TNNC1

Last update 08 May 2025

Basic Info

Synonyms

TN-C, TNNC, TNNC1

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Introduction

Troponin is the central regulatory protein of striated muscle contraction. Tn consists of three components: Tn-I which is the inhibitor of actomyosin ATPase, Tn-T which contains the binding site for tropomyosin and Tn-C. The binding of calcium to Tn-C abolishes the inhibitory action of Tn on actin filaments.

100 Clinical Results associated with TNNC1

100 Translational Medicine associated with TNNC1

0 Patents (Medical) associated with TNNC1

143

Literatures (Medical) associated with TNNC1

15 Mar 2025·The FASEB Journal

A satellite cell‐dependent epigenetic fingerprint in skeletal muscle identity genes after lifelong physical activity

Article

Author: Wen, Yuan ; Dupont‐Versteegden, Esther E. ; Chambers, Toby L. ; Freeman, Willard M. ; Murach, Kevin A. ; Englund, Davis A. ; Wren, Jonathan D. ; Dungan, Cory M. ; Porter, Hunter L.

AbstractSatellite cells comprise a small proportion of mononuclear cells in adult skeletal muscle. Despite their relative rarity, satellite cells have critical functions in muscle adaptation, particularly during prolonged exercise training. The mechanisms by which satellite cells mediate skeletal muscle responsiveness to physical activity throughout the lifespan are still being defined, but epigenetic regulation may play a role. To explore this possibility, we analyzed global DNA methylation patterns in muscle tissue from female mice that engaged in lifelong voluntary unweighted wheel running with or without satellite cells. Satellite cells were ablated in adulthood using the tamoxifen‐inducible Pax7‐DTA model. Compared to sedentary mice, wheel running for 13 months caused muscle DNA methylation differences in the promoter regions of numerous muscle fiber‐enriched genes—Cacgn1, Dnm2, Mlip, Myl1, Myom2, Mstn, Sgca, Sgcg, Tnnc1, Tnni2, Tpm1, and Ttn—only when satellite cells were present. These genes relate to muscle fiber identity, cytoarchitecture, and size as well as overall muscle function. Epigenetic alterations to such genes are consistent with previously observed histological and in vivo impairments to running adaptation after satellite cell depletion in these same mice. Musk promoter region methylation was affected only in the absence of satellite cells with lifelong running relative to sedentary; this dovetails with work showing that satellite cells influence skeletal muscle innervation. Defining the epigenetic effects of satellite cells on identity genes in muscle fibers after lifelong physical activity provides new directions for how these rare stem cells can promote muscle adaptation and function throughout the lifespan.

01 Mar 2025·Animal Bioscience

Transcriptome analysis revealed the mechanism of skeletal muscle growth and development in different hybrid sheep

Article

Author: Li, Shuang ; Zhang, Zijun ; Cao, Hongguo ; Ling, Yinghui ; Yang, Wangxin ; Lou, Mengyu ; Zhang, Sihuan

Objective: This study aimed to analyze the molecular mechanism of heterosis in East Friesian sheep×Hu sheep (EH) hybrid sheep and Suffolk×EH (SHE) hybrid sheep (Ovis aries).Methods: In this research, the growth performance data of Hu sheep (H), EH and SHE from birth to 8 months of age were analyzed. Three 8-month-old sheep of each of the three strains (9 sheep in total) were chosen and their longissimus dorsi muscles were collected for transcriptome sequencing. We verified the expression of seven differentially expressed genes (DEGs) by real-time quantitative reverse transcription polymerase chain reaction (RT-qPCR).Results: The results showed: (1) body weight and chest circumference of EH were significantly greater than H (p<0.05), except at 4 months of age. Body weight and chest circumference of SHE was significantly higher than EH (p<0.05), except at 6 months of age. (2) 310 DEGs were screened in the EH and H, gene ontology and Kyoto encyclopedia of genes and genomes showed DEGs were mainly concentrate on the categories of actin cytoskeleton, calcium binding, cGMP-PKG and mitogen-activated protein kinase (MAPK) signaling pathway, which correlating the development of skeletal muscle and energy metabolism. 329 DEGs were screened in the SHE and EH. DEGs were mainly enriched in extracellular matrix-receptor interactions and cell adhesion molecules. (3) Protein–protein interaction screening yielded five (MYL2, TNNI1, TNNI3, MYH11, TNNC1) and three (SOX10, COL2A1, MPZ) pivotal DEGs regulating muscle development in EH and SHE. (4) RT-qPCR test results were consistent with transcriptome sequencing.Conclusion: This study provides candidate genes for improving sheep growth traits. It provides a theoretical basis for analyzing the mechanism of muscle development in crossbred sheep.

01 Feb 2025·Journal of the American College of Cardiology

Genes Associated With Hypertrophic Cardiomyopathy

Article

Author: Walsh, Roddy ; Adduru, Mhy-Lanie ; Hespe, Sophie ; Muiño-Mosquera, Laura ; McNally, Elizabeth M ; Ware, James S ; Josephs, Katherine ; Brown, Emily E ; Bagnall, Richard D ; Thaxton, Courtney ; Waddell, Amber ; Reuter, Chloe ; Jordan, Elizabeth ; Peters, Stacey ; Callewaert, Bert ; Asatryan, Babken ; Hoffman-Andrews, Lily ; Anderson, Kailyn ; Wayburn, Bess ; Mayers, Megan ; Stafford, Fergus ; Chahal, C Anwar A ; Jarinova, Olga ; Parikh, Victoria ; Bronicki, Lucas ; Murray, Brittney ; Ingles, Jodie ; Owens, Emma ; James, Cynthia A ; Landstrom, Andrew P

BACKGROUNDHypertrophic cardiomyopathy (HCM) is an inherited cardiac condition affecting ∼1 in 500 and exhibits marked genetic heterogeneity. Previously published in 2019, 57 HCM-associated genes were curated providing the first systematic evaluation of gene-disease validity.OBJECTIVESThe authors report work by the Clinical Genome Resource Hereditary Cardiovascular Disease (HCVD) Gene Curation Expert Panel (GCEP) to reappraise the clinical validity of previously curated and new putative HCM genes.METHODSThe Clinical Genome Resource systematic gene curation framework was used to reclassify the gene-disease relationships for HCM and related syndromic entities involving left ventricular hypertrophy. Genes previously curated were included if their classification was not definitive, and if the time since curation was >2 to 3 years. New genes with literature assertions for HCM were included for initial evaluation. Existing genes were curated for new inheritance patterns where evidence existed. Curations were presented on twice monthly calls, with the HCVD GCEP composed of 29 individuals from 21 institutions across 6 countries.RESULTSThirty-one genes were recurated and an additional 5 new potential HCM-associated genes were curated. Among the recurated genes, 17 (55%) genes changed classification: 1 limited and 4 disputed (from no known disease relationship), 9 disputed (from limited), and 3 definitive (from moderate). Among these, 3 (10%) genes had a clinically relevant upgrade, including TNNC1, a 9th sarcomere gene with definitive HCM association. With new evidence, 2 genes were curated for multiple inheritance patterns (TRIM63, disputed for autosomal dominant but moderate for autosomal recessive; ALPK3, strong for autosomal dominant and definitive for recessive). CSRP3 was curated for a semidominant mode of inheritance (definitive). Nine (29%) genes were downgraded to disputed, further discouraging clinical reporting of variants in these genes. Five genes recently reported to cause HCM were curated: RPS6KB1 and RBM20 (limited), KLHL24 and MT-TI (moderate), and FHOD3 (definitive).CONCLUSIONSWe report 29 genes with definitive, strong, or moderate evidence of causation for HCM or isolated left ventricular hypertrophy, including sarcomere, sarcomere-associated, and syndromic conditions.

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TNNC1

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