SH3BP2

Chr 4AD

SH3 domain binding protein 2

Also known as: 3BP-2, 3BP2, CRBM, CRPM, RES4-23

The protein functions as a cytoplasmic adaptor that binds to SH3 domains of signaling proteins including ABL1 and SYK tyrosine kinases, positively regulating transcriptional activity in immune cells. Mutations cause cherubism, a rare bone disorder characterized by painless bilateral enlargement of the jaws that typically manifests in early childhood. Inheritance is autosomal dominant, and the gene shows very low constraint against loss-of-function variants.

Summary from RefSeq, OMIM, UniProt
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Primary Disease Associations & Inheritance

CherubismMIM #118400
AD
1
Active trials
10
Pubs (1 yr)
23
P/LP submissions
0%
P/LP missense
1.14
LOEUF
GOF
Mechanism· G2P
Clinical SummarySH3BP2
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
23 unique Pathogenic / Likely Pathogenic· 196 VUS of 400 total submissions
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Clinical Trials
1 active or recruiting trial — potential therapeutic options may be available
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GeneReview available — SH3BP2
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
1.14LOEUF
pLI 0.000
Z-score 1.02
OE 0.78 (0.551.14)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
0.29Z-score
OE missense 0.96 (0.881.05)
344 obs / 359.6 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.78 (0.551.14)
00.351.4
Missense OE0.96 (0.881.05)
00.61.4
Synonymous OE1.15
01.21.6
LoF obs/exp: 20 / 25.6Missense obs/exp: 344 / 359.6Syn Z: -1.45
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
limitedSH3BP2-related cherubismGOFAD
DN
0.6455th %ile
GOF
0.5071th %ile
LOF
0.4234th %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
GOF1 literature citation

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.

Literature Evidence

GOFGain-of-function missense mutations in the SH3BP2 gene cause cherubism, an autosomal dominant disorder associated with severe craniofacial developmental defects in children.PMID:31999934

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

ClinVar Variant Classifications

400 submitted variants in ClinVar

Classification Summary

Pathogenic21
Likely Pathogenic2
VUS196
Likely Benign153
Benign7
Conflicting3
21
Pathogenic
2
Likely Pathogenic
196
VUS
153
Likely Benign
7
Benign
3
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
21
0
21
Likely Pathogenic
0
0
2
0
2
VUS
8
176
11
1
196
Likely Benign
0
2
74
77
153
Benign
0
0
7
0
7
Conflicting
3
Total817811578382

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

View in ClinVar →

Protein Context — Lollipop Plot

SH3BP2 · 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 ↗