TNNI3

Chr 19ARAD

troponin I3, cardiac type

Also known as: CMD1FF, CMD2A, CMH7, RCM1, TNNC1, cTnI

Cardiac troponin I is the inhibitory subunit of the troponin complex that regulates calcium-sensitive contraction in cardiac muscle by controlling actin-myosin interactions. Mutations cause multiple forms of cardiomyopathy including hypertrophic, restrictive, and dilated cardiomyopathy with both autosomal dominant and autosomal recessive inheritance patterns. The gene shows moderate constraint against loss-of-function variants (LOEUF 0.69), and comprehensive clinical management guidelines are available through GeneReviews.

OMIMResearchSummary from RefSeq, OMIM, UniProt
MultiplemechanismAR/ADLOEUF 0.694 OMIM phenotypes
Clinical SummaryTNNI3
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Gene-Disease Validity (ClinGen)
arrhythmogenic right ventricular cardiomyopathy · ADNo Known Disease Relationship

No known disease relationship

4 total gene-disease associations curated

Population Constraint (gnomAD)
Constrained for loss-of-function variants (OE-LoF 0.30) despite low pLI — interpret in context.
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Clinical Trials
3 active or recruiting trials — potential therapeutic options may be available

Population Genetics & Constraint

gnomAD v4 — loss-of-function & missense intolerance

Tolerant — LoF & missense variants common in population
LoF Constraint
0.69LOEUF
pLI 0.096
Z-score 2.35
OE 0.30 (0.150.69)
Tolerant

Typical tolerance to LoF variation

Missense Constraint
1.28Z-score
OE missense 0.68 (0.570.81)
89 obs / 130.2 exp
Tolerant

Mild missense constraint

Observed / Expected Ratios
LoF OE0.30 (0.150.69)
00.351.4
Missense OE0.68 (0.570.81)
00.61.4
Synonymous OE1.08
01.21.6
LoF obs/exp: 4 / 13.2Missense obs/exp: 89 / 130.2Syn Z: -0.44
Curated Mechanism (G2P)Gene2Phenotype (DDG2P) ↗
definitiveTNNI3-related hypertrophic cardiomyopathyOTHERAD
DN
0.74top 25%
GOF
0.5954th %ile
LOF
0.2969th %ile

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

DNprediction above median · 1 literature citation
LOF1 literature citation

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.

Literature Evidence

DNA splice site mutation in TNNI3 causing RCM has never been reported before and probably causes a truncated protein with a severe dominant negative effect.PMID:21533915
LOFThe TNNI3p.98trunc showed pure haploinsufficiency, increased Ca2+ -sensitivity and impaired length-dependent activation.PMID:28436080

Predictions from Badonyi M, Marsh JA. PLoS ONE. 2024;19(8):e0307312.

ClinVar Variant Classifications

0 submitted variants in ClinVar

Protein Context — Lollipop Plot

TNNI3 · 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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