TNR

Chr 1AR

tenascin R

Also known as: NEDSTO, TN-R

The protein is a neural extracellular matrix glycoprotein that regulates neurite outgrowth, neural cell adhesion, and sodium channel clustering at nodes of Ranvier within the central nervous system. Biallelic mutations cause a neurodevelopmental disorder with nonprogressive spasticity and transient opisthotonus, inherited in an autosomal recessive pattern. The gene shows significant constraint against loss-of-function variants (LOEUF 0.34), suggesting intolerance to protein loss.

OMIMResearchSummary from RefSeq, OMIM, UniProt
MultiplemechanismARLOEUF 0.341 OMIM phenotype
Clinical SummaryTNR
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Gene-Disease Validity (ClinGen)
neurodevelopmental disorder, nonprogressive, with spasticity and transient opisthotonus · ARDefinitive

Definitive — sufficient evidence for diagnostic panels

Population Constraint (gnomAD)
Moderately constrained gene (pLI 0.52) — some intolerance to loss-of-function variants.
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ClinVar Variants
41 unique Pathogenic / Likely Pathogenic· 220 VUS of 329 total submissions

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

LoF intolerant — likely haploinsufficient
LoF Constraint
0.34LOEUF
pLI 0.524
Z-score 6.14
OE 0.22 (0.150.34)
Highly constrained

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

Missense Constraint
1.60Z-score
OE missense 0.84 (0.790.90)
685 obs / 813.0 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.22 (0.150.34)
00.351.4
Missense OE0.84 (0.790.90)
00.61.4
Synonymous OE1.04
01.21.6
LoF obs/exp: 16 / 72.4Missense obs/exp: 685 / 813.0Syn Z: -0.51
DN
0.6358th %ile
GOF
0.5856th %ile
LOF
0.4529th %ile

This gene has evidence for multiple mechanisms of pathogenicity (loss-of-function and dominant-negative). The Badonyi & Marsh model scores dominant-negative highest among its predictions, but genomic evidence (constraint, ClinVar variant spectrum, and literature) most strongly supports loss-of-function (haploinsufficiency). Different variants in this gene may act through different mechanisms — interpret in context of the specific variant.

LOF22% of P/LP variants are LoF · LOEUF 0.34
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. Mechanism ranking also informed by gnomAD constraint, ClinVar, and ClinGen data.

ClinVar Variant Classifications

329 submitted variants in ClinVar

Classification Summary

Pathogenic36
Likely Pathogenic5
VUS220
Likely Benign42
Benign14
Conflicting4
36
Pathogenic
5
Likely Pathogenic
220
VUS
42
Likely Benign
14
Benign
4
Conflicting

Curated Variants Distribution

Classified variants from ClinVar · 5 ACMG categories

ClassificationLoFMissense + InframeNon-codingSynonymousTotal
Pathogenic
7
2
27
0
36
Likely Pathogenic
2
2
1
0
5
VUS
1
207
12
0
220
Likely Benign
0
11
2
29
42
Benign
0
3
3
8
14
Conflicting
4
Total102254537321

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

View in ClinVar →

Protein Context — Lollipop Plot

TNR · 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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