TNNT2_HUMAN TNNT2 ELISA tesk kit
- Known as:
- TNNT2_HUMAN TNNT2 Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen17160
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- TNNT2_HUMAN TNNT2 ELISA tesk kit
Related genes to: TNNT2_HUMAN TNNT2 ELISA tesk kit
- Gene:
- TNNT2 NIH gene
- Name:
- troponin T2, cardiac type
- Previous symbol:
- CMH2, CMD1D
- Synonyms:
- CMPD2
- Chromosome:
- 1q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-09-27
- Date modifiied:
- 2019-04-23
Related products to: TNNT2_HUMAN TNNT2 ELISA tesk kit
Related articles to: TNNT2_HUMAN TNNT2 ELISA tesk kit
- Dilated cardiomyopathy (DCM) and arrhythmogenic cardiomyopathy (ACM) are progressive cardiac muscle disorders with phenotypic and genetic overlap. Although a male predominance is noted in DCM/ACM, it remains unclear whether this extends to specific genetic subtypes or reflects variation in disease stage and whether sex influences age-dependent disease onset across pediatric and adult groups. - Source: PubMed
Publication date: 2026/05/20
Stroeks Sophie L V MBart Nicole KRossano JosephClaggett BrianBeelen Nina JBuchan Rachel JDay SharleneFornaro AlessandraHalliday Brian PWheeler Matthew THammersley Daniel JHelms AdamHeymans Astrid B MHo Carolyn YKhan Sadiya SLin KimLota AmritMerlo MarcoMestroni LuisaOlivotto IacopoOwens AnjaliSeidman Christine EShore SupriyaSinnette CorineSinagra GianfrancoStevenson Lynne WStewart Garrick CTheotakis PantazisVenner Max F G H MWare James STaylor Matthew R GVerdonschot Job A JWilsbacher LisaPrasad SanjayHeymans Stephane RParikh Victoria NTayal UpasanaLakdawala Neal K - Bunge has been used traditionally for cardiovascular disorders, but its specific roles in stem cell cardiac differentiation remain unclear. In this study, we examined whether Bunge (SM) promotes cardiomyocyte differentiation from mouse embryonic stem cells (mESCs) and defined its underlying mechanism. To dynamically monitor cardiac differentiation, we established a -H2B-mCherry reporter mESC line that retained normal pluripotency and differentiation capacity. Using an embryoid body-based differentiation system, we found that SM exerted a distinct temporal effect on lineage progression: treatment during the early differentiation window inhibited pluripotency maintenance, proliferation, and mesodermal development, whereas administration during the cardiac precursor stage markedly enhanced cardiomyocyte formation, as indicated by increased beating embryoid bodies and upregulation of , , , , and . Mechanistically, transcriptomic and protein analyses showed that SM suppressed canonical Wnt/β-catenin signaling, including downregulation of , , , , and , while Wnt activation WAY262611 partially reversed these effects. Further compound screening identified tanshinone IIA (Tan IIA) as the principal active constituent of SM, which largely recapitulated the pro-cardiogenic and Wnt-inhibitory effects of the crude extract. Together, these findings identify SM and Tan IIA as stage-dependent regulators of mESC fate and support their potential utility in natural product-based strategies for improving stem cell-derived cardiomyocyte generation. - Source: PubMed
Publication date: 2026/04/26
Lu GuotaoSun QiRen WeiYang JihongYang Fan - Dilated cardiomyopathy (DCM) is a primary myocardial disorder characterized by progressive ventricular dilatation and impaired myocardial systolic contractility, and it represents the most common form of cardiomyopathy globally. DCM drives a substantial worldwide disease burden, thus presenting a formidable and persistent challenge to global public health systems. The pathogenesis of DCM is marked by extreme etiological heterogeneity: 30%-50% of cases have a familial origin, with genetic determinants serving as the core driver of disease onset and progression. With the rapid advancement and widespread application of next-generation sequencing (NGS) technologies, a growing repertoire of DCM-causative genes has been successfully identified. These genes encode key functional proteins that regulate multiple core physiological processes in cardiomyocytes, including sarcomeric structure maintenance, intracellular signal transduction, and myocardial energy homeostasis. DCM-causing genes can be classified into multiple categories according to their functions. Sarcomeric protein genes (such as TTN, MYH7, and TNNT2) disrupt sarcomere assembly and contractile function through mechanisms such as haploinsufficiency and the toxic peptide hypothesis; mutations in nuclear membrane protein genes (such as LMNA and EMD) cause abnormal nuclear structure and disordered mechanotransduction signals; ion channel genes (such as SCN5A, CACNA1C, and RYR2) affect electrophysiological balance and calcium handling; desmosome-related genes (such as DSC2 and DSP) are associated with abnormal cell junctions and dysregulation of the Wnt/β-catenin pathway; KLF13, ETS1, and BMP10 are possible candidate genes for DCM with limited research; loss of function of RBM20 leads to abnormal splicing of TTN, CamkIIδ, RyR2, etc. and causes nuclear import defects as well as cytoplasmic RBM20-RNP granule toxicity, thereby driving ventricular dilation. These genes drive myocardial remodeling through common signaling pathways (such as ERK and TGF-β). Potential treatment strategies include gene-level interventions, targeted pathway inhibitors, and myosin activators. However, genetic heterogeneity results in a narrow applicable population for single-gene therapies. Future research needs to shift from targeting individual genes to improving the common pathological environment to achieve broad-spectrum treatment. Exploring upstream prevention of mutations or activation of endogenous repair mechanisms provides new directions for the treatment of DCM. - Source: PubMed
Publication date: 2026/03/28
Zhang XiaoZhang XinyuChen YunruHuan NaWang ChenglongZhang Dawu - Dilated cardiomyopathy (DCM) is the most prevalent pediatric cardiomyopathy and has a poor prognosis. Although heart transplantation is the only curative option, the severe donor shortage in Japan underscores an urgent need for alternative therapies. Here, we generated induced pluripotent stem cell (iPSC) lines from two unrelated children with the same TNNT2-R151W mutation. We then investigated the cellular characteristics of the cardiomyocytes derived from these iPSC lines (R151W iPSC-CMs) and evaluated their contractile function in pillar-based engineered heart tissue (EHT). We also assessed the therapeutic potential of overexpressing wild-type TNNT2 in patient-derived iPSCs (wtTNNT2-OE-iPSCs). R151W-iPSC-CMs exhibited pronounced sarcomere disarray, attenuated Ca transient amplitude, prolonged time to peak, and delayed decay tau. These characteristics are indicative of failing myocardium and were restored in wtTNNT2-OE-iPSC-CMs. Pillar-based EHT assays revealed a substantial decrease in contractile force in R151W-EHTs compared to wtTNNT2-OE-EHTs, which is suggestive of the systolic dysfunction observed clinically in DCM. Collectively, these results provide the first functional evidence that the TNNT2-R151W mutation leads to pediatric DCM by causing sarcomere insufficiency and disturbances in Ca handling. Our patient-specific iPSC-EHT platform faithfully recapitulates key features of pediatric DCM and could offer a robust system for mechanistic studies and drug testing. Furthermore, phenotypic rescue upon overexpression of wild-type TNNT2 suggests that this allele is amenable to a gene replacement approach aimed at restoring wild-type function in TNNT2-mutant cardiomyopathies. - Source: PubMed
Publication date: 2026/01/06
Nagashima ToshiakiMiki KenjiTsuchida MasaruWhitehouse JuliaTakei-Sasozaki IkueHigashiyama YukiIshida HidekazuKashino KunioMiyagawa Shigeru - This study aims to characterize the clinical and genetic features of a sporadic case of dilated cardiomyopathy (DCM) associated with a TNNT2 variant and to review the variant spectrum of the TNNT2 gene in the Chinese DCM population. - Source: PubMed
Publication date: 2026/03/26
Chen XinglinHuang ZhengjieZheng QiZha LingfengTang TingtingCheng Xiang