SORBS2

Chr 4

sorbin and SH3 domain containing 2

Also known as: ARGBP2, PRO0618

The SORBS2 protein functions as an adapter that assembles signaling complexes linking ABL kinases to the actin cytoskeleton and regulates pancreatic cell adhesion. Mutations cause autosomal recessive intellectual disability with seizures and spasticity, typically presenting in early childhood. This gene is highly constrained against loss-of-function variants, suggesting that complete protein loss is not well tolerated.

Summary from RefSeq, UniProt
Research Assistant →
0
Active trials
20
Pubs (1 yr)
116
P/LP submissions
0%
P/LP missense
0.40
LOEUF
Multiple*
Mechanism· predicted
Clinical SummarySORBS2
Population Constraint (gnomAD)
Constrained for loss-of-function variants (OE-LoF 0.26) despite low pLI — interpret in context.
📋
ClinVar Variants
115 unique Pathogenic / Likely Pathogenic· 197 VUS of 369 total submissions
Some data sources returned errors (1)

ensembl: TimeoutError: The operation was aborted due to timeout

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Moderate LoF intolerance
LoF Constraint
0.40LOEUF
pLI 0.036
Z-score 5.08
OE 0.26 (0.170.40)
Moderately constrained

More LoF-intolerant than ~75% of genes

Missense Constraint
0.11Z-score
OE missense 0.99 (0.931.05)
687 obs / 695.0 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.26 (0.170.40)
00.351.4
Missense OE0.99 (0.931.05)
00.61.4
Synonymous OE1.06
01.21.6
LoF obs/exp: 14 / 54.5Missense obs/exp: 687 / 695.0Syn Z: -0.80
DN
0.74top 25%
GOF
0.6735th %ile
LOF
0.48top 25%

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

369 submitted variants in ClinVar

Classification Summary

Pathogenic103
Likely Pathogenic12
VUS197
Likely Benign16
Benign6
103
Pathogenic
12
Likely Pathogenic
197
VUS
16
Likely Benign
6
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
103
0
103
Likely Pathogenic
0
0
12
0
12
VUS
0
168
29
0
197
Likely Benign
0
11
4
1
16
Benign
0
1
1
4
6
Total01801495334

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

View in ClinVar →

Protein Context — Lollipop Plot

SORBS2 · 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.

Search ClinicalTrials.gov →
Clinical Literature
Open Research Assistant →
Full-Text Mentions
NLP-detected gene mentions in article bodies · via PubTator3
PubTator3
Top 5 full-text resultsSearch PubTator3 ↗
Recent Gene-Specific Literature
Gene in title · MEDLINE · newest first
Europe PMC