Protein / target

Neuron-specific calcium-binding protein hippocalcin

Encoded byHPCAP84074Homo sapiensSwiss-Prot

UniProt: P84074 Ensembl: ENSG00000121905 HGNC: HGNC:5144 NCBI Gene: 3208

Small-molecule tractable

Druggability

Structure with Ligand

Research papers

Protein at a glance

Biological role

Identical protein binding

Strongest disease association

Diabetes Mellitus, Type 2

Via encoding gene HPCA · Genetic evidence · score 0.14

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

Calcium-binding protein that may play a role in the regulation of voltage-dependent calcium channels.

View complete UniProt function annotation

Calcium-binding protein that may play a role in the regulation of voltage-dependent calcium channels (PubMed:28398555). May also play a role in cyclic-nucleotide-mediated signaling through the regulation of adenylate and guanylate cyclases (By similarity)

Subcellular location

Cytoplasm, cytosolMembrane

Domains and Gene Ontology detail (29)

Domains & features

EF-hand 1EF-hand 2EF-hand 3EF-hand 4

Gene Ontology

Caxon
Ccytoplasm
Ccytosol
Cdendrite cytoplasm
Cdendrite membrane
Cdendritic spine head
Cglutamatergic synapse
Cmembrane
Cneuronal cell body membrane
Cperikaryon
Factin binding
Fcalcium ion binding

193 aa · 22 kDa

Biological roles

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

Synaptic signallingGO

View supporting evidence

Synaptic signalling

·glutamatergic synapse
·regulation of postsynaptic neurotransmitter receptor internalization

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 HPCA

Gene-level evidence surfaced through the gene HPCAthat 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.

Neurodegenerative Diseases

0.23Preliminary

Pathway evidence dominant · Open Targets 0.34 · no direct causal or clinical evidence

Diabetes Mellitus, Type 2

0.14Preliminary

Genetic evidence dominant · Open Targets 0.09

lissencephaly due to TUBA1A mutation

0.12Preliminary

Animal model evidence dominant · Open Targets 0.04 · no direct causal or clinical evidence

Central Nervous System Neoplasms

0.06Preliminary

RNA expression evidence dominant · Open Targets 0.03 · no direct causal or clinical evidence

Diabetes Mellitus

0.05Preliminary

Genetic evidence dominant · Open Targets 0.03

View evidence synthesis (5)

Neurodegenerative DiseasesPreliminary

0.23

agreement 0.05–0.40

Pathway99%Literature1%

Open Targets aggregate 0.34 · 2 independent evidence families · no direct causal or clinical evidence

Diabetes Mellitus, Type 2Preliminary

0.14

agreement 0.02–0.26

Genetic100%

Open Targets aggregate 0.09 · 1 independent evidence family

lissencephaly due to TUBA1A mutationPreliminary

0.12

agreement 0.00–0.35

Animal model100%

Open Targets aggregate 0.04 · 1 independent evidence family · no direct causal or clinical evidence

Central Nervous System NeoplasmsPreliminary

0.06

agreement 0.00–0.24

RNA expression97%Literature3%

Open Targets aggregate 0.03 · 2 independent evidence families · no direct causal or clinical evidence

Diabetes MellitusPreliminary

0.05

agreement 0.00–0.19

Genetic83%Literature17%

Open Targets aggregate 0.03 · 2 independent evidence families

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

Neurodegenerative Diseases0.34

Diabetes Mellitus, Type 20.09

lissencephaly due to TUBA1A mutation0.04

Central Nervous System Neoplasms0.03

Diabetes Mellitus0.03

Huntington's Disease0.03

Tractability

Small molecules — Emerging

Feasibility evidence (structure with ligand) — no clinical-stage drug of this modality recorded.

Antibodies — Emerging

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

Protein degraders — Emerging

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

View underlying tractability evidence (4)

SM · Structure with LigandAB · UniProt loc med confPR · Database UbiquitinationPR · Half-life Data

Raw Open Targets tractability assessment buckets, by modality.

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

Epigallocatechin gallate improves neuronal damage in animal model of ischemic stroke and glutamate-exposed neurons via modulation of hippocalcin expression.10 cites

Park DJ · PloS one · 2024

Recent

Epigallocatechin gallate improves neuronal damage in animal model of ischemic stroke and glutamate-exposed neurons via modulation of hippocalcin expression.

Park DJ · PloS one · 2024

Europe PMC papers linked directly to this protein.