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Protein / target

Sialoadhesin

Encoded bySIGLEC1Q9BZZ2Homo sapiensSwiss-Prot
Antibody-tractable
Druggability
UniProt loc high conf
1
Research papers

Protein at a glance

Biological role

Carbohydrate binding

Strongest disease association

Neoplasms

Via encoding gene SIGLEC1 · Genetic evidence · score 0.55

Research activity

Emerging research

1 papers · latest 2019

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

Macrophage-restricted adhesion molecule that mediates sialic-acid dependent binding to lymphocytes, including granulocytes, monocytes, natural killer cells, B-cells and CD8 T-cells.

View complete UniProt function annotation

Macrophage-restricted adhesion molecule that mediates sialic-acid dependent binding to lymphocytes, including granulocytes, monocytes, natural killer cells, B-cells and CD8 T-cells. Plays a crucial role in limiting bacterial dissemination by engaging sialylated bacteria to promote effective phagocytosis and antigen presentation for the adaptive immune response (PubMed:12940982, PubMed:33489013). Mediates the uptake of various enveloped viruses via sialic acid recognition and subsequently induces the formation of intracellular compartments filled with virions (VCCs) (PubMed:28129379). In turn, enhances macrophage-to-T-cell transmission of several viruses including HIV-1 or SARS-CoV-2 (PubMed:28129379, PubMed:34782760). Acts as an endocytic receptor mediating clathrin dependent endocytosis. Preferentially binds to alpha-2,3-linked sialic acid (PubMed:12940982). Binds to SPN/CD43 on T-cells (By similarity). May play a role in hemopoiesis. Plays a role in the inhibition of antiviral innate immune by promoting TBK1 degradation via TYROBP and TRIM27-mediated ubiquitination (PubMed:26358190)

Subcellular location

Cell membraneSecreted
Domains and Gene Ontology detail (29)

Domains & features

Ig-like V-typeIg-like C2-type 1Ig-like C2-type 2Ig-like C2-type 3Ig-like C2-type 4Ig-like C2-type 5Ig-like C2-type 6Ig-like C2-type 7Ig-like C2-type 8Ig-like C2-type 9Ig-like C2-type 10Ig-like C2-type 11Ig-like C2-type 12Ig-like C2-type 13Ig-like C2-type 14Ig-like C2-type 15

Gene Ontology

  • Cearly endosome
  • Cextracellular region
  • Clate endosome
  • Cmembrane
  • Cplasma membrane
  • Fcarbohydrate binding
  • Fvirion binding
  • Pcell-cell adhesion
  • Pcell-matrix adhesion
  • Pclathrin-dependent endocytosis of virus by host cell
  • Pinflammatory response
  • Pnegative regulation of type I interferon production

1709 aa · 183 kDa · 3 isoforms

Biological roles

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

Immune signallingUniProt · GO
View supporting evidence

Immune signalling

  • ·Macrophage-restricted adhesion molecule that mediates sialic-acid dependent binding to l…
  • ·inflammatory response

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 SIGLEC1

Gene-level evidence surfaced through the gene SIGLEC1that 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.

Neoplasms
0.61Moderately supported

Genetic evidence dominant · Open Targets 0.33

Ovarian neoplasm
0.47Limited support

Genetic evidence dominant · Open Targets 0.28

Neurodegenerative Diseases
0.28Preliminary

Pathway evidence dominant · Open Targets 0.42 · no direct causal or clinical evidence

Infections
0.14Preliminary

Literature evidence dominant · Open Targets 0.11 · no direct causal or clinical evidence

COVID-19
0.13Preliminary

Literature evidence dominant · Open Targets 0.11 · no direct causal or clinical evidence

View evidence synthesis (5)
NeoplasmsModerately supported
0.61
agreement 0.470.75
Genetic79%Literature21%

Open Targets aggregate 0.33 · 2 independent evidence families

Ovarian neoplasmLimited support
0.47
agreement 0.330.61
Genetic92%Literature8%

Open Targets aggregate 0.28 · 2 independent evidence families

Neurodegenerative DiseasesPreliminary
0.28
agreement 0.110.46
Pathway97%Literature3%

Open Targets aggregate 0.42 · 2 independent evidence families · no direct causal or clinical evidence

InfectionsPreliminary
0.14
agreement 0.000.41
Literature100%

Open Targets aggregate 0.11 · 1 independent evidence family · no direct causal or clinical evidence

COVID-19Preliminary
0.13
agreement 0.000.40
Literature100%

Open Targets aggregate 0.11 · 1 independent evidence family · no direct causal or clinical evidence

This ranking differs from Open Targets' own: re-weighting moves genetically-evidenced diseases above more heavily co-mentioned ones. 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 Diseases0.42
Neoplasms0.33
Ovarian neoplasm0.28
Infections0.11
COVID-190.11
Breast Neoplasms0.11
Colorectal Neoplasms0.10

Tractability

AntibodiesEmerging

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

View underlying tractability evidence (4)
AB · UniProt loc high confAB · GO CC high confAB · UniProt loc med confAB · UniProt SigP or TMHMM

Raw Open Targets tractability assessment buckets, by modality.

Research activity

1 papers · to 2019

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

Most cited

Recent

Europe PMC papers linked directly to this protein.