BIN3
Bridging integrator 3
Also known as: BIN3_HUMAN
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- Q9NQY0
- Gene
- BIN3
- Ensembl
- ENSG00000147439
- Chromosome
- 8
- Canonical length
- 253 aa
- Protein class
- Plasma proteins, Predicted intracellular proteins
OverviewNCBI Gene
The product of this gene is a member of the BAR domain protein family. The encoded protein is comprised solely of a BAR domain which is predicted to form coiled-coil structures and proposed to mediate dimerization, sense and induce membrane curvature, and bind small GTPases. BAR domain proteins have been implicated in endocytosis, intracellular transport, and a diverse set of other processes. [provided by RefSeq, Jul 2008]
Canonical amino-acid sequenceUniProt
253 residues, UniProt reviewed canonical sequence.
>Q9NQY0|BIN3
1 MSWIPFKIGQ PKKQIVPKTV ERDFEREYGK LQQLEEQTRR LQKDMKKSTD ADLAMSKSAV
61 KISLDLLSNP LCEQDQDLLN MVTALDTAMK RMDAFNQEKV NQIQKTVIEP LKKFGSVFPS
121 LNMAVKRREQ ALQDYRRLQA KVEKYEEKEK TGPVLAKLHQ AREELRPVRE DFEAKNRQLL
181 EEMPRFYGSR LDYFQPSFES LIRAQVVYYS EMHKIFGDLS HQLDQPGHSD EQRERENEAK
241 LSELRALSIV ADDLocalizationUniProt · AlphaFold · HPA
Whether an antibody against BIN3 can act on the native protein depends on physical access: surface and secreted proteins are reachable by circulating antibodies, intracellular proteins usually are not.
- Antibody reachability
- Intracellular
- Secreted
- No
- Transmembrane segments
- 0
- Mean surface accessibility (rSASA)
- 0.36
- Highest tissue expression
- 41 nTPM
Expression across tissuesHPA
Tissue
- bone marrow: 41 nTPM
- choroid plexus: 34 nTPM
- adrenal gland: 31 nTPM
- adipose tissue: 19 nTPM
- breast: 19 nTPM
- kidney: 18 nTPM
Single-cell type
- neutrophils: 362 nCPM
- breast myoepithelial cells: 198 nCPM
- neutrophil progenitors: 186 nCPM
- adrenal cortex cells: 163 nCPM
- müller glia: 158 nCPM
- schwann cells: 142 nCPM
Immune cell
- neutrophil: 95 nTPM
- eosinophil: 82 nTPM
- basophil: 67 nTPM
- T-reg: 47 nTPM
- total PBMC: 42 nTPM
- NK-cell: 39 nTPM
Brain region
- choroid plexus: 11 nTPM
- hippocampal formation: 9.5 nTPM
- cerebral cortex: 9 nTPM
- medulla oblongata: 8.9 nTPM
- white matter: 8.2 nTPM
- hypothalamus: 8 nTPM
Genetic constraint and essentialitygnomAD · DepMap
Does the body need this protein intact? Low LOEUF or a strong DepMap dependency means loss or blockade of the protein is likely to be felt.
- gnomAD LOEUF (loss-of-function intolerance)
- 1.6
- gnomAD pLI
- 0
- gnomAD missense Z
- -0.3
- DepMap mean gene effect
- 0.16
- DepMap dependency class
- none
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 4% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
- actin filament organization
- cytoskeleton-dependent cytokinesis
- endocytosis
- intracellular protein localization
- myoblast migration involved in skeletal muscle regeneration
- plasma membrane tubulation
- regulation of lamellipodium assembly
- skeletal muscle fiber development
- unidimensional cell growth
- actin cortical patch localization
Molecular functions
Cellular components
Protein domainsUniProt · Pfam · InterPro
- BAR domain
- AH/BAR domain superfamily
- BAR domain
- Bridging integrator 3, BAR domain
- Bridging integrator 3/RVS161-like
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of BIN3 in the human serome: UniProt-annotated complex subunits plus reported interactors. Each links to its own Seroatlas record.
Antibody and autoantibody relevanceSeroatlas analysis
Seroatlas reads BIN3 as an antibody target. Whether an autoantibody or antibody against BIN3 could matter depends on whether native BIN3 is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
BIN3 is annotated as predominantly intracellular. Intracellular proteins are common autoantibody markers, becoming visible to the immune system after cell injury or altered processing, but are usually markers of disease rather than direct drivers.
Annotation status
The present source text does not explicitly label BIN3 as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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