SIN3A

Chr 15AD

SIN3 transcription regulator family member A

Also known as: CHR15DELq24, DEL15Q24, WITKOS

The protein is a transcriptional regulatory protein that mediates gene repression through protein-protein interactions via its paired amphipathic helix domains, including interactions with the Mad-Max transcriptional repressor complex. Loss-of-function mutations cause Witteveen-Kolk syndrome, an autosomal dominant neurodevelopmental disorder. The gene is highly intolerant to loss-of-function variants, consistent with haploinsufficiency as the disease mechanism.

GeneReviewsOMIMResearchSummary from RefSeq, OMIM, UniProt, Mechanism
LOFmechanismADLOEUF 0.071 OMIM phenotype
Clinical SummarySIN3A
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Gene-Disease Validity (ClinGen)
SIN3A-related intellectual disability 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
24 unique Pathogenic / Likely Pathogenic· 155 VUS of 300 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 — SIN3A
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
0.07LOEUF
pLI 1.000
Z-score 7.50
OE 0.01 (0.000.07)
Highly constrained

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

Missense Constraint
4.39Z-score
OE missense 0.54 (0.490.59)
386 obs / 717.0 exp
Constrained

Highly missense-constrained (top ~0.1%)

Observed / Expected Ratios
LoF OE0.01 (0.000.07)
00.351.4
Missense OE0.54 (0.490.59)
00.61.4
Synonymous OE0.98
01.21.6
LoF obs/exp: 1 / 67.4Missense obs/exp: 386 / 717.0Syn Z: 0.19
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
strongSIN3A-related syndromic intellectual disabilityLOFAD
DN
0.2399th %ile
GOF
0.2597th %ile
LOF
0.85top 5%

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

LOFprediction above median · 1 literature citation · 88% of P/LP variants are LoF · LOEUF 0.07

Literature Evidence

LOFHaploinsufficiency of SIN3A and mutations in KDM1A cause syndromes similar to RREB1 haploinsufficiency suggesting genetic perturbation of the RREB1-SIN3A-KDM1A complex represents a new category of RASopathy-like syndromes arising through epigenetic reprogramming of MAPK pathway genes.PMID:32938917

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

300 submitted variants in ClinVar

Classification Summary

Pathogenic16
Likely Pathogenic8
VUS155
Likely Benign87
Benign9
Conflicting6
16
Pathogenic
8
Likely Pathogenic
155
VUS
87
Likely Benign
9
Benign
6
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
15
0
1
0
16
Likely Pathogenic
6
1
1
0
8
VUS
1
144
10
0
155
Likely Benign
0
4
26
57
87
Benign
0
1
5
3
9
Conflicting
6
Total221504360281

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

View in ClinVar →

Protein Context — Lollipop Plot

SIN3A · protein map & ClinVar variants

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

3D Protein StructureAlphaFold
Clinical Literature
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