Affinage

TNNI3K

Serine/threonine-protein kinase TNNI3K · UniProt Q59H18

Length
835 aa
Mass
92.9 kDa
Annotated
2026-06-10
41 papers in source corpus 21 papers cited in narrative 21 extracted findings
Cross-family judge faithfulness: 9/9 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

TNNI3K is a cardiomyocyte-enriched dual-specificity (Tyr and Ser/Thr) kinase that functions at the sarcomere to tune myofilament contractility, cardiac geometry, conduction, and stress responses (PMID:23085512, PMID:33084860). Its kinase activity, rather than mere protein abundance, drives cardiac remodeling—including sarcomere length reduction and titin isoform changes—as established by kinase-dead transgenic comparison, and the protein localizes to the sarcomere Z disc (PMID:23085512). Activity is autoregulated: dimerization and the N-terminal ANK domain are required for autophosphorylation, while the C-terminal Ser-rich domain and the binding partner AOP-1 negatively regulate catalysis (PMID:17660584, PMID:18205602). TNNI3K physically binds cardiac troponin I and phosphorylates it (at Ser43/Thr143 and Ser22/Ser23), enhancing cardiomyocyte contraction, and supports contractile reserve through PKA signaling (PMID:23369981, PMID:23472207, PMID:33084860). Cardiac-specific transcription is governed by MEF2C binding to a critical MEF2 site in the promoter (PMID:18021318). The kinase has context-dependent roles in disease: it promotes ischemia/reperfusion injury by increasing mitochondrial superoxide and activating p38 MAPK, such that pharmacologic inhibition at reperfusion reduces infarct size, yet it is cardioprotective during acute viral myocarditis (PMID:24132636, PMID:41745317). TNNI3K also modulates atrioventricular conduction and restrains the frequency of mononuclear diploid cardiomyocytes by acting at distinct cell-cycle stages (PMID:23236294, PMID:31589606, PMID:37597489). Human variants establish a bidirectional genotype-phenotype relationship: gain-of-function alleles that enhance autophosphorylation cause supraventricular tachycardia, conduction disease, and dilated cardiomyopathy, whereas loss-of-kinase-function alleles cause concentric ventricular remodeling, impaired contractility, and junctional ectopic tachycardia (PMID:30010057, PMID:33084860, PMID:37199186, PMID:38424693). Crystal structures of the kinase domain bound to small-molecule inhibitors have enabled structure-guided design of selective, cardioprotective compounds (PMID:26355916, PMID:34699203).

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 2007 Medium

    Established the basic enzymatic identity and intramolecular regulation of TNNI3K, defining it as an autoregulated dual-specificity kinase before any substrate or pathway was known.

    Evidence In vitro kinase assays with domain deletion/mutagenesis

    PMID:17660584

    Open questions at the time
    • No physiological substrate identified
    • Activation mechanism of dimerization not structurally resolved
  2. 2007 Medium

    Identified AOP-1 as a direct ANK-domain partner that inhibits kinase activity, providing the first regulatory protein interaction.

    Evidence Yeast two-hybrid, in vitro binding, co-IP, and kinase assay

    PMID:18205602

    Open questions at the time
    • In vivo relevance of AOP-1 inhibition untested
    • Stoichiometry and structural basis of inhibition unknown
  3. 2007 Medium

    Explained the cardiac-restricted expression of TNNI3K by identifying MEF2C as the critical transcriptional driver at its promoter.

    Evidence Promoter mutational analysis, EMSA supershift, co-transfection

    PMID:18021318

    Open questions at the time
    • Upstream regulators of MEF2C-driven expression not defined
    • Does not address post-transcriptional control
  4. 2009 High

    Linked TNNI3K dosage to cardiac disease susceptibility in vivo, showing expression level modulates cardiomyopathy progression across genetic backgrounds.

    Evidence Double-transgenic and pressure-overload mouse models with genetic mapping

    PMID:19763165

    Open questions at the time
    • Molecular substrate driving disease acceleration not identified at this stage
    • Distinction between kinase activity and abundance not yet resolved
  5. 2012 High

    Demonstrated that kinase activity itself, not overexpression, drives remodeling, and localized the protein to the Z disc—anchoring TNNI3K function to the sarcomere.

    Evidence Kinase-dead vs. wild-type transgenic mice, proteomics, immunofluorescence

    PMID:23085512

    Open questions at the time
    • Direct substrate at the Z disc not proven in this study
    • Mechanism linking phosphorylation to titin isoform change unknown
  6. 2012 High

    Identified TNNI3K as a quantitative modulator of atrioventricular conduction, connecting it to a discrete electrophysiological phenotype.

    Evidence Expression QTL mapping and ECG in congenic/transgenic mice

    PMID:23236294

    Open questions at the time
    • Molecular target mediating PR prolongation not defined
    • Cell type responsible (conduction system vs. myocyte) not resolved
  7. 2013 Medium

    Identified cardiac troponin I as a direct substrate and binding partner, establishing the molecular link between TNNI3K and myofilament contractility.

    Evidence Co-IP, yeast two-hybrid, in vitro and in vivo phosphorylation, cardiomyocyte contraction measurements

    PMID:23369981 PMID:23472207

    Open questions at the time
    • Reported phosphosite assignments differ between studies (Ser43/Thr143 vs Ser22/Ser23)
    • Single-lab findings without independent reciprocal validation
  8. 2013 High

    Defined a pathological role in ischemia/reperfusion injury via mitochondrial superoxide and p38 MAPK, and validated pharmacologic inhibition as cardioprotective.

    Evidence Small-molecule inhibition in mouse I/R model with superoxide, p38, and infarct readouts

    PMID:24132636

    Open questions at the time
    • Direct substrate linking TNNI3K to mitochondrial superoxide not identified
    • Mechanism coupling kinase to p38 activation unresolved
  9. 2014 Medium

    Provided first human genetic evidence implicating a TNNI3K missense mutation in disease through a dominant-negative loss-of-function mechanism.

    Evidence In vitro aggregation assay, in silico docking, human ventricular IHC

    PMID:24925317

    Open questions at the time
    • Dominant-negative mechanism inferred, not directly demonstrated
    • Limited to one carrier's tissue
  10. 2015 High

    Delivered the first crystal structure of the kinase domain bound to an inhibitor, enabling rational drug design against TNNI3K.

    Evidence X-ray crystallography of TNNI3K-inhibitor complex

    PMID:26355916

    Open questions at the time
    • Structure of full-length protein and ANK domain not solved
    • Active-state/dimer structure not determined
  11. 2019 High

    Showed kinase activity is required for TNNI3K to restrain mononuclear diploid cardiomyocyte frequency, connecting it to cardiomyocyte ploidy and oxidative stress.

    Evidence Kinase-dead knock-in mice, cardiomyocyte ploidy analysis, in vitro kinase assay of human variants

    PMID:31589606

    Open questions at the time
    • Substrate controlling ploidy not identified
    • Mechanistic convergence with oxidative stress not detailed
  12. 2021 High

    Established that loss of kinase activity causes concentric remodeling and reduced contractile reserve via impaired PKA signaling, revealing a beneficial physiological role distinct from its injury-promoting role.

    Evidence Knockout and knock-in (K489R, I686T) mouse models with contractility, calcium, and PKA assays

    PMID:33084860

    Open questions at the time
    • Direct link between TNNI3K and PKA pathway not biochemically defined
    • Substrate mediating contractile reserve unclear
  13. 2021 Medium

    Achieved selective inhibitor design over related kinases using diarylurea co-crystal structures, yielding a cardioprotective tool compound.

    Evidence X-ray crystallography of inhibitor complexes, structure-based chemistry, mouse I/R model

    PMID:34699203

    Open questions at the time
    • Primarily medicinal-chemistry; in vivo efficacy limited validation
    • Long-term safety/specificity not addressed
  14. 2023 Medium

    Consolidated the bidirectional genotype-phenotype model, showing gain-of-autophosphorylation variants cause DCM/arrhythmia while a depleted-activity variant is benign.

    Evidence Autophosphorylation assays, NGS, co-segregation, UK Biobank burden testing

    PMID:37199186

    Open questions at the time
    • Mechanism by which enhanced autophosphorylation drives disease not resolved
    • Single-lab functional assays
  15. 2023 Medium

    Refined the cardiomyocyte proliferation role by showing TNNI3K acts at both S-phase entry and cytokinesis.

    Evidence Single-cell analysis of ventricular cardiomyocytes with Tnni3k knockout

    PMID:37597489

    Open questions at the time
    • Substrate/effector at each cell-cycle stage unknown
    • Single method, single lab
  16. 2024 Medium

    Extended the loss-of-function arm of the genotype-phenotype map to congenital junctional ectopic tachycardia via reduced-activity variants, and showed natural loss-of-kinase alleles occur across species.

    Evidence Autophosphorylation assays of human and canine variants with co-segregation

    PMID:38424693 PMID:38828440

    Open questions at the time
    • Limited family sizes
    • Mechanistic link from reduced activity to specific arrhythmia not established
  17. 2026 Medium

    Revealed a cardioprotective role for kinase activity in acute viral myocarditis, contrasting its injury-promoting role in I/R and underscoring context-dependent function.

    Evidence Knockout and kinase-dead knock-in mice with CVB3 infection and histological inflammation quantification

    PMID:41745317

    Open questions at the time
    • Substrate mediating anti-inflammatory effect unknown
    • Why long-term damage is unaffected not explained

Open questions

Synthesis pass · forward-looking unresolved questions
  • The unifying biochemical mechanism that reconciles TNNI3K's opposing roles—injury-promoting in I/R yet protective in myocarditis and for contractile reserve—remains unresolved, as does how a single set of substrates produces both gain- and loss-of-function disease.
  • No structural model of the active dimer or ANK regulation
  • Substrates beyond cTnI driving mitochondrial, conduction, and ploidy phenotypes not identified
  • Mechanistic coupling of kinase activity to p38 and PKA pathways undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 4 GO:0016740 transferase activity 3
Localization
GO:0005856 cytoskeleton 1
Pathway
R-HSA-162582 Signal Transduction 2 R-HSA-1640170 Cell Cycle 2 R-HSA-397014 Muscle contraction 2
Partners
AOP-1TNNI3

Evidence

Reading pass · 21 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2007 TNNI3K exhibits dual-specificity kinase activity (Tyr and Ser/Thr), forms dimers or oligomers required for activation, the C-terminal Ser-rich domain negatively regulates kinase activity, and the N-terminal ANK domain is necessary for autophosphorylation. In vitro kinase assay, domain deletion/mutagenesis analysis General physiology and biophysics Medium 17660584
2007 Antioxidant protein 1 (AOP-1) interacts with the ANK motif of TNNI3K (identified by yeast two-hybrid, confirmed by in vitro binding assay and co-expression), co-localizes with TNNI3K, and inhibits TNNI3K kinase activity in vitro. Yeast two-hybrid screen, in vitro binding assay, co-immunoprecipitation, confocal immunofluorescence, in vitro kinase assay Biochemistry. Biokhimiia Medium 18205602
2007 MEF2C binds to the TNNI3K/CARK promoter at a conserved MEF2 site that is the most critical cis-acting element for cardiac-specific transcription; MEF2C antisense reduces CARK transcript levels. Promoter truncation/mutational analysis, EMSA (supershift), co-transfection assays Journal of cellular and molecular medicine Medium 18021318
2008 TNNI3K overexpression promotes differentiation of P19CL6 cells into cardiomyocytes, suppresses p38/JNK-mediated apoptosis (reduced annexin-V+ cells, Bax, and p38/JNK phosphorylation), and improves cardiac function in a mouse myocardial infarction model. Cell transfection/overexpression, flow cytometry (apoptosis), Western blot (p38/JNK phosphorylation), intramyocardial cell injection in MI mouse model American journal of physiology. Heart and circulatory physiology Medium 18552163
2009 TNNI3K expression accelerates cardiac dysfunction in the Calsequestrin transgenic mouse model of cardiomyopathy and in a pressure-overload model; high TNNI3K transcript levels correlate with increased disease susceptibility, while a splice-activating intronic SNP causes nonsense-mediated decay and loss of detectable protein in resistant strains. Transgenic mouse models (TNNI3K/Csq double transgenic, pressure overload), genetic mapping, RT-PCR, Western blot PLoS genetics High 19763165
2012 TNNI3K is a dual-function kinase (Tyr and Ser/Thr activity) in vivo; its kinase activity (not merely overexpression) drives cardiac remodeling including sarcomere length reduction and titin isoform changes, as shown by kinase-dead transgenic mice lacking these effects; TNNI3K protein localizes to the sarcomere Z disc. Transgenic mice (wild-type vs. kinase-dead TNNI3K), in vitro kinase assay, proteomics, immunofluorescence/immunostaining, pressure-overload model Journal of molecular and cellular cardiology High 23085512
2012 Tnni3k mRNA level positively correlates with PR interval duration in mice; overexpression of hTNNI3K in DBA/2J mice prolongs the PR interval, identifying Tnni3k as a modulator of atrio-ventricular conduction. Expression QTL mapping, ECG measurements in congenic and transgenic mouse lines, correlation analysis of mRNA and PR interval PLoS genetics High 23236294
2013 TNNI3K phosphorylates cardiac troponin I (cTnI) at Ser43 and Thr143 in vitro and in adult rat cardiomyocytes (not at Ser23/24 or Ser44); TNNI3K overexpression increases and knockdown decreases cTnI phosphorylation at these sites; increased TNNI3K/cTnI interaction enhances cardiomyocyte contraction. Co-immunoprecipitation, in vitro kinase assay, adult rat cardiomyocyte overexpression/knockdown, cardiomyocyte contraction measurements Brazilian journal of medical and biological research Medium 23369981
2013 TNNI3K physically interacts with cTnI (confirmed by co-immunoprecipitation and yeast two-hybrid), induces cTnI phosphorylation at Ser22/Ser23 in vivo and in vitro, and promotes concentric cardiac hypertrophy with enhanced cardiac function in transgenic mice; phosphoamino acid analysis confirmed TNNI3K is a protein-tyrosine kinase. Yeast two-hybrid, co-immunoprecipitation, in vivo and in vitro phosphorylation assays, transgenic mouse echocardiography PloS one Medium 23472207
2013 TNNI3K promotes ischemia/reperfusion injury through increased mitochondrial superoxide production, impaired mitochondrial function, and p38 MAPK activation; pharmacologic TNNI3K inhibition reduces mitochondrial superoxide, p38 activation, and infarct size when delivered at reperfusion. Small-molecule inhibitor treatment in mouse I/R model, mitochondrial superoxide measurement, p38 MAPK phosphorylation assay, infarct size measurement, echocardiography Science translational medicine High 24132636
2014 A missense mutation G526D in the TNNI3K kinase domain causes abnormal peptide aggregation in vitro; in silico docking predicts altered but energetically favorable dimerization; ventricular tissue from a carrier shows reduced TNNI3K protein staining with nuclear/sarcoplasmic inclusions, implicating dominant-negative loss-of-function. In vitro aggregation assay, in silico docking, immunohistochemistry of human ventricular tissue Human molecular genetics Medium 24925317
2015 X-ray crystal structure of a purine inhibitor (compound 1) bound to TNNI3K confirmed Type I binding mode to the kinase domain, enabling rational structure-guided inhibitor design and delineation of structure-activity relationships. X-ray crystallography of TNNI3K-inhibitor complex Journal of medicinal chemistry High 26355916
2018 The TNNI3K p.Glu768Lys variant displays enhanced kinase autophosphorylation activity compared to wild-type TNNI3K, and co-segregates with disease in 23 affected individuals across 3 independent families presenting with supraventricular tachycardia, conduction disturbance, and DCM. Autophosphorylation kinase assay, next-generation sequencing, co-segregation analysis Heart rhythm Medium 30010057
2019 Tnni3k function requires its kinase activity (shown by kinase-dead allele in mice); Tnni3k regulates the frequency of mononuclear diploid cardiomyocytes and converges with oxidative stress in this regulation; common human TNNI3K kinase domain variants substantially compromise kinase activity in vitro. In vitro kinase assay of human variants, kinase-dead knock-in mouse model, cardiomyocyte ploidy analysis PLoS genetics High 31589606
2021 Loss of TNNI3K kinase activity (null allele, kinase-dead K489R, or hypomorphic I686T variant) causes concentric ventricular remodeling, impaired cardiomyocyte contractility, defective calcium dynamics, and reduced PKA signaling in response to isoproterenol in cultured cardiomyocytes, demonstrating a beneficial role for TNNI3K in maintaining normal cardiac geometry and contractile reserve. Tnni3k knockout and knock-in mouse models, echocardiography, cardiomyocyte contractility and calcium imaging, PKA signaling assay in culture Human molecular genetics High 33084860
2021 X-ray crystal structures of TNNI3K with diarylurea inhibitors enabled structure-based design of selective TNNI3K inhibitors over VEGFR2, p38α, and B-Raf; a tool compound (GSK329) showed cardioprotective effects in a mouse I/R model. X-ray crystallography of TNNI3K-inhibitor complexes, structure-based medicinal chemistry, in vivo I/R mouse model Journal of medicinal chemistry Medium 34699203
2023 Novel TNNI3K variants p.Ile512Thr and p.His592Tyr show increased autophosphorylation activity and co-segregate with DCM, conduction disease, and supraventricular tachycardia; a likely benign variant (p.Arg556_Asn590del) shows depleted autophosphorylation, suggesting enhanced autophosphorylation drives pathogenicity. TNNI3K autophosphorylation assay, next-generation sequencing, co-segregation analysis, UK Biobank burden testing Circulation. Genomic and precision medicine Medium 37199186
2023 Tnni3k influences both early S-phase entry and the completion of cell division (cytokinesis) in cardiomyocytes, demonstrating roles at distinct stages of the cell cycle. Retrospective single-cell analysis of ventricular cardiomyocyte suspensions to identify post-division cells, genetic loss-of-function (Tnni3k knockout) Journal of molecular and cellular cardiology Medium 37597489
2024 Two TNNI3K variants (p.Leu577Phe and p.Pro742Leu) associated with congenital junctional ectopic tachycardia demonstrate substantially reduced kinase activity in autophosphorylation assays, linking loss of kinase function to this arrhythmia. Autophosphorylation kinase assay, next-generation sequencing, co-segregation analysis Clinical genetics Medium 38424693
2024 A naturally occurring polymorphism in the canine Tnni3k gene (prevalent in West Highland White Terriers) eliminates Tnni3k kinase activity, demonstrating that natural loss-of-kinase-function alleles exist across species. In vitro kinase assay of canine Tnni3k polymorphic variant microPublication biology Medium 38828440
2026 Tnni3k kinase activity is cardioprotective during acute CVB3 viral myocarditis: Tnni3k knockout and kinase-dead knock-in mice show increased cardiac inflammation and macrophage infiltration compared to wild-type, while long-term damage is comparable. Tnni3k knockout and kinase-dead knock-in mouse models, CVB3 infection, histological quantification of inflammation and macrophage infiltration Journal of cardiovascular development and disease Medium 41745317

Source papers

Stage 0 corpus · 41 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2009 Tnni3k modifies disease progression in murine models of cardiomyopathy. PLoS genetics 77 19763165
2013 Inhibition of the cardiomyocyte-specific kinase TNNI3K limits oxidative stress, injury, and adverse remodeling in the ischemic heart. Science translational medicine 57 24132636
2011 Quantitative trait locus analysis, pathway analysis, and consomic mapping show genetic variants of Tnni3k, Fpgt, or H28 control susceptibility to viral myocarditis. Journal of immunology (Baltimore, Md. : 1950) 48 21525387
2014 TNNI3K mutation in familial syndrome of conduction system disease, atrial tachyarrhythmia and dilated cardiomyopathy. Human molecular genetics 46 24925317
2012 Dissection of a quantitative trait locus for PR interval duration identifies Tnni3k as a novel modulator of cardiac conduction. PLoS genetics 42 23236294
2012 Overexpression of TNNI3K, a cardiac-specific MAPKKK, promotes cardiac dysfunction. Journal of molecular and cellular cardiology 37 23085512
2015 Identification of Purines and 7-Deazapurines as Potent and Selective Type I Inhibitors of Troponin I-Interacting Kinase (TNNI3K). Journal of medicinal chemistry 36 26355916
2019 Tnni3k alleles influence ventricular mononuclear diploid cardiomyocyte frequency. PLoS genetics 30 31589606
2008 Overexpression of TNNI3K, a cardiac-specific MAP kinase, promotes P19CL6-derived cardiac myogenesis and prevents myocardial infarction-induced injury. American journal of physiology. Heart and circulatory physiology 30 18552163
2018 Whole exome sequencing identifies a novel mutation (c.333 + 2T > C) of TNNI3K in a Chinese family with dilated cardiomyopathy and cardiac conduction disease. Gene 27 29355681
2018 Supraventricular tachycardias, conduction disease, and cardiomyopathy in 3 families with the same rare variant in TNNI3K (p.Glu768Lys). Heart rhythm 23 30010057
2013 TNNI3K, a cardiac-specific kinase, promotes physiological cardiac hypertrophy in transgenic mice. PloS one 23 23472207
2017 ACE2, CALM3 and TNNI3K polymorphisms as potential disease modifiers in hypertrophic and dilated cardiomyopathies. Molecular and cellular biochemistry 19 28744816
2013 TNNI3K is a novel mediator of myofilament function and phosphorylates cardiac troponin I. Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas 18 23369981
2010 Identification of a gp41 core-binding molecule with homologous sequence of human TNNI3K-like protein as a novel human immunodeficiency virus type 1 entry inhibitor. Journal of virology 18 20592080
2020 Discovery of novel TNNI3K inhibitor suppresses pyroptosis and apoptosis in murine myocardial infarction injury. European journal of medicinal chemistry 17 32344181
2018 4,6-Diaminopyrimidines as Highly Preferred Troponin I-Interacting Kinase (TNNI3K) Inhibitors. Journal of medicinal chemistry 17 29561151
2015 TNNI3K in cardiovascular disease and prospects for therapy. Journal of molecular and cellular cardiology 17 25787061
2021 The Diverse Roles of TNNI3K in Cardiac Disease and Potential for Treatment. International journal of molecular sciences 16 34203974
2007 Identification of the dual specificity and the functional domains of the cardiac-specific protein kinase TNNI3K. General physiology and biophysics 16 17660584
2007 Mef2c is an essential regulatory element required for unique expression of the cardiac-specific CARK gene. Journal of cellular and molecular medicine 16 18021318
2007 AOP-1 interacts with cardiac-specific protein kinase TNNI3K and down-regulates its kinase activity. Biochemistry. Biokhimiia 15 18205602
2016 GSK114: A selective inhibitor for elucidating the biological role of TNNI3K. Bioorganic & medicinal chemistry letters 14 27246618
2020 Identification of a nonsense mutation in TNNI3K associated with cardiac conduction disease. Journal of clinical laboratory analysis 11 32529721
2017 Overexpression of Cardiac-Specific Kinase TNNI3K Promotes Mouse Embryonic Stem Cells Differentiation into Cardiomyocytes. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 11 28135716
2021 The prevalent I686T human variant and loss-of-function mutations in the cardiomyocyte-specific kinase gene TNNI3K cause adverse contractility and concentric remodeling in mice. Human molecular genetics 10 33084860
2021 A Novel Missense Mutation in TNNI3K Causes Recessively Inherited Cardiac Conduction Disease in a Consanguineous Pakistani Family. Genes 10 34440456
2020 New Insights into 4-Anilinoquinazolines as Inhibitors of Cardiac Troponin I-Interacting Kinase (TNNi3K). Molecules (Basel, Switzerland) 10 32272798
2023 Tnni3k influences cardiomyocyte S-phase activity and proliferation. Journal of molecular and cellular cardiology 9 37597489
2018 Over-expression of TNNI3K is associated with early-stage carcinogenesis of cholangiocarcinoma. Molecular carcinogenesis 8 30334579
2022 Whole-Exome Sequencing Identifies a Novel Variant (c.1538T > C) of TNNI3K in Arrhythmogenic Right Ventricular Cardiomyopathy. Frontiers in cardiovascular medicine 6 35274013
2021 Identification of Diarylurea Inhibitors of the Cardiac-Specific Kinase TNNI3K by Designing Selectivity Against VEGFR2, p38α, and B-Raf. Journal of medicinal chemistry 6 34699203
2023 Genetic Burden of TNNI3K in Diagnostic Testing of Patients With Dilated Cardiomyopathy and Supraventricular Arrhythmias. Circulation. Genomic and precision medicine 5 37199186
2024 Reduced kinase function in two ultra-rare TNNI3K variants in families with congenital junctional ectopic tachycardia. Clinical genetics 3 38424693
2025 A de novo TNNI3K variant aggravates the pathogenicity of DMD-associated early-onset cardiomyopathy: a case report. Frontiers in genetics 2 40134720
2009 TNNI3K could be a novel molecular target for the treatment of cardiac diseases. Recent patents on cardiovascular drug discovery 2 19925440
2024 A kinase-dead natural polymorphism in the canine Tnni3k gene. microPublication biology 1 38828440
2019 Correction to: ACE2, CALM3 and TNNI3K polymorphisms as potential disease modifiers in hypertrophic and dilated cardiomyopathies. Molecular and cellular biochemistry 1 30488312
2026 Tnni3k Is Cardioprotective in Viral Myocarditis. Journal of cardiovascular development and disease 0 41745317
2025 Clockwise bundle branch re-entrant ventricular tachycardia in a teenage patient as the first manifestation of dilated cardiomyopathy associated with the p.Ile512Leu TNNI3k variant: a case report. European heart journal. Case reports 0 40904527
2025 Design and synthesis of 4-azaindoles derivatives: targeting the cardiac troponin I-interacting kinase (TNNI3K). Bioorganic & medicinal chemistry 0 40974855

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