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Protein / target

Calretinin

Encoded byCALB2P22676Homo sapiensSwiss-Prot
UniProt: P22676Ensembl: ENSG00000172137HGNC: HGNC:1435NCBI Gene: 794
Degrader-tractable
Druggability
Half-life Data
1
Research papers

Protein at a glance

Biological role

Calcium ion binding

Strongest disease association

Pre-Eclampsia

Via encoding gene CALB2 · Genetic evidence · score 0.45

Research activity

Emerging research

1 papers · latest 2023

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 involved in calcium homeostasis and signal transduction.

View complete UniProt function annotation

Calcium-binding protein involved in calcium homeostasis and signal transduction. It plays a critical role in buffering intracellular calcium levels and modulating calcium-dependent signaling pathways (PubMed:2001709). Predominantly expressed in specific neuronal populations, influences synaptic plasticity and neuronal excitability, contributing to learning and memory (By similarity). During embryonic development, it facilitates neuronal differentiation and maturation (By similarity)

Subcellular location

SynapseCell projection, dendrite
Domains and Gene Ontology detail (21)

Domains & features

EF-hand 1EF-hand 2EF-hand 3EF-hand 4EF-hand 5EF-hand 6

Gene Ontology

  • Ccuticular plate
  • Ccytosol
  • Cdendriole
  • Cdendrite
  • Cgap junction
  • Cnucleus
  • Cparallel fiber to Purkinje cell synapse
  • Cstereocilium
  • Csynapse
  • Cterminal bouton
  • Fcalcium ion binding
  • Fcalcium ion binding involved in regulation of presynaptic cytosolic calcium ion concentration

271 aa · 32 kDa

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 CALB2

Gene-level evidence surfaced through the gene CALB2that 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.

Pre-Eclampsia
0.48Limited support

Genetic evidence dominant · Open Targets 0.28

Corneal Neovascularization
0.45Limited support

Genetic evidence dominant · Open Targets 0.28

Atrial Fibrillation
0.38Limited support

Genetic evidence dominant · Open Targets 0.23

Schizophrenia
0.36Preliminary

Animal model evidence dominant · Open Targets 0.11 · no direct causal or clinical evidence

Coronary Artery Disease
0.34Limited support

Genetic evidence dominant · Open Targets 0.20

View evidence synthesis (5)
Pre-EclampsiaLimited support
0.48
agreement 0.34–0.62
Genetic91%Literature9%

Open Targets aggregate 0.28 · 2 independent evidence families

Corneal NeovascularizationLimited support
0.45
agreement 0.33–0.57
Genetic100%

Open Targets aggregate 0.28 · 1 independent evidence family

Atrial FibrillationLimited support
0.38
agreement 0.24–0.52
Genetic99%Literature1%

Open Targets aggregate 0.23 · 2 independent evidence families

SchizophreniaPreliminary
0.36
agreement 0.19–0.54
Animal model73%Literature27%

Open Targets aggregate 0.11 · 2 independent evidence families · no direct causal or clinical evidence

Coronary Artery DiseaseLimited support
0.34
agreement 0.20–0.47
Genetic96%Literature4%

Open Targets aggregate 0.20 · 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
Pre-Eclampsia0.28
Corneal Neovascularization0.28
Atrial Fibrillation0.23
Coronary Artery Disease0.20
Miyoshi myopathy0.11
Schizophrenia0.11

Tractability

Protein degraders — Emerging

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

View underlying tractability evidence (1)
PR · Half-life Data

Raw Open Targets tractability assessment buckets, by modality.

Research activity

1 papers · to 2023

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

Most cited

Calretinin-expressing islet cells are a source of pre- and post-synaptic inhibition of non-peptidergic nociceptor input to the mouse spinal cord.12 cites

Davis OC · Scientific reports · 2023

Recent

Calretinin-expressing islet cells are a source of pre- and post-synaptic inhibition of non-peptidergic nociceptor input to the mouse spinal cord.

Davis OC · Scientific reports · 2023

Europe PMC papers linked directly to this protein.