Affinage

TNNI1

Troponin I, slow skeletal muscle · UniProt P19237

Length
187 aa
Mass
21.7 kDa
Annotated
2026-04-28
85 papers in source corpus 20 papers cited in narrative 20 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

TNNI1 (slow skeletal troponin I, ssTnI) is the inhibitory subunit of the troponin complex expressed in slow-twitch skeletal muscle and fetal/neonatal cardiac muscle, where it functions as a primary determinant of myofilament calcium sensitivity and pH resistance of contraction. In the heart, TNNI1 is the dominant TnI isoform during fetal life and is replaced postnatally by cardiac TnI (cTnI) in a thyroid hormone–regulated transcriptional switch; its expression directly sets the elevated Ca²⁺ sensitivity characteristic of immature myocardium and, because it lacks the PKA phosphorylation sites present in cTnI, abolishes β-adrenergic modulation of Ca²⁺ sensitivity and slows cardiac relaxation (PMID:9144257, PMID:10226156, PMID:27353610, PMID:11112997). Isoform-specific residues in the C-terminal helix 4—particularly H132 and coordinated positions Q157/A164/E166/H173—govern the enhanced Ca²⁺ sensitivity and acid resistance by altering the electrostatic TnI–TnC interaction that tunes Ca²⁺ binding affinity of TnC (PMID:17602701, PMID:24853739). Loss-of-function mutation in the TNNI1 tropomyosin-binding domain (p.K175*) causes autosomal dominant proximal arthrogryposis with type 1 fiber pathology, establishing TNNI1 as essential for slow skeletal muscle fiber integrity (PMID:34934811).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 1990 High

    Cloning of the human TNNI1 cDNA established it as a conserved, slow-twitch-skeletal-muscle-restricted troponin I isoform mapping to chromosome 1, providing the molecular identity needed for subsequent functional studies.

    Evidence cDNA cloning, Northern blot, somatic cell hybrid mapping, in vitro myogenic differentiation

    PMID:2365354

    Open questions at the time
    • No functional data on contractile regulation at this stage
    • Expression in fetal heart not yet recognized
  2. 1997 High

    Gene transfer of ssTnI into adult cardiomyocytes demonstrated that it stoichiometrically replaces cTnI in myofilaments and increases Ca²⁺ sensitivity while conferring resistance to acidic pH, answering whether TnI isoform identity alone determines myofilament Ca²⁺ responsiveness.

    Evidence Adenoviral gene transfer into adult rat cardiomyocytes; permeabilized single-cell force–Ca²⁺ measurements

    PMID:9144257

    Open questions at the time
    • Mechanism at the residue level unknown
    • In vivo consequences not yet tested
  3. 1999 High

    Complete genetic replacement of cTnI by ssTnI in transgenic mice revealed that ssTnI expression abolishes PKA-dependent contractile modulation and impairs diastolic function, establishing that the absence of PKA phosphorylation sites in ssTnI accounts for its inability to support β-adrenergic relaxation enhancement.

    Evidence Transgenic mouse hearts; permeabilized and intact cardiomyocyte measurements; in vivo hemodynamics

    PMID:10226156

    Open questions at the time
    • Relative contribution of TnI vs. phospholamban phosphorylation to relaxation not resolved
    • Structural basis of isoform-specific PKA effects unknown
  4. 2000 High

    Using cTnI-knockout mice, thyroid hormone was identified as the transcriptional regulator of postnatal ssTnI downregulation in the heart, answering whether the isoform switch depends on cTnI protein accumulation or an independent hormonal signal.

    Evidence cTnI-KO mice; pharmacological hyper-/hypothyroid manipulation; Northern and Western blots

    PMID:11112997

    Open questions at the time
    • Transcription factor mediating T3 repression of TNNI1 not identified
    • Upstream cis-regulatory elements only partially mapped
  5. 2003 High

    X-ray diffraction and mechanical measurements in ssTnI-transgenic hearts showed that PKA-mediated enhancement of length-dependent activation requires cTnI phosphorylation, resolving the question of whether myofilament lattice spacing changes from MyBP-C phosphorylation alone suffice for this response.

    Evidence Skinned myocyte mechanics; X-ray diffraction of lattice spacing; PKA treatment in transgenic mouse fibers

    PMID:12562915

    Open questions at the time
    • Molecular link between TnI phosphorylation and interfilament spacing not defined
  6. 2004 High

    Epistatic analysis crossing ssTnI-transgenic with phospholamban-knockout mice quantified the relative contribution of cTnI phosphorylation to in vivo relaxation during β-adrenergic stimulation, showing a significant, independent role beyond Ca²⁺ reuptake.

    Evidence In situ cardiac hemodynamics in double-mutant mice; isoproterenol challenge

    PMID:14985072

    Open questions at the time
    • Quantitative partitioning between TnI and other myofilament targets of PKA remains approximate
  7. 2006 High

    Cross-species analysis in guinea pig and sheep hearts demonstrated that the fetal-to-postnatal decline in cardiac Ca²⁺ sensitivity tracks ssTnI protein level, establishing ssTnI expression as the primary determinant of the high Ca²⁺ sensitivity of immature myocardium.

    Evidence Western blot; skinned cardiac strip force–Ca²⁺ measurements across developmental stages in two species

    PMID:16679402

    Open questions at the time
    • Contribution of concurrent titin isoform changes not fully separated from TnI effects
  8. 2007 High

    Systematic mutagenesis identified H132 in ssTnI helix 4 as the key residue conferring isoform-specific pH resistance, answering which structural element distinguishes ssTnI from cTnI in acid sensitivity.

    Evidence Adenoviral transfer of ssTnI point mutants into adult cardiomyocytes; force–Ca²⁺ at physiological and acidic pH

    PMID:17602701

    Open questions at the time
    • Structural mechanism by which H132 protonation state alters TnI–TnC interaction not resolved at atomic level
  9. 2008 Medium

    Promoter analysis identified a CREB site and CCAAT box within 300 bp upstream of TNNI1 as critical for cardiac expression and showed direct T3-mediated transcriptional repression, partially answering how thyroid hormone silences TNNI1 postnatally.

    Evidence Promoter deletion/reporter assays; EMSA; ChIP in cardiac myocytes; T3 treatment

    PMID:18357515

    Open questions at the time
    • Identity of the thyroid hormone receptor/co-repressor complex acting on the TNNI1 promoter not established
    • In vivo validation of promoter elements lacking
  10. 2014 High

    Molecular dynamics and mutagenesis of four coordinated helix-4 residues (Q157/A164/E166/H173) revealed the structural mechanism: ssTnI-type residues alter the R171–TnC E15 electrostatic interaction, increasing TnC Ca²⁺ binding affinity and thereby slowing relaxation.

    Evidence Adenoviral gene transfer of cTnI helix-4 mutants; sarcomere shortening; MD simulation with free energy perturbation

    PMID:24853739

    Open questions at the time
    • No experimental high-resolution structure of the ssTnI–TnC complex to validate the simulation
  11. 2014 High

    ssTnI expression in adult transgenic hearts conferred protection against pressure-overload hypertrophy by maintaining energy charge through increased pyruvate/glucose oxidation, revealing an unexpected link between TnI isoform identity and cardiac metabolic adaptation.

    Evidence Transgenic mouse TAC model; echocardiography; isolated perfused heart metabolic flux; gene expression

    PMID:25424393

    Open questions at the time
    • Whether metabolic protection is a direct consequence of altered crossbridge kinetics or an indirect signaling effect is unresolved
  12. 2016 High

    Quantitative correlation in human pediatric cardiac tissue confirmed ssTnI as the primary determinant of neonatal myofibrillar Ca²⁺ sensitivity, translating the animal findings directly to human cardiac physiology.

    Evidence Western blot of ssTnI in human surgical samples; myofibril force–Ca²⁺ measurements across age

    PMID:27353610

    Open questions at the time
    • Small sample size inherent to surgical tissue; regional heterogeneity not fully addressed
  13. 2021 Medium

    Identification of a heterozygous nonsense variant (p.K175*) in the TNNI1 tropomyosin-binding domain causing proximal arthrogryposis with slow-fiber pathology established TNNI1 as a disease gene for congenital contracture syndromes.

    Evidence Trio exome sequencing; muscle biopsy histopathology and electron microscopy

    PMID:34934811

    Open questions at the time
    • No in vitro functional reconstitution of the truncated protein
    • Only a single family reported
    • Mechanism of Z-disk streaming from TnI truncation unknown

Open questions

Synthesis pass · forward-looking unresolved questions
  • The atomic-resolution structure of the ssTnI-containing troponin complex, the precise transcription factor complex mediating thyroid hormone repression of TNNI1, and whether the metabolic protection conferred by ssTnI expression results from altered crossbridge energetics or secondary signaling remain unresolved.
  • No high-resolution structure of the ssTnI–TnC–TnT ternary complex
  • Transcription factor identity for T3-mediated TNNI1 silencing unknown
  • Causality of ssTnI-driven metabolic shift not separated from mechanical effects

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 5 GO:0008092 cytoskeletal protein binding 3
Localization
GO:0005856 cytoskeleton 3 GO:0005634 nucleus 1
Pathway
R-HSA-397014 Muscle contraction 7
Partners
TNNC1TNNT1TNNT2TPM1
Complex memberships
troponin complex

Evidence

Reading pass · 20 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1997 Adenovirus-mediated gene transfer of ssTnI (TNNI1) into adult cardiac myocytes results in nearly complete stoichiometric replacement of endogenous cTnI in the myofilament, lowers the threshold Ca2+ for activated contraction, and enhances contractile Ca2+ sensitivity under both physiological and acidic pH conditions, demonstrating isoform-specific functional effects on myofilament Ca2+ activation. Adenoviral gene transfer into adult rat cardiac myocytes; permeabilized single-cell force-Ca2+ measurements; Western blot for myofilament protein stoichiometry Proceedings of the National Academy of Sciences of the United States of America High 9144257
1999 Transgenic mice with complete cardiomyocyte replacement of cTnI by ssTnI (TNNI1) show increased myofilament Ca2+ sensitivity, loss of PKA-dependent contractile response (because ssTnI lacks PKA phosphorylation sites), slowed intracellular Ca2+ decay, prolonged re-lengthening, and impaired diastolic function in vivo, establishing that cTnI is required for normal beta-adrenergic relaxation and Ca2+-sensitivity regulation. Transgenic mouse model; permeabilized cardiomyocyte force-Ca2+ measurements; intact cell Ca2+ imaging; in vivo hemodynamics; Western blot The Journal of physiology High 10226156
2002 Gene transfer of ssTnI (TNNI1) and HCM mutant cTnI (cTnIR146G) into adult cardiac myocytes reveals that ssTnI incorporates more efficiently into the myofilament than cTnIR146G, yet both increase Ca2+ sensitivity of tension; critically, ssTnI protects against acidic pH-induced decreases in Ca2+ sensitivity whereas HCM mutants (cTnIR146G and ssTnIR115G) do not, identifying the pH-sensitive domain as an isoform-specific functional determinant. Adenoviral gene transfer; permeabilized myocyte force-Ca2+ measurements at physiological and acidic pH; Western blot for myofilament incorporation Circulation research High 12242271
2003 In transgenic mice where cTnI is replaced by ssTnI (TNNI1), PKA-mediated phosphorylation of MyBP-C (but not ssTnI) decreases myofilament lattice spacing and does not alter Ca2+ responsiveness, demonstrating that length-dependent activation (LDA) enhancement by PKA requires cTnI phosphorylation, and that ssTnI expression reduces LDA while increasing basal Ca2+ sensitivity. Skinned myocyte force-Ca2+ measurements; X-ray diffraction of myofilament lattice spacing; PKA treatment; transgenic mouse model The Journal of physiology High 12562915
2004 In situ hemodynamic measurements in mice expressing ssTnI instead of cTnI (with or without phospholamban) demonstrate that PKA-mediated phosphorylation of cTnI significantly contributes to the enhanced rate of cardiac relaxation during beta-adrenergic stimulation, since hearts expressing unphosphorylatable ssTnI show significantly blunted -dP/dt responses to isoproterenol. In situ cardiac hemodynamics; transgenic mouse models (ssTnI-TG, PLB-KO crossed with ssTnI-TG); beta-adrenergic stimulation with isoproterenol Cardiovascular research High 14985072
2007 Site-directed mutagenesis of ssTnI with substitutions at specific residues (R125Q, H132A, V134E) transferred into adult cardiac myocytes via gene transfer identifies histidine 132 (H132 in ssTnI, corresponding to cTnI) as the key residue determining isoform-specific pH sensitivity of myofilament Ca2+ activation, while helix-4 residues control both Ca2+ and pH sensitivity differences between TnI isoforms. Adenoviral gene transfer of ssTnI point mutants; permeabilized myocyte force-Ca2+ measurements at physiological and acidic pH; sarcomere shortening measurements in intact myocytes Journal of molecular and cellular cardiology High 17602701
2007 Skinned cardiac fiber measurements using the fetal TnT isoform with either cardiac TnI or ssTnI (TNNI1) show that the TnI isoform modulates the severity of TnT mutation effects: fetal troponin isoforms (including ssTnI) confer a cardioprotective functional phenotype with less severe Ca2+ sensitivity changes compared to adult isoforms, consistent with a physiological role for ssTnI in fetal heart protection. Skinned cardiac fiber force measurements; actomyosin ATPase assay; TnT displacement/reconstitution in skinned fibers The Journal of biological chemistry Medium 18032382
2000 Using cardiac TnI knockout mice, thyroid hormone (T3/thyroxine) is identified as a regulator of ssTnI (TNNI1) gene inactivation in the heart: hyperthyroid conditions abbreviate ssTnI expression duration and accelerate postnatal downregulation, while hypothyroid conditions prolong ssTnI expression, demonstrating that ssTnI downregulation occurs independently of cTnI protein and is regulated transcriptionally by thyroid hormone. Northern blot and Western blot analysis; cTnI knockout mice; pharmacological hyperthyroid/hypothyroid manipulation; time-course analysis Journal of molecular and cellular cardiology High 11112997
2008 Functional characterization of the mouse ssTnI (TNNI1) gene promoter identifies conserved GA-rich sequences, a CREB binding site, and a CCAAT box within the first 300 bp upstream of the transcription start site as critical for cardiac myocyte expression; EMSA and ChIP assays confirm protein binding to the CREB site in cardiac nuclear extracts, and thyroid hormone T3 causes significant inhibitory transcriptional regulation of ssTnI in myocardial cells. Promoter deletion/transfection assays; EMSA; ChIP; thyroid hormone treatment; luciferase reporter assays in cardiac myocytes Journal of biomedical science Medium 18357515
2012 In transgenic mice expressing ssTnI in adult cardiomyocytes treated with propylthiouracil to revert MHC to beta-isoform, ssTnI increases crossbridge recruitment rate (b) 3.8-fold more in the presence of beta-MHC than alpha-MHC, while ssTnI-mediated increase in myofilament Ca2+ sensitivity (pCa50) is substantially blunted in beta-MHC fibers, demonstrating a functional interplay between MHC and TnI isoforms that tunes cardiac contractile dynamics. Detergent-skinned cardiac muscle fiber bundles; force-Ca2+ measurements; ATPase activity; crossbridge kinetics modeling; propylthiouracil-induced MHC isoform switch in transgenic mice The Journal of physiology High 22966157
2014 Molecular dynamics simulation and gene transfer of cTnI with helix-4 ssTnI substitutions (Q157R/A164H/E166V/H173N) into adult cardiac myocytes demonstrates that four specific evolutionary residues in cTnI helix 4 confer enhanced relaxation performance; ssTnI-like substitutions increase contractility and slow relaxation by altering the electrostatic interaction between TnI R171 and cTnC E15, thereby increasing Ca2+ binding affinity of TnC. Adenoviral gene transfer; sarcomere shortening measurements; molecular dynamics simulation; free energy perturbation calculation of Ca2+ binding Biophysical journal High 24853739
2014 Adult transgenic mouse hearts expressing ssTnI (TNNI1) instead of cTnI are protected from pressure overload (TAC): ssTnI-TAC hearts show markedly reduced hypertrophic remodeling, preserved diastolic function, and maintained energy charge, mediated by reduced pyruvate dehydrogenase kinase 4 expression enabling increased pyruvate/glucose oxidation and reduced anaplerotic flux. Transgenic mouse model; aortic banding (TAC); echocardiography; isolated perfused heart metabolic flux measurements; gene expression analysis Circulation. Heart failure High 25424393
2016 In Drosophila, the single TnI gene wupA (ortholog of human TNNI1) can localize to the nucleus, and its overexpression transcriptionally upregulates InR, Rap1, and Dilp8, promoting cell proliferation; loss of wupA reduces proliferation and antagonizes oncogenic Ras/Notch/Lgl mutations via Flower- and Sparc-dependent cell competition. In human tumors, TNNI1 knockdown restrains non-small-cell lung carcinoma xenograft growth. Drosophila gain- and loss-of-function genetics; xenograft mouse model with TNNI1 knockdown; nuclear localization imaging; transcriptional target analysis Oncotarget Medium 27437768
2017 Hypertrophic cardiomyopathy cTnC mutations reconstituted into rabbit soleus fibers and bovine masseter myofibrils (which contain ssTnI/TNNI1) show that troponin complexes containing ssTnI attenuate the Ca2+ sensitization caused by cTnC A8V and D145E but enhance it for C84Y, demonstrating that the TnI isoform within the troponin complex is a critical determinant of how cTnC mutations affect Ca2+ regulation in slow skeletal muscle. Skinned fiber reconstitution with purified troponin subunits; isometric force measurements; ATPase activity assay; bovine masseter myofibril reconstitution Frontiers in physiology High 28473771
2021 A heterozygous nonsense variant in TNNI1 (c.523A>T, p.K175*) within the tropomyosin-binding site near the C-terminus causes autosomal dominant proximal arthrogryposis with type 1 muscle fiber abnormalities and Z-disk streaming, establishing that TNNI1 loss-of-function in the tropomyosin-binding domain disrupts slow skeletal muscle fiber integrity and causes joint contractures. Trio-based exome sequencing; muscle biopsy with histopathology and electron microscopy; clinicopathologic correlation Neurology. Genetics Medium 34934811
2006 In guinea pig and sheep hearts, ssTnI (TNNI1) and cTnI are co-expressed during fetal development and the isoform switch is completed before birth (not triggered by birth), concurrent with titin isoform changes; skinned fibers from guinea pig show high Ca2+ sensitivity that corresponds to high ssTnI expression and declines as ssTnI is replaced by cTnI, demonstrating that ssTnI expression level directly determines the Ca2+ sensitivity of cardiac force development across species. Western blot for TnI isoforms; skinned cardiac strip force-Ca2+ measurements; titin isoform analysis by gel electrophoresis; selective titin proteolysis American journal of physiology. Heart and circulatory physiology High 16679402
2016 In pediatric patients with conotruncal heart defects, ssTnI (TNNI1) expression in right ventricular tissue declines monoexponentially postnatally (half-time ~5.8 months), and Ca2+ sensitivity of myofibril contraction correlates directly with ssTnI expression level throughout this developmental transition, establishing ssTnI as the primary determinant of elevated neonatal myofibrillar Ca2+ sensitivity in human hearts. Western blot quantification of ssTnI in human surgical tissue; myofibril mechanical measurements (force-Ca2+ and kinetics); correlation analysis across patients of different ages Journal of the American Heart Association High 27353610
1990 Isolation of the human TNNI1 cDNA demonstrates that the slow skeletal TnI protein is highly conserved across species, shows tissue-specific expression restricted to slow-twitch skeletal muscle, is induced during myogenic differentiation, and maps to chromosome 1q12-qter. cDNA cloning; Northern blot analysis; somatic cell hybrid mapping; in vitro myogenic differentiation Genomics High 2365354
2016 PKA treatment of slow-twitch skeletal muscle fibers phosphorylates MyBP-C but not ssTnI (TNNI1), and this phosphorylation increases power output ~30%, while incorporation of unphosphorylated cTnI thin filaments into skinned cardiac myocytes decreases isometric force (reversed by PKA), and unphosphorylated cTnI speeds force development rates, demonstrating molecule-specific roles in PKA-mediated contractility modulation. Skinned cardiac myocyte mechanical measurements; slow-twitch skeletal fiber PKA treatment; thin filament reconstitution; force, rate, and power measurements Archives of biochemistry and biophysics Medium 26854722
2013 Ankrd1 co-immunoprecipitates with the androgen receptor (AR) and acts as a transcriptional repressor of AR; when Ankrd1 is overexpressed in myoblasts, testosterone significantly reduces TnnI1 (TNNI1) mRNA levels, demonstrating that TNNI1 expression in skeletal muscle is regulated through an Ankrd1-AR transcriptional axis. Co-immunoprecipitation; reporter gene assays; RT-PCR for TNNI1 mRNA; Ankrd1 overexpression in L6.AR myoblasts Biochemical and biophysical research communications Low 23811403

Source papers

Stage 0 corpus · 85 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2014 Acquisition of a quantitative, stoichiometrically conserved ratiometric marker of maturation status in stem cell-derived cardiac myocytes. Stem cell reports 183 25358788
1999 Impaired cardiomyocyte relaxation and diastolic function in transgenic mice expressing slow skeletal troponin I in the heart. The Journal of physiology 182 10226156
2016 Overexpression of Tbx20 in Adult Cardiomyocytes Promotes Proliferation and Improves Cardiac Function After Myocardial Infarction. Circulation 132 26841808
2003 Troponin I in the murine myocardium: influence on length-dependent activation and interfilament spacing. The Journal of physiology 130 12562915
2015 TNNI1, TNNI2 and TNNI3: Evolution, regulation, and protein structure-function relationships. Gene 108 26526134
2017 Skeletal Muscle-Specific Overexpression of PGC-1α Induces Fiber-Type Conversion through Enhanced Mitochondrial Respiration and Fatty Acid Oxidation in Mice and Pigs. International journal of biological sciences 107 29104506
1997 Slow skeletal troponin I gene transfer, expression, and myofilament incorporation enhances adult cardiac myocyte contractile function. Proceedings of the National Academy of Sciences of the United States of America 107 9144257
1990 cDNA sequence, tissue-specific expression, and chromosomal mapping of the human slow-twitch skeletal muscle isoform of troponin I. Genomics 84 2365354
2015 Combinatorial polymer matrices enhance in vitro maturation of human induced pluripotent stem cell-derived cardiomyocytes. Biomaterials 65 26204225
2021 ERRγ enhances cardiac maturation with T-tubule formation in human iPSC-derived cardiomyocytes. Nature communications 64 34155205
2020 Cardiomyocyte cell cycling, maturation, and growth by multinucleation in postnatal swine. Journal of molecular and cellular cardiology 53 32710980
2007 A troponin T mutation that causes infantile restrictive cardiomyopathy increases Ca2+ sensitivity of force development and impairs the inhibitory properties of troponin. The Journal of biological chemistry 52 18032382
2015 Time course and side-by-side analysis of mesodermal, pre-myogenic, myogenic and differentiated cell markers in the chicken model for skeletal muscle formation. Journal of anatomy 51 26278933
2002 Myofilament calcium sensitivity and cardiac disease: insights from troponin I isoforms and mutants. Circulation research 51 12242271
2016 Myogenic differentiation potential of human tonsil-derived mesenchymal stem cells and their potential for use to promote skeletal muscle regeneration. International journal of molecular medicine 48 27035161
2012 Changes in serum fast and slow skeletal troponin I concentration following maximal eccentric contractions. Journal of science and medicine in sport 48 22795680
2006 Developmental changes in passive stiffness and myofilament Ca2+ sensitivity due to titin and troponin-I isoform switching are not critically triggered by birth. American journal of physiology. Heart and circulatory physiology 48 16679402
2000 Structural characterization of the human fast skeletal muscle troponin I gene (TNNI2). Gene 43 10721725
1996 Troponin I isoform expression is developmentally regulated in differentiating embryonic stem cell-derived cardiac myocytes. Developmental dynamics : an official publication of the American Association of Anatomists 36 9019244
2004 Troponin I phosphorylation plays an important role in the relaxant effect of beta-adrenergic stimulation in mouse hearts. Cardiovascular research 33 14985072
2010 Association of 3 polymorphisms in porcine troponin I genes (TNNI1 and TNNI2) with meat quality traits. Journal of applied genetics 32 20145300
2007 Single amino acid substitutions define isoform-specific effects of troponin I on myofilament Ca2+ and pH sensitivity. Journal of molecular and cellular cardiology 32 17602701
2010 The embryonic genes Dkk3, Hoxd8, Hoxd9 and Tbx1 identify muscle types in a diet-independent and fiber-type unrelated way. BMC genomics 28 20230627
2016 Molecule specific effects of PKA-mediated phosphorylation on rat isolated heart and cardiac myofibrillar function. Archives of biochemistry and biophysics 27 26854722
2019 Binary Colloidal Crystals Drive Spheroid Formation and Accelerate Maturation of Human-Induced Pluripotent Stem Cell-Derived Cardiomyocytes. ACS applied materials & interfaces 26 30614683
2018 Acute oral administration of L-leucine upregulates slow-fiber- and mitochondria-related genes in skeletal muscle of rats. Nutrition research (New York, N.Y.) 25 30122194
2016 Troponin-I enhances and is required for oncogenic overgrowth. Oncotarget 24 27437768
1995 Differential expression of TnI and TnT isoforms in rabbit heart during the perinatal period and during cardiovascular stress. Journal of molecular and cellular cardiology 24 7760375
2000 Thyroid hormone regulates slow skeletal troponin I gene inactivation in cardiac troponin I null mouse hearts. Journal of molecular and cellular cardiology 23 11112997
1996 Cardiac and skeletal muscle troponin I isoforms are encoded by a dispersed gene family on mouse chromosomes 1 and 7. Mammalian genome : official journal of the International Mammalian Genome Society 22 8903721
2021 Integrative transcriptomic, proteomic, and machine learning approach to identifying feature genes of atrial fibrillation using atrial samples from patients with valvular heart disease. BMC cardiovascular disorders 21 33509101
2021 Elevation of fast but not slow troponin I in the circulation of patients with Becker and Duchenne muscular dystrophy. Muscle & nerve 21 33683712
2004 Troponin I isoform expression in human and experimental atrial fibrillation. Circulation 21 15289369
2021 Effect of dietary L-theanine supplementation on skeletal muscle fiber type transformation in vivo. The Journal of nutritional biochemistry 19 34517095
2017 Hypertrophic Cardiomyopathy Cardiac Troponin C Mutations Differentially Affect Slow Skeletal and Cardiac Muscle Regulation. Frontiers in physiology 19 28473771
2014 Metabolic efficiency promotes protection from pressure overload in hearts expressing slow skeletal troponin I. Circulation. Heart failure 19 25424393
2022 Comparative Transcriptome Analysis of Slow-Twitch and Fast-Twitch Muscles in Dezhou Donkeys. Genes 18 36140778
2009 The molecular structures and expression patterns of zebrafish troponin I genes. Gene expression patterns : GEP 17 19602390
2019 Adult human cardiac stem cell supplementation effectively increases contractile function and maturation in human engineered cardiac tissues. Stem cell research & therapy 16 31801634
2018 Improvement of Dystrophic Muscle Fragility by Short-Term Voluntary Exercise through Activation of Calcineurin Pathway in mdx Mice. The American journal of pathology 16 30142334
2012 Induction of cardiac myogenic lineage development differs between mesenchymal and satellite cells and is accelerated by bone morphogenetic protein-4. Journal of molecular and cellular cardiology 16 22709559
2013 Ankrd1 is a transcriptional repressor for the androgen receptor that is downregulated by testosterone. Biochemical and biophysical research communications 15 23811403
2010 Identification of three novel SNPs and association with carcass traits in porcine TNNI1 and TNNI2. Molecular biology reports 14 20182806
2023 A Revised Perspective on the Evolution of Troponin I and Troponin T Gene Families in Vertebrates. Genome biology and evolution 12 36518048
2022 Comparative transcriptomic analysis reveals region-specific expression patterns in different beef cuts. BMC genomics 12 35596128
2016 Postnatal Development of Right Ventricular Myofibrillar Biomechanics in Relation to the Sarcomeric Protein Phenotype in Pediatric Patients with Conotruncal Heart Defects. Journal of the American Heart Association 11 27353610
2010 Temporal expression of TnI fast and slow isoforms in biceps femoris and masseter muscle during pig growth. Animal : an international journal of animal bioscience 10 22444701
2008 Functional characterization of mouse fetal TnI gene promoters in myocardial cells. Journal of biomedical science 10 18357515
2014 Molecular determinants of cardiac myocyte performance as conferred by isoform-specific TnI residues. Biophysical journal 9 24853739
2010 Molecular cloning and comparative characterization of the porcine troponin I family. Animal biotechnology 9 20024788
1993 Assignment of the human slow skeletal muscle troponin gene (TNNI1) to 1q32 by fluorescence in situ hybridisation. Cytogenetics and cell genetics 9 8428521
2025 TMT-labelled quantitative proteomics reveals the mechanism of Rhodotorula mucilaginosa on proteolysis of dry-cured ham: Structural protein degradation, amino acid release and taste improvement. Food chemistry 8 39848055
2023 Validation of protein biological markers of lamb meat quality characteristics based on the different muscle types. Food chemistry 8 37392625
2019 Regular aerobic exercise-ameliorated troponin I carbonylation to mitigate aged rat soleus muscle functional recession. Experimental physiology 8 30820991
2019 Transcriptional regulatory region and DNA methylation analysis of TNNI1 gene promoters in Gaoyou duck skeletal muscle (Anas platyrhynchos domestica). British poultry science 8 30968708
2016 Three slow skeletal muscle troponin genes in small-tailed Han sheep (Ovis aries): molecular cloning, characterization and expression analysis. Molecular biology reports 8 27295221
2014 Influence of a constitutive increase in myofilament Ca(2+)-sensitivity on Ca(2+)-fluxes and contraction of mouse heart ventricular myocytes. Archives of biochemistry and biophysics 8 24480308
2024 Integrated 4D Analysis of Intramuscular Fat Deposition: Quantitative Proteomic and Transcriptomic Studies in Wannanhua Pig Longissimus Dorsi Muscle. Animals : an open access journal from MDPI 7 38200898
2012 The effects of slow skeletal troponin I expression in the murine myocardium are influenced by development-related shifts in myosin heavy chain isoform. The Journal of physiology 7 22966157
2024 Muscle Transcriptome Analysis of Mink at Different Growth Stages Using RNA-Seq. Biology 6 38785766
2023 Identification of Potential Sex-Specific Biomarkers in Pigs with Low and High Intramuscular Fat Content Using Integrated Bioinformatics and Machine Learning. Genes 6 37761835
2022 Effects of feeding restriction on skeletal muscle development and functional analysis of TNNI1 in New Zealand white rabbits. Animal biotechnology 6 36520026
2019 Myocardial-specific ablation of Jumonji and AT-rich interaction domain-containing 2 (Jarid2) leads to dilated cardiomyopathy in mice. The Journal of biological chemistry 6 30700554
2005 Thyroid hormone inhibits slow skeletal TnI expression in cardiac TnI-null myocardial cells. Tissue & cell 6 15695175
2024 Roles of programmed death-1 and muscle innate lymphoid cell-derived interleukin 13 in sepsis-induced intensive care unit-acquired weakness. Journal of cachexia, sarcopenia and muscle 5 39016179
2003 Gene transfer of troponin I isoforms, mutants, and chimeras. Advances in experimental medicine and biology 5 15098664
2024 Explorations on Key Module and Hub Genes Affecting IMP Content of Chicken Pectoralis Major Muscle Based on WGCNA. Animals : an open access journal from MDPI 4 38338044
2024 Transcriptome analysis revealed the mechanism of skeletal muscle growth and development in different hybrid sheep. Animal bioscience 4 39483021
2022 Cas9/AAV9-Mediated Somatic Mutagenesis Uncovered the Cell-Autonomous Role of Sarcoplasmic/Endoplasmic Reticulum Calcium ATPase 2 in Murine Cardiomyocyte Maturation. Frontiers in cell and developmental biology 4 35433671
2021 TNNI1 Mutated in Autosomal Dominant Proximal Arthrogryposis. Neurology. Genetics 4 34934811
2010 Real-time reverse transcription-PCR expression profiling of porcine troponin I family in three different types of muscles during development. Molecular biology reports 4 20376701
2024 Abnormal genes and pathways that drive muscle contracture from brachial plexus injuries: Towards machine learning approach. SLAS technology 3 39033877
2024 Identification and analysis of differentially expressed lncRNAs and their ceRNA networks in DMD/mdx primary myoblasts. Scientific reports 3 39390091
2017 Novel Muscle-Specific Genes TCAP, TNNI1, and FHL1 in Cattle: SNVs, Linkage Disequilibrium, Combined Genotypes, Association Analysis of Growth Performance, and Carcass Quality Traits and Expression Studies. Animal biotechnology 3 29095095
2005 The miscommunicative cardiac cell: when good proteins go bad. Annals of the New York Academy of Sciences 3 16093482
2025 Methimazole disrupted skeletal ossification and muscle fiber transition in Bufo gargarizans larvae. Ecotoxicology and environmental safety 2 39793290
2025 Effects of Fermented Liquid Feed on Growth Performance, Meat Quality, and Intestinal Microbiota of Yuedong Black Pigs. Animals : an open access journal from MDPI 2 41007902
2024 Genetic background of walking ability and its relationship with leg defects, mortality, and performance traits in turkeys (Meleagris gallopavo). Poultry science 2 38788487
2024 Differential analysis of ubiquitin-proteomics in skeletal muscle of Duroc pigs and Tibetan fragrant pigs. Frontiers in veterinary science 2 39280835
2023 Distinct mononuclear diploid cardiac subpopulation with minimal cell-cell communications persists in embryonic and adult mammalian heart. Frontiers of medicine 2 37294383
2023 Transcriptomics profiling reveal the heterogeneity of white and brown adipocyte. Journal of bioenergetics and biomembranes 1 37906396
2022 The functional verification and analysis of Fugu promoter of cardiac gene tnni1a in zebrafish. Cells & development 1 35787465
2026 Metabolic and cellular physiological differences between embryonic breast and leg muscle satellite cells in chickens. Poultry science 0 41865652
2025 Promotion of maturation in CDM3-induced embryonic stem cell-derived cardiomyocytes by palmitic acid. Bio-medical materials and engineering 0 39331088
2020 [Effects of electroacupuncture combined with passive stretch exercise on disused muscle atrophy and expression of skeletal troponin in mice]. Zhen ci yan jiu = Acupuncture research 0 32959554