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Protein / target

Dysbindin

Encoded byDTNBP1Q96EV8Homo sapiensSwiss-Prot
UniProt: Q96EV8Ensembl: ENSG00000047579HGNC: HGNC:17328NCBI Gene: 84062
Antibody-tractable
Druggability
UniProt loc high conf
1
Research papers

Protein at a glance

Biological role

Negative regulation of dendritic spine morphogenesis

Strongest disease association

Carcinoma, Squamous Cell

Via encoding gene DTNBP1 · Genetic evidence · score 0.52

Research activity

Emerging research

1 papers · latest 2024

Derived from structured UniProt, Open Targets and literature data on this page.

Protein profile

UniProt 2026_02

Canonical identity and biological annotation from UniProt.

Function overview

Component of the BLOC-1 complex, a complex that is required for normal biogenesis of lysosome-related organelles (LRO), such as platelet dense granules and melanosomes.

View complete UniProt function annotation

Component of the BLOC-1 complex, a complex that is required for normal biogenesis of lysosome-related organelles (LRO), such as platelet dense granules and melanosomes. In concert with the AP-3 complex, the BLOC-1 complex is required to target membrane protein cargos into vesicles assembled at cell bodies for delivery into neurites and nerve terminals. The BLOC-1 complex, in association with SNARE proteins, is also proposed to be involved in neurite extension. Associates with the BLOC-2 complex to facilitate the transport of TYRP1 independent of AP-3 function. Plays a role in synaptic vesicle trafficking and in neurotransmitter release. Plays a role in the regulation of cell surface exposure of DRD2. May play a role in actin cytoskeleton reorganization and neurite outgrowth. May modulate MAPK8 phosphorylation. Appears to promote neuronal transmission and viability through regulating the expression of SNAP25 and SYN1, modulating PI3-kinase-Akt signaling and influencing glutamatergic release. Regulates the expression of SYN1 through binding to its promoter. Modulates prefrontal cortical activity via the dopamine/D2 pathway

Subcellular location

CytoplasmCytoplasmic vesicle membraneEndosome membraneMelanosome membranePostsynaptic densityEndoplasmic reticulumNucleusCytoplasmic vesicle, secretory vesicle, synaptic vesicle membranePostsynaptic cell membrane
Domains and Gene Ontology detail (40)

Gene Ontology

  • Caxon
  • Caxon cytoplasm
  • CBLOC-1 complex
  • Ccytoplasm
  • Ccytosol
  • Cdendritic spine
  • Cendoplasmic reticulum membrane
  • Cendosome membrane
  • Cglutamatergic synapse
  • Cgrowth cone
  • Chippocampal mossy fiber to CA3 synapse
  • Cmelanosome membrane

351 aa · 39 kDa · 3 isoforms

Biological roles

What this protein does, drawn together from its UniProt function, Gene Ontology terms and Reactome pathways.

Excitatory neurotransmissionUniProt · GOCell proliferation & survivalUniProtHaemostasisUniProt · GO
View supporting evidence

Excitatory neurotransmission

  • ·Component of the BLOC-1 complex, a complex that is required for normal biogenesis of lys…
  • ·glutamatergic synapse

Cell proliferation & survival

  • ·Component of the BLOC-1 complex, a complex that is required for normal biogenesis of lys…

Haemostasis

  • ·Component of the BLOC-1 complex, a complex that is required for normal biogenesis of lys…
  • ·platelet dense granule organization

Concepts derived from UniProt GO Reactome — each badge above shows which sources supported that role.

Translational evidence

Open Targets 26

Why this target matters therapeutically, strongest evidence first. Disease associations are gene-level (via the gene that encodes this protein) and open into the full confidence synthesis; the development universe, tractability and safety annotations are target-level, from Open Targets.

Strongest disease associations · via encoding gene DTNBP1

Gene-level evidence surfaced through the gene DTNBP1 that encodes this protein — not a direct protein–disease relationship. Ranked by Forefront's causal-directness weighting, so genetically- and clinically-evidenced diseases lead over ones that merely share the literature.

Schizophrenia
0.55Moderately supported

Genetic evidence dominant · Open Targets 0.32

Carcinoma, Squamous Cell
0.52Moderately supported

Genetic evidence dominant · Open Targets 0.32

Pericarditis
0.48Limited support

Genetic evidence dominant · Open Targets 0.29

View evidence synthesis (3)
SchizophreniaModerately supported
0.55
agreement 0.41–0.69
Genetic79%Literature21%

Open Targets aggregate 0.32 · 2 independent evidence families

Carcinoma, Squamous CellModerately supported
0.52
agreement 0.40–0.64
Genetic100%

Open Targets aggregate 0.32 · 1 independent evidence family

PericarditisLimited support
0.48
agreement 0.36–0.60
Genetic100%

Open Targets aggregate 0.29 · 1 independent evidence family

The evidence agreement range shows how closely the independent evidence families agree — it is not a statistical confidence interval, and nothing here is fitted to outcome data. Derived from Open Targets evidence types under Forefront weighting; the per-type scores above show the calculation.

Show all associations
Schizophrenia0.32
Carcinoma, Squamous Cell0.32
Pericarditis0.29

Tractability

Antibodies — Emerging

Feasibility evidence (uniprot loc high conf and uniprot loc med conf) — no clinical-stage drug of this modality recorded.

Protein degraders — Emerging

Feasibility evidence (uniprot ubiquitination and database ubiquitination) — no clinical-stage drug of this modality recorded.

View underlying tractability evidence (6)
AB · UniProt loc high confAB · UniProt loc med confAB · GO CC med confPR · UniProt UbiquitinationPR · Database UbiquitinationPR · Half-life Data

Raw Open Targets tractability assessment buckets, by modality.

Safety-related annotations

methamphetamine psychosisClinPGxnot studiedClinPGxpsychosisClinPGx

Terms indexed against this target in Open Targets' safety data, with their datasource. These are annotations, not causal claims: the direction of effect (whether activation or inhibition is implicated), species and evidence strength are not captured here, so an entry does not mean that modulating this target is known to cause that condition.

Research activity

1 papers · to 2024

Papers linked directly to this protein. This is the protein's own literature — descriptor-derived papers are kept separate below.

Most cited

Loss of dysbindin-1 in excitatory neurons in mice impacts NMDAR-dependent behaviors, neuronal morphology and synaptic transmission in the ventral hippocampus.1 cites

Bhardwaj SK · Scientific reports · 2024

Recent

Loss of dysbindin-1 in excitatory neurons in mice impacts NMDAR-dependent behaviors, neuronal morphology and synaptic transmission in the ventral hippocampus.

Bhardwaj SK · Scientific reports · 2024

Europe PMC papers linked directly to this protein.