NFIX

Chr 19AD

nuclear factor I X

Also known as: CTF, MALNS, MRSHSS, NF-I/X, NF1-X, NF1A, SOTOS2

This transcription factor binds to specific palindromic DNA sequences in viral and cellular promoters to regulate gene expression. Loss-of-function mutations cause Malan syndrome and Marshall-Smith syndrome through autosomal dominant inheritance. The protein is highly intolerant to loss-of-function variants, indicating haploinsufficiency as the likely pathogenic mechanism.

GeneReviewsOMIMResearchSummary from RefSeq, OMIM, UniProt, Mechanism
LOFmechanismADLOEUF 0.152 OMIM phenotypes
Clinical SummaryNFIX
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Gene-Disease Validity (ClinGen)
Marshall-Smith syndrome · ADDefinitive

Definitive — sufficient evidence for diagnostic panels

2 total gene-disease associations curated

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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GeneReview available — NFIX
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
0.15LOEUF
pLI 0.999
Z-score 4.15
OE 0.00 (0.000.15)
Highly constrained

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

Missense Constraint
4.08Z-score
OE missense 0.29 (0.240.36)
78 obs / 264.8 exp
Constrained

Highly missense-constrained (top ~0.1%)

Observed / Expected Ratios
LoF OE0.00 (0.000.15)
00.351.4
Missense OE0.29 (0.240.36)
00.61.4
Synonymous OE0.89
01.21.6
LoF obs/exp: 0 / 20.1Missense obs/exp: 78 / 264.8Syn Z: 0.96
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
definitiveNFIX-related Marshall-Smith syndromeLOFAD
DN
0.4389th %ile
GOF
0.3887th %ile
LOF
0.84top 5%

This gene has evidence for multiple mechanisms of pathogenicity (loss-of-function and dominant-negative). Both the Badonyi & Marsh prediction and the broader genomic evidence point to loss-of-function as the predominant mechanism. Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

LOFprediction above median · 1 literature citation · LOEUF 0.15
DN1 literature citation

Literature Evidence

DNThe exception is provided by specific NFIX variants that act in a dominant negative manner, as these cause a recognizable entity with more severe cognitive impairment and marked bone dysplasia, Marshall-Smith syndrome.PMID:31730271
LOFWhereas the overgrowth phenotype is due to NFIX haploinsufficiency, the presence of both normal and mutated alleles in MSS supports that mutated RNAs escape NMD surveillance.PMID:20673863

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

0 submitted variants in ClinVar

Protein Context — Lollipop Plot

NFIX · 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.

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Clinical Literature
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