S100B

Chr 21

S100 calcium binding protein B

Also known as: NEF, S100, S100-B, S100beta

S100B encodes a small calcium- and zinc-binding protein highly expressed in astrocytes that acts as a neurotrophic factor promoting astrocytosis and axonal proliferation. Mutations cause autosomal dominant epileptic encephalopathy with variable age of onset, primarily affecting the central nervous system. The gene shows low constraint to loss-of-function variation (pLI 0.04, LOEUF 1.73), and comprehensive clinical information is available in GeneReviews.

Summary from RefSeq, UniProt
Research Assistant →
2
Active trials
326
Pubs (1 yr)
96
P/LP submissions
P/LP missense
1.73
LOEUF
Multiple*
Mechanism· predicted
Clinical SummaryS100B
Population Constraint (gnomAD)
Low constraint (pLI 0.04) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
90 unique Pathogenic / Likely Pathogenic· 28 VUS of 123 total submissions
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Clinical Trials
2 active or recruiting trials — potential therapeutic options may be available
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GeneReview available — S100B
Authoritative clinical overview · Recommended first read
Open GeneReview ↗

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.73LOEUF
pLI 0.044
Z-score 0.55
OE 0.66 (0.261.73)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
0.40Z-score
OE missense 0.84 (0.661.09)
43 obs / 51.0 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.66 (0.261.73)
00.351.4
Missense OE0.84 (0.661.09)
00.61.4
Synonymous OE0.89
01.21.6
LoF obs/exp: 2 / 3.0Missense obs/exp: 43 / 51.0Syn Z: 0.38
DN
0.84top 10%
GOF
0.90top 5%
LOF
0.1598th %ile

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

GOFprediction above median
DNprediction 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

123 submitted variants in ClinVar

Classification Summary

Pathogenic82
Likely Pathogenic8
VUS28
Likely Benign1
Benign3
82
Pathogenic
8
Likely Pathogenic
28
VUS
1
Likely Benign
3
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories· variant type breakdown unavailable

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
82
Likely Pathogenic
8
VUS
28
Likely Benign
1
Benign
3
Total122

Counts from ClinVar esearch · Updated hourly

View in ClinVar →

Protein Context — Lollipop Plot

S100B · protein map & ClinVar variants

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

Clinical Literature
Open Research Assistant →
Key Publications
Landmark & review papers · by relevance
PubMed
Top 5 results · since 2015Search PubMed ↗