SGPP2

Chr 2

sphingosine-1-phosphate phosphatase 2

Also known as: SPP2, SPPase2

The protein is a sphingosine-1-phosphate phosphatase that degrades the bioactive signaling molecule sphingosine-1-phosphate, regulating sphingolipid metabolism and inflammatory signaling pathways. Mutations cause autosomal recessive spastic paraplegia with onset typically in childhood or adolescence, characterized by progressive lower limb spasticity and weakness. The gene shows low constraint against loss-of-function variants, consistent with its recessive inheritance pattern.

Summary from RefSeq, UniProt
Research Assistant →
0
Active trials
12
Pubs (1 yr)
32
P/LP submissions
0%
P/LP missense
0.95
LOEUF
Multiple*
Mechanism· predicted
Clinical SummarySGPP2
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
32 unique Pathogenic / Likely Pathogenic· 52 VUS of 92 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.95LOEUF
pLI 0.003
Z-score 1.70
OE 0.48 (0.260.95)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
0.07Z-score
OE missense 0.99 (0.881.11)
193 obs / 195.9 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.48 (0.260.95)
00.351.4
Missense OE0.99 (0.881.11)
00.61.4
Synonymous OE1.20
01.21.6
LoF obs/exp: 6 / 12.5Missense obs/exp: 193 / 195.9Syn Z: -1.43
DN
0.77top 25%
GOF
0.6640th %ile
LOF
0.2677th %ile

This gene has evidence for multiple mechanisms of pathogenicity (dominant-negative and gain-of-function). Both the Badonyi & Marsh prediction and the broader genomic evidence point to dominant-negative as the predominant mechanism. Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

DNprediction above median
GOFprediction above median

Note: In-silico variant effect predictors (SIFT, PolyPhen, REVEL, CADD) may underestimate pathogenicity of missense variants in genes with GOF or DN mechanisms. Consider functional evidence and clinical context.

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312.

ClinVar Variant Classifications

92 submitted variants in ClinVar

Classification Summary

Pathogenic31
Likely Pathogenic1
VUS52
Likely Benign4
31
Pathogenic
1
Likely Pathogenic
52
VUS
4
Likely Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
31
0
31
Likely Pathogenic
0
0
1
0
1
VUS
0
50
2
0
52
Likely Benign
0
4
0
0
4
Benign
0
0
0
0
0
Total05434088

LoF = frameshift, stop gained/lost, canonical splice · Counts from ClinVar esearch · Updated hourly

View in ClinVar →

Protein Context — Lollipop Plot

SGPP2 · protein map & ClinVar variants

Showing all ClinVar variants across the protein. Search a specific variant to highlight its position.

Clinical Trials

Active and recruiting trials from ClinicalTrials.gov

No active trials found for this gene.

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Clinical Literature
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