CLIA Cardiac muscle troponin T,cTnT,Homo sapiens,Human,TNNT2,TnTc,Troponin T, cardiac muscle
- Known as:
- CLIA Cardiac muscle troponin T,cTnT,Homo sapiens,Human,TNNT2,TnTc,Troponin T, cardiac muscle
- Catalog number:
- U1339h
- Product Quantity:
- 96T
- Category:
- -
- Supplier:
- EIAab
- Gene target:
- CLIA Cardiac muscle troponin cTnT Homo sapiens Human TNNT2 TnTc Troponin cardiac
Related genes to: CLIA Cardiac muscle troponin T,cTnT,Homo sapiens,Human,TNNT2,TnTc,Troponin T, cardiac muscle
- 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: CLIA Cardiac muscle troponin T,cTnT,Homo sapiens,Human,TNNT2,TnTc,Troponin T, cardiac muscle
Related articles to: CLIA Cardiac muscle troponin T,cTnT,Homo sapiens,Human,TNNT2,TnTc,Troponin T, cardiac muscle
- The prevention and management of cancer therapy-related cardiac dysfunction (CTRCD) have become increasingly important. Recent studies have revealed the crucial role of genetics in determining the susceptibility to development of CTRCD. We present a case of a 65-year-old woman with breast cancer who developed recurrent CTRCD following low-dose chemotherapy, despite lacking conventional cardiovascular risk factors. Her medical history included anthracycline-associated cardiomyopathy, and her condition deteriorated significantly after treatment with HER2-targeted therapies. Through the use of multimodal imaging, we detected severe left ventricular systolic dysfunction. Further investigation with genetic testing revealed a likely pathogenic variant in the TNNT2 gene, suggesting a genetic predisposition to CTRCD. This case implies the potential role of genetic screening in identifying patients at risk for CTRCD and advocates for personalized chemotherapy and cardioprotective strategies. - Source: PubMed
Publication date: 2024/04/14
Lee So-YoungKim Hoon SeokJung Mi-HyangChang SuyonKim MyungshinYoun Jong-ChanChung Woo-BaekJung Hae Ok - Cellular therapy holds immense promise to remuscularize the damaged myocardium but is practically hindered by limited allogeneic sources of cardiac-committed cells that engraft stably in the recipient heart after transplantation. Here, we demonstrate that the pericardial tissue harbors myogenic stem cells (pSCs) that are activated in response to inflammatory signaling after myocardial infarction (MI). The pSCs derived from the MI rats (MI-pSCs) show and cardiac commitment characterized by cardiac-specific Tnnt2 expression and formation of rhythmic contraction in culture. Bulk RNA-seq analysis reveals significant upregulation of a panel of genes related to cardiac/myogenic differentiation, paracrine factors, and extracellular matrix in the activated pSCs compared to the control pSCs (Sham-pSCs). Notably, we define MyoD as a key factor that governs the process of cardiac commitment, as siRNA-mediated gene silencing results in a significant reduction of myogenic potential. Injection of the cardiac-committed cells into the infarcted rat heart leads to long-term survival and stable engraftment in the recipient myocardium. Therefore, these findings point to pericardial myogenic progenitors as an attractive candidate for cardiac cell-based therapy to remuscularize the damaged myocardium. - Source: PubMed
Publication date: 2024/03/27
Zhao JianfengRui LimeiOuyang WeiliHao YingcaiLiu YusongTang JianfengDing ZhehengTeng ZenghuiLiu XueqingZhu HongtaoDing Zhaoping - Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiomyopathy. It follows an autosomal dominant inheritance pattern in most cases, with incomplete penetrance and heterogeneity. It is familial in 60% of cases and most of these are caused by pathogenic variants in the core sarcomeric genes (, , , , , , , ). Genetic testing using targeted disease-specific panels that utilize next-generation sequencing (NGS) and include sarcomeric genes with the strongest evidence of association and syndrome-associated genes is highly recommended for every HCM patient to confirm the diagnosis, identify the molecular etiology, and guide screening and management. The yield of genetic testing for a disease-causing variant is 30% in sporadic cases and up to 60% in familial cases and in younger patients with typical asymmetrical septal hypertrophy. Genetic testing remains challenging in the interpretation of results and classification of variants. Therefore, in 2015 the American College of Medical Genetics and Genomics (ACMG) established guidelines to classify and interpret the variants with an emphasis on the necessity of periodic reassessment of variant classification as genetic knowledge rapidly expands. The current guidelines recommend focused cascade genetic testing regardless of age in phenotype-negative first-degree relatives if a variant with decisive evidence of pathogenicity has been identified in the proband. Genetic test results in family members guide longitudinal clinical surveillance. At present, there is emerging evidence for genetic test application in risk stratification and management but its implementation into clinical practice needs further study. Promising fields such as gene therapy and implementation of artificial intelligence in the diagnosis of HCM are emerging and paving the way for more effective screening and management, but many challenges and obstacles need to be overcome before establishing the practical implications of these new methods. - Source: PubMed
Publication date: 2024/03/19
Abbas Mohammed TiseerBaba Ali NimaFarina Juan MMahmoud Ahmed KPereyra MilagrosScalia Isabel GKamel Moaz ABarry TimothyLester Steven JCannan Charles RMital RohitWilansky SusanFreeman William KChao Chieh-JuAlsidawi SaidAyoub ChadiArsanjani Reza - - Source: PubMed
Publication date: 2024/02/15
Liu HuiyiHan XiaoningChu SongyunMa WeiDing WenhuiLi JianpingJiang Yimeng - Yudong black goats (YDGs) are a local breed in southwest China that possess unique meat qualities and produce a high meat yield, making them ideal models for studying goat meat quality. Castration may decrease off-odors, significantly change metabolites and improve meat quality. Using multi-omics techniques, this study focused on Yudong black goat wethers (YDW, n = 4) and Yudong black bucks (YDB, n = 4). The findings revealed that 33 differentially expressed genes (DEGs) and 279 significantly changed metabolites (SCMs) influenced goat meat quality by affecting fat accumulation and lipolysis regulatory processes. Herein, several candidate genes (, , , and , etc.) were identified that play a role in regulating meat quality, non-castrated and castrated, alongside a series of metabolites that may serve as potential meat quality biomarkers. Lipids (triglycerides, oxidized lipids_5-iso PGF2VI, ceramide (t18:1/36:2(2OH)) and Carnitine C20:5, etc.) were significantly higher in the castrated goats. These results revealed that lipids and hydrophilic metabolites were affected by castration, which might be beneficial in terms of goat meat quality. This study aimed to investigate the differences in meat quality between uncastrated and castrated male goats and the possible molecular regulatory mechanisms. - Source: PubMed
Publication date: 2023/12/27
Yang SongjianZhang XinyueLi XingchunZheng JikangZhao LeFan ChengliZhao Yongju