STT3B

Chr 3AR

STT3 oligosaccharyltransferase complex catalytic subunit B

Also known as: CDG1X, SIMP, STT3-B

STT3B encodes a catalytic subunit of the oligosaccharyl transferase complex that transfers oligosaccharides to asparagine residues during protein N-glycosylation in the endoplasmic reticulum. Mutations cause congenital disorder of glycosylation type Ix, inherited in an autosomal recessive pattern. The gene is highly constrained against loss-of-function variants, indicating that complete loss of function is likely incompatible with normal development.

GeneReviewsOMIMResearchSummary from RefSeq, OMIM, UniProt
LOFmechanismARLOEUF 0.251 OMIM phenotype
Clinical SummarySTT3B
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Gene-Disease Validity (ClinGen)
congenital disorder of glycosylation · ARLimited

Limited evidence — not for standalone diagnostic reporting

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
18 unique Pathogenic / Likely Pathogenic· 99 VUS of 274 total submissions
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GeneReview available — STT3B
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
0.25LOEUF
pLI 0.999
Z-score 5.29
OE 0.12 (0.060.25)
Highly constrained

Highly LoF-intolerant (top ~10% of genes)

Missense Constraint
3.76Z-score
OE missense 0.49 (0.430.55)
205 obs / 422.2 exp
Constrained

Highly missense-constrained (top ~0.1%)

Observed / Expected Ratios
LoF OE0.12 (0.060.25)
00.351.4
Missense OE0.49 (0.430.55)
00.61.4
Synonymous OE1.02
01.21.6
LoF obs/exp: 5 / 42.0Missense obs/exp: 205 / 422.2Syn Z: -0.18
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
limitedSTT3B-related congenital disorder of glycosylationLOFAR

Predictions shown for reference only — model trained on dominant genes, not applicable to AR conditions.

DN
0.4686th %ile
GOF
0.4086th %ile
LOF
0.68top 25%

The Badonyi & Marsh prediction model was trained exclusively on dominant disease genes. Predictions are not reliable for genes with autosomal recessive inheritance and are shown at reduced opacity for reference only.

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

274 submitted variants in ClinVar

Classification Summary

Pathogenic17
Likely Pathogenic1
VUS99
Likely Benign97
Benign35
Conflicting2
17
Pathogenic
1
Likely Pathogenic
99
VUS
97
Likely Benign
35
Benign
2
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
0
1
16
0
17
Likely Pathogenic
0
0
1
0
1
VUS
0
96
2
1
99
Likely Benign
0
1
45
51
97
Benign
0
1
31
3
35
Conflicting
2
Total0999555251

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

View in ClinVar →

Protein Context — Lollipop Plot

STT3B · 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
Open Research Assistant →