NSD1

Chr 5AD

nuclear receptor binding SET domain protein 1

Also known as: ARA267, KMT3B, SOTOS, SOTOS1, STO

This protein functions as a histone methyltransferase that enhances androgen receptor transactivation and acts as a bifunctional transcriptional regulator in the nucleus. Mutations cause Sotos syndrome and Weaver syndrome through an autosomal dominant inheritance pattern. The pathogenic mechanism involves loss of function, as the protein is highly intolerant to loss-of-function variants.

GeneReviewsOMIMResearchSummary from RefSeq, OMIM, UniProt, Mechanism
LOFmechanismADLOEUF 0.101 OMIM phenotype
Clinical SummaryNSD1
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Gene-Disease Validity (ClinGen)
Sotos syndrome · ADDefinitive

Definitive — sufficient evidence for diagnostic panels

Population Constraint (gnomAD)
Highly constrained gene — heterozygous loss-of-function variants are very rare in the population (pLI 1.00). One damaged copy is likely sufficient to cause disease.
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ClinVar Variants
89 unique Pathogenic / Likely Pathogenic· 185 VUS of 500 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 — NSD1
Authoritative clinical overview · Recommended first read
Open GeneReview ↗

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Dual constrained — LoF & missense intolerant
LoF Constraint
0.10LOEUF
pLI 1.000
Z-score 9.31
OE 0.05 (0.020.10)
Highly constrained

Among the most LoF-intolerant genes (~top 3%)

Missense Constraint
3.41Z-score
OE missense 0.75 (0.710.79)
1065 obs / 1427.7 exp
Constrained

Highly missense-constrained (top ~0.1%)

Observed / Expected Ratios
LoF OE0.05 (0.020.10)
00.351.4
Missense OE0.75 (0.710.79)
00.61.4
Synonymous OE1.00
01.21.6
LoF obs/exp: 5 / 110.6Missense obs/exp: 1065 / 1427.7Syn Z: 0.08
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
definitiveNSD1-related Sotos syndromeLOFAD
definitiveNSD1-related Beckwith-Wiedemann syndromeOTHERAD
DN
0.2399th %ile
GOF
0.2398th %ile
LOF
0.86top 5%

The highest-scoring mechanism for this gene is loss-of-function (haploinsufficiency).

LOFprediction above median · 1 literature citation · 65% of P/LP variants are LoF · LOEUF 0.10

Literature Evidence

LOFHaploinsufficiency of NSD1 causes Sotos syndrome.PMID:11896389

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312. Mechanism ranking also informed by gnomAD constraint, ClinVar, and ClinGen data.

ClinVar Variant Classifications

500 submitted variants in ClinVar

Classification Summary

Pathogenic51
Likely Pathogenic38
VUS185
Likely Benign134
Benign55
Conflicting5
51
Pathogenic
38
Likely Pathogenic
185
VUS
134
Likely Benign
55
Benign
5
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
36
11
4
0
51
Likely Pathogenic
22
13
3
0
38
VUS
4
171
6
4
185
Likely Benign
0
35
39
60
134
Benign
0
9
43
3
55
Conflicting
5
Total622399567468

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

View in ClinVar →

Protein Context — Lollipop Plot

NSD1 · protein map & ClinVar variants

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

3D Protein StructureAlphaFold
Clinical Literature
Open Research Assistant →