SH2D4A

Chr 8

SH2 domain containing 4A

Also known as: PPP1R38, SH2A

The SH2D4A protein enables phosphatase binding and inhibits estrogen-induced cell proliferation by competing with phospholipase C gamma for estrogen receptor binding, and may function in T-cell development. Mutations cause autosomal recessive developmental and epileptic encephalopathy with movement abnormalities, typically presenting in infancy with seizures, developmental delay, and movement disorders. The gene shows tolerance to loss-of-function variation (pLI near zero), consistent with the recessive inheritance pattern observed clinically.

Summary from RefSeq, UniProt
Research Assistant →
0
Active trials
3
Pubs (1 yr)
78
P/LP submissions
0%
P/LP missense
1.42
LOEUF
Multiple*
Mechanism· predicted
Clinical SummarySH2D4A
Population Constraint (gnomAD)
Low constraint (pLI 0.00) — loss-of-function variants are relatively tolerated in the population.
📋
ClinVar Variants
78 unique Pathogenic / Likely Pathogenic· 99 VUS of 211 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
1.42LOEUF
pLI 0.000
Z-score -0.28
OE 1.05 (0.801.42)
Tolerant

Highly tolerant — LoF variants common in population

Missense Constraint
-2.17Z-score
OE missense 1.39 (1.271.53)
334 obs / 239.6 exp
Tolerant

Tolerant to missense variation

Observed / Expected Ratios
LoF OE1.05 (0.801.42)
00.351.4
Missense OE1.39 (1.271.53)
00.61.4
Synonymous OE1.34
01.21.6
LoF obs/exp: 32 / 30.4Missense obs/exp: 334 / 239.6Syn Z: -2.59
DN
0.6842th %ile
GOF
0.7028th %ile
LOF
0.3355th %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

211 submitted variants in ClinVar

Classification Summary

Pathogenic75
Likely Pathogenic3
VUS99
Likely Benign5
Benign1
75
Pathogenic
3
Likely Pathogenic
99
VUS
5
Likely Benign
1
Benign

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
0
75
0
75
Likely Pathogenic
0
0
3
0
3
VUS
0
80
19
0
99
Likely Benign
0
1
4
0
5
Benign
0
0
1
0
1
Total0811020183

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

View in ClinVar →

Protein Context — Lollipop Plot

SH2D4A · protein map & ClinVar variants

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

3D Protein StructureAlphaFold

Clinical Trials

Active and recruiting trials from ClinicalTrials.gov

No active trials found for this gene.

Search ClinicalTrials.gov →
Clinical Literature
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