for clustering of AMPA receptor subunits GluR2-4 at the postsynaptic density of spiral ganglion neuron (SGN) afferent synapses in the cochlea; Bai1-deficient mice have normal inner hair cells but fail to transmit auditory information to SGNs, indicating BAI1 is essential for trafficking or anchoring AMPA receptors at cochlear ribbon synapses. |
Bai1 knockout mice, immunostaining for AMPA receptor subunits, auditory brainstem response and hearing threshold measurement, confocal and electron microscopy of synapses |
Cell reports |
High |
38564333
|
| 2025 |
C1q acts through BAI1 to drive neural stem cell (NSC) quiescence via two parallel BAI1-dependent mechanisms: (1) BAI1-dependent negative regulation of MDM2 causing cell cycle suppression through p53; (2) endocytic internalization of the C1q-BAI1 complex driving regulation of p32 (C1qBP) and metabolic reprogramming toward aerobic glycolysis. These functions were validated in human NSCs and in a mouse spinal cord injury model. |
BAI1 loss-of-function, MDM2/p53 pathway assay, endocytosis assay, metabolic profiling, in vivo spinal cord injury model with hNSC transplant |
Nature communications |
Medium |
41381494
|
| 2025 |
ADGRB1/BAI1 is required for astrocyte-mediated phagocytosis of excitatory presynaptic elements; Adgrb1-knockout astrocytes show reduced phagocytic capacity, less engulfment of presynaptic material, and a higher density of excitatory synapses in vivo, indicating BAI1 mediates synaptic pruning by astrocytes. |
Adgrb1 knockout mice, cultured astrocyte phagocytosis assay, immunostaining of pre- and post-synaptic markers, RNA-seq of KO astrocytes |
Experimental neurology |
Medium |
40930306
|