Ask about this productRelated genes to: TNNI1 antibody
- Gene:
- TNNI1 NIH gene
- Name:
- troponin I1, slow skeletal type
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1989-12-11
- Date modifiied:
- 2016-10-05
Related products to: TNNI1 antibody
Related articles to: TNNI1 antibody
- This study explored the effects of dietary riboflavin supplementation on breast meat quality, muscle fiber characteristics, metabonomics, transcriptomics, and phosphoproteomics of Pekin ducks. A total of 96 14-day-old ducks were randomly allotted to two treatment groups, each with 8 replicates of 6 birds, and were fed diets supplemented with 0 or 10 mg/kg riboflavin for 28 days. Compared to the control group without riboflavin supplementation, dietary riboflavin supplementation significantly increased breast muscle shear force, myofiber diameter, perimeter, and cross-sectional area, as well as myofibril diameter. Dietary riboflavin supplementation increased gene expression involved in myogenic differentiation of breast muscle in Pekin ducks, including MYOD, MRF4, and MYF5. Breast muscle metabolomics revealed that riboflavin stimulated fatty acid beta oxidation, as most carnitine-related metabolites were upregulated. Transcriptomics analysis revealed that riboflavin upregulated seven genes involved in muscle contraction (MYO3A, MYO5B, MYH11, MYBPC1, TNNI1, TNNT2, A2M), and ten genes involved in fatty acid synthesis, oxidation, and transport processes, which may contribute to enhanced intramuscular fat content. Furthermore, phosphoproteomics analysis indicated dietary riboflavin supplementation altered the phosphorylation levels of proteins involved in muscle contraction and glycolysis (PGM1, ENO1, and TPI1), which may lead to an increase in pH. In conclusion, riboflavin supplementation in the diet improved the breast meat quality and fiber development of ducks probably by activating fatty acid beta oxidation, synthesis, and transport, as well as muscle contraction, while simultaneously depressing glycolysis process. - Source: PubMed
Publication date: 2026/06/22
Wu QingyiShao QingZhou WeiZhuang LeiJin YongyanZhou ZhengkuiXie MingHou ShuishengTang Jing - Troponin I 1 (TNNI1) encodes the slow skeletal isoform of troponin I and is essential for the regulation of contraction in slow-twitch skeletal muscle. However, the developmental and tissue-specific expression of TNNI1-related genes across vertebrates remains incompletely characterized. In zebrafish, multiple tnni genes have been identified, including four tnni1-related paralogs (tnni1a, tnni1b, tnni1c, and tnni1d), which share high sequence similarity. While individual tnni genes have been partially characterized, a systematic comparison of the spatial and temporal expression patterns of these tnni1 paralogs during embryogenesis remains lacking. Here, we analyzed and compared the spatial and temporal expression patterns of the four tnni1 paralogs during zebrafish embryogenesis to assess their potential functional divergence. Multiple sequence alignment revealed that proteins encoded by zebrafish Tnni1 paralogs are highly conserved relative to mammalian TNNI1, with paralog-specific divergence primarily in the N-terminal region. Whole-mount in situ hybridization showed that tnni1a is first detected in the embryonic heart and was later expressed in cranial and hypaxial muscles. tnni1b was expressed in bilateral cardiac precursor cells, exhibited the strongest and most sustained cardiac expression among the paralogs, and was subsequently expressed in extraocular, craniofacial, hypaxial, and trunk muscles. In contrast, tnni1c and tnni1d were initially expressed in somites, displayed weaker or transient cardiac expression, and were later broadly expressed in extraocular, craniofacial, and hypaxial muscles. Taken together, these findings indicate that zebrafish tnni1 paralogs exhibit distinct yet partially overlapping spatiotemporal expression profiles, supporting partial subfunctionalization following gene duplication during cardiac and skeletal muscle development. - Source: PubMed
Publication date: 2026/07/11
Kim EunmiLee HaeniLim Hyun-JoungKim Geun-Young - This study aimed to integrate multiple datasets for the identification of atrial fibrillation (AF)-related differentially expressed genes (DEGs), analyze their underlying mechanisms through functional enrichment and machine learning, construct diagnostic models, and explore immune-metabolic interactions to provide novel biomarkers and theoretical foundations. Gene expression datasets were integrated and normalized, with batch effects removed using principal component analysis. Differential expression analysis, functional enrichment analysis (Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathways), and machine learning-based feature gene selection and model construction were performed. Shapley additive explanations analysis was utilized to interpret the constructed models, while gene set enrichment analysis, gene set variation analysis, and immune cell infiltration analysis were conducted to investigate the associations between feature genes and immune infiltration. After integrating and normalizing gene expression data and eliminating batch effects via principal component analysis, 6 DEGs were identified, including 4 upregulated and 2 down-regulated ones. Functional enrichment analysis showed these DEGs were significantly enriched in neuro-related biological processes and pathways, indicating their key roles in AF pathogenesis. Five key feature genes were selected using LASSO, random forest, and support vector machine-recursive feature elimination algorithms. They had significant expression differences between the AF and control groups (P < .001) and were located on distinct chromosomes. The constructed random forest and support vector machine models performed excellently (area under the curve ≥ 0.85). Shapley additive explanations analysis revealed TNNI1 contributed most to model prediction, with its expression significantly positively correlated with immune cell infiltration. Gene set enrichment analysis and gene set variation analysis analyses further showed feature genes participated in AF pathogenesis by regulating immune modulation, metabolic pathways, and autophagy. Immune cell infiltration analysis found altered proportions of T-cell subsets and M0 macrophages in the AF group, along with complex links between feature gene expression and immune cell function. This study systematically elucidated the unique gene expression patterns and key regulatory pathways associated with AF, clarifying the crucial roles of feature genes in immune regulation, metabolic imbalance, and cellular dysfunction. These findings provide a theoretical basis and potential therapeutic targets for understanding AF pathogenesis and developing targeted treatment strategies. - Source: PubMed
Maimaiti MierzhatiPaerhati AizizhaLiu ShenhongDu XianglinBai Wen - Although the Kazakh horse is a dual-purpose breed renowned for both milk and meat production, the extent to which surgical castration alters gene expression in its muscles has not yet been fully elucidated. In this study, left longissimus dorsi muscle (LDM) samples were obtained from six Kazakh stallions (W group) and six Kazakh geldings (S group) to comparatively evaluate meat quality parameters, examine histological characteristics in tissue sections, and apply transcriptomic profiling to comprehensively explore the principal regulatory pathways and candidate genes through which surgical castration modulates LDM growth. The results demonstrated that surgical castration did not induce significant alterations in meat color or pH-related parameters. However, cooking loss and shear force values were markedly diminished, accompanied by a marked decrease in muscle fiber cross-sectional area. Transcriptomic analysis identified 848 differentially expressed genes (DEGs) in total, comprising 415 upregulated and 433 markedly downregulated DEGs, which were predominantly enriched in key biological pathways, including actin cytoskeleton regulation. Moreover, eleven core candidate genes, including MYL2, MYL3, and TNNI1, were further screened and identified. - Source: PubMed
Publication date: 2026/06/18
Li ZexuRen WanluWang RanLi LulingMa ShikunSu YiShan DehaxiHuang QiupingWang Jianwen - Generating mature human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) remains a major obstacle to accurate disease modeling and cardiac repair. As the transcription factor Irx3 is a key determinant of ventricular conduction system fate in mice, we hypothesized that suppressing IRX3 expression accelerates human working cardiomyocyte differentiation. Here, we demonstrate that depleting IRX3 enhances hiPSC-CM differentiation. IRX3-knockout (KO) hiPSCs generated a greater number of cardiomyocytes with elevated expression of TNNI1 and CX43. Notably, IRX3-KO cardiomyocytes exhibited improved electrophysiological properties, more uniform mitochondrial distribution, better sarcomere organization, and enhanced intercellular connectivity. We observed that IRX3 expression peaks during the early stages of cardiomyocyte differentiation, whereas IRX3-KO cardiac progenitors have increased expression of GATA4, NKX2-5, and TBX5, as well as enhanced cell proliferation. These integrative analyses indicate that IRX3 influences cardiomyocyte differentiation by modulating the gene regulatory networks driven by GATA4, NKX2-5, and TBX5, providing functional evidence linking gene regulatory networks to the structural and electrophysiological development of cardiomyocytes. Collectively, these findings identify IRX3 as a key regulator of early cardiac commitment and highlight the potential of IRX3 suppression to enhance the molecular and functional phenotype of hiPSC-derived cardiomyocytes. - Source: PubMed
Publication date: 2026/06/16
Ribeiro Kalthof AgathaFerreira Nikolas DreschSilva Caio MateusCordeiro Valadão IuriPinheiro de Sousa IguaracyBertoldi Ester Riserio MatosLima Vanessa MoraisTuraca Lauro ThiagoBarbosa Ana Beatriz Ruiz AfonsoFonseca-Alaniz Miriam HelenaConcordet Jean-PaulNeri Elida AdalgisaKrieger Jose E