CausalSentinel

Protein Dossier — LYG1 (Lysozyme g-like protein 1)

MR feasibility tier: A — Published pQTL-MR estimates exist for this protein (retrieved below - not computed here).

1. Published MR estimates (retrieved, not computed)

Outcome beta se p method nSNP cis/trans coloc
Femoral neck bone mineral density 0.142 0.0646 0.0279 Wald ratio 1 trans NA
Lumbar spine bone mineral density 0.0983 0.073 0.178 Wald ratio 1 trans NA
Birth weight -0.0341 0.0288 0.237 Wald ratio 1 trans NA
Low grade serous ovarian cancer -0.351 0.298 0.239 Wald ratio 1 trans NA
Invasive mucinous ovarian cancer 0.269 0.248 0.279 Wald ratio 1 trans NA
ER-negative Breast cancer (Combined Oncoarray; iCOGS; GWAS meta analysis) 0.0864 0.0816 0.29 Wald ratio 1 trans NA
Ovarian cancer 0.0797 0.0837 0.341 Wald ratio 1 trans NA
High grade serous ovarian cancer 0.0785 0.0993 0.429 Wald ratio 1 trans NA
Breast cancer (Combined Oncoarray; iCOGS; GWAS meta analysis) -0.0341 0.0437 0.435 Wald ratio 1 trans NA

2. pQTL instrument availability (Tier-B probe)

No prot-* pQTL GWAS dataset found for this protein (matched by UniProt accession and symbol).

3. GWAS Catalog results — traits with signal at this locus

4 association rows across 4 traits (3 genome-wide significant rows). Associations are loci, not causal claims; the mapped gene at a locus is not necessarily the effector gene.

Trait best p lead SNP n assoc study MR status
Late effect (PheCode 1012) 1e-12 rs532494959 1 GCST90479760 no MR -> candidate analysis
Heel bone mineral density 2e-11 rs62153852 1 GCST006433 no MR -> candidate analysis
ICD10 D25: Leiomyoma of uterus 4e-11 rs12475639 1 GCST90454204 no MR -> candidate analysis
IgG glycosylation 4e-7 rs2200578 1 GCST001848 no MR -> candidate analysis

4. Phenome map — where this gene is a genetic locus, vs. where MR exists

Top diseases by Open Targets association (of 35 total). Associations are loci, not causal claims. The causal-status column is a four-state triage per pair: established (curated) = a curated clinical assertion exists (ClinGen/G2P/GEL/Orphanet/ClinVar — any validity level, MR adds little); exploratory rare-variant signal = ExWAS burden evidence without curation — a candidate NEW gene-disease relationship; common-variant locus = GWAS signal, classic pQTL-MR territory; multi-layer = burden+GWAS together, an allelic-series candidate (the strongest causal setup). Burden estimand is carrier-vs-noncarrier, not per-SD MR.

Disease genetic assoc. burden (ExWAS) causal status MR status
inflammatory bowel disease 0.337 common-variant locus no MR -> candidate analysis
uterine corpus leiomyoma 0.163 common-variant locus no MR -> candidate analysis
placental abruption 0.081 common-variant locus no MR -> candidate analysis
Uterine leiomyoma 0.057 common-variant locus no MR -> candidate analysis
male reproductive organ cancer 0.049 common-variant locus no MR -> candidate analysis
mathematical ability 0.048 common-variant locus no MR -> candidate analysis
Cachexia 0.041 common-variant locus no MR -> candidate analysis
intelligence 0.037 common-variant locus no MR -> candidate analysis
Splenomegaly 0.032 common-variant locus no MR -> candidate analysis

Of the 9 rows above, 9 have no MR estimate in this resource. Across all retrieved diseases for this gene: 0 exploratory rare-variant signal(s), 0 multi-layer (allelic-series candidate) pair(s). Final triage still belongs to a statistical geneticist.

5. Downstream annotation (druggability & safety preview)

Layer Result
ChEMBL druggability not available — no ChEMBL target (undrugged)
gnomAD constraint pLI=1.9e-05, LOEUF=1.18 — LoF-tolerant
GWAS Catalog 24 unique SNPs / 48 rows
ClinVar 51 records; 3 pathogenic in sample of 30
PharmGKB/ClinPGx no annotations

Caveats declared by the tools

Sources

Provenance