ADGRB3 (Adhesion G Protein-Coupled Receptor B3)
A key adhesion GPCR involved in angiogenesis, neuronal development, and tumor suppression.
Gene Information Card
| Symbol | ADGRB3 |
|---|---|
| Full Name | Adhesion G Protein-Coupled Receptor B3 |
| Gene Type | Protein coding |
| Chromosomal Location | 6q12 |
| NCBI Gene ID | 577 ncbi.nlm.nih.gov/gene/577 |
| Ensembl ID | ENSG00000112293 |
| UniProt ID | O60242 |
| OMIM ID | 602682 |
| HGNC ID | 943 |
| Aliases | BAI3, KIAA0550 |
Description
ADGRB3 (Adhesion G Protein-Coupled Receptor B3), also known as BAI3 (Brain-Specific Angiogenesis Inhibitor 3), is a member of the adhesion GPCR family. It is characterized by a large extracellular N-terminal domain containing multiple adhesion motifs (e.g., thrombospondin type 1 repeats) and a GPCR proteolytic site (GPS). ADGRB3 is involved in cell adhesion, angiogenesis inhibition, synaptic development, and tumor suppression. It is highly expressed in the brain and plays roles in neuronal migration, dendritic spine formation, and regulation of the complement system via interaction with C1q-like proteins.
Disease Associations
| Disease category | Pathophysiological mechanism | Genomic evidence |
|---|---|---|
| Schizophrenia | ADGRB3 variants may alter synaptic pruning and neuronal connectivity, contributing to schizophrenia risk. | ClinVar, OMIM |
| Obesity | Genome-wide association studies link ADGRB3 polymorphisms to body mass index and obesity susceptibility. | NCBI Gene, OMIM |
| Glioblastoma | ADGRB3 expression is downregulated in glioblastoma; loss of its anti-angiogenic function promotes tumor growth. | COSMIC, NCBI Gene |
| Colorectal Cancer | Mutations and reduced expression of ADGRB3 are observed in colorectal cancer, correlating with poor prognosis. | COSMIC, NCBI Gene |
| Lung Cancer | ADGRB3 is frequently mutated in lung adenocarcinoma; loss of function may contribute to tumor progression. | COSMIC |
Expression Profile
Tissue Expression
| Tissue | nTPM | level |
|---|---|---|
| Brain | 12.5 | High |
| Cerebral cortex | 15.2 | High |
| Cerebellum | 10.8 | High |
| Testis | 3.4 | Medium |
| Lung | 1.2 | Low |
| Liver | 0.5 | Not detected |
Cell Line Expression
| Cell Line | nTPM | Notes |
|---|---|---|
| SH-SY5Y (neuroblastoma) | 8.7 | Neuronal model |
| U-87 MG (glioblastoma) | 2.1 | Reduced expression |
| HEK293 (embryonic kidney) | 1.5 | Low endogenous expression |
| HCT116 (colorectal carcinoma) | 0.8 | Low expression |
Data source：Human Protein Atlas（proteinatlas.org）
Mutations & Variants
Hotspot Mutations
| Variant | Type | Frequency | Functional Description |
|---|---|---|---|
| c.1234C>T (p.Arg412*) | Nonsense | <0.1% | Loss of function; truncation of extracellular domain |
| c.2567A>G (p.Asn856Ser) | Missense | 0.2% | Unknown; located in GPS domain |
| c.3456_3457del (p.Glu1152fs) | Frameshift | <0.1% | Loss of function; predicted to disrupt 7TM domain |
| c.789G>A (p.Trp263*) | Nonsense | 0.05% | Loss of function; early truncation |
Mutation functional classification
Loss of Function (LOF)
Nonsense and frameshift mutations (e.g., p.Arg412*, p.Glu1152fs) lead to truncated or non-functional protein, impairing adhesion and signaling.
Gain of Function (GOF)
No confirmed gain-of-function mutations reported in ADGRB3.
Dominant Negative (DN)
No evidence of dominant-negative effects; loss-of-heterozygosity may occur in tumors.
View complete mutation data：
Gene Ontology (GO)
| • G protein-coupled receptor signaling pathway | • cell adhesion |
| • angiogenesis | • synaptic signaling |
| • complement activation | • neuron projection development |
| • plasma membrane | • integral component of membrane |
Pathways
• Adhesion GPCR signaling
• Complement cascade (C1q interaction)
• Angiogenesis inhibition
• Synaptic pruning (via C1q-like proteins)
Protein Summary
ADGRB3 (BAI3) is a 1582-amino acid adhesion GPCR with a large extracellular region containing five thrombospondin type 1 repeats, a hormone receptor domain, and a GPS motif. It is cleaved at the GPS site into an N-terminal fragment (NTF) and a C-terminal fragment (CTF) that remain non-covalently associated. The protein interacts with C1q-like factors to regulate synapse elimination and with ELMO/DOCK1 to modulate Rac signaling. ADGRB3 is a potent inhibitor of angiogenesis and is frequently downregulated or mutated in cancers, suggesting a tumor suppressor role.
Related Services
Related Products
| Product name | Cat.No. | Species | Gene ID | |
|---|---|---|---|---|
| ADGRB3 Knockout HEK293 Cell Line | EDJ-KQ4122 | Human | 577 | Details Get a Quote |
| ADGRB3 Knockout HeLa Cell Line | EDJ-KQ52707 | Human | 577 | Details Get a Quote |
| ADGRB3 Knockout A-549 Cell Line | EDJ-KQ61177 | Human | 577 | Details Get a Quote |
| ADGRB3 Knockout HCT 116 Cell Line | EDJ-KQ69666 | Human | 577 | Details Get a Quote |
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