TBX5 antibody - N-terminal region (ARP33403_P050)
- Known as:
- TBX5 (anti-) - N-terminal region (ARP33403_P050)
- Catalog number:
- arp33403_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- TBX5 antibody - N-terminal region (ARP33403_P050)
Related genes to: TBX5 antibody - N-terminal region (ARP33403_P050)
- Gene:
- TBX5 NIH gene
- Name:
- T-box 5
- Previous symbol:
- HOS
- Synonyms:
- -
- Chromosome:
- 12q24.21
- Locus Type:
- gene with protein product
- Date approved:
- 1997-05-22
- Date modifiied:
- 2019-04-23
Related products to: TBX5 antibody - N-terminal region (ARP33403_P050)
Related articles to: TBX5 antibody - N-terminal region (ARP33403_P050)
- Cardiac hypertrophy, characterized by an increase in the size of cardiac myocytes, is an adaptive response to increased workload on the cardiac tissue following physiological stimuli, such as exercise, and pathological conditions, such as hypertension or valvular heart disease. Typically, physiological hypertrophy induced by various exercise modalities leads to beneficial adaptations, such as improved contractile function and increased oxidative capacity. Understanding the molecular mechanisms underlying physiological cardiac hypertrophy is crucial for developing targeted therapeutic strategies. This review provides a comprehensive overview of current knowledge of physiological cardiac hypertrophy, with a particular focus on adaptations induced by various exercise modalities. We delved into the potential cellular and molecular pathways involved in physiological hypertrophy including IGF1/PI3K/AKT, angiotensin2, hepatocyte growth factor, platelet-derived growth factor. MAPK/ERK cascade, calcineurin, Neurogelin2 and downstream transcriptional factors such as HAND2, GATA4, MEF2, NKX2.5, TBX5, NFAT, c/EBPβ, CITED4, PHLPP, as well as the role of microRNAs (miRNAs) like miR-222 and miR-17 in mediating these adaptations. Furthermore, we used comparative tables to illustrate the differential effects of endurance, high-intensity interval training (HIIT), and resistance training on structural, molecular, and functional cardiac parameters, as markers of physiological hypertrophy. We also presented pathway-specific percentage changes observed across different exercise training modalities to highlight key differences. The discussion integrated these findings to explore translational perspectives and to offer the most beneficial exercise training schedules that induce physiological hypertrophy. - Source: PubMed
Publication date: 2026/03/31
Gharaat Mohammad AliSheykhlouvand MohsenChoobdari Hamid RezaSuzuki KatsuhikoArazi Hamid - Early heart development involves heart tube elongation, looping, and axial patterning, yet these processes remain difficult to study experimentally. While pluripotent stem cell-derived heart organoids model cardiomyocyte differentiation, they do not recapitulate early morphogenetic events. Here, we generate elongating heart organoids (EHOs) from human induced pluripotent stem cells that undergo coordinated elongation and looping-like curvature, resembling early cardiac morphogenesis. EHOs establish a venous-to-arterial axis with spatially organized sinus venosus-like, atrial, and ventricular cardiomyocytes, and exhibit sequential propagation of contractile activity along this axis. Single-cell transcriptomics and trajectory analyses, together with pulse-labeling, support a model in which progressive incorporation of cardiac cells from proliferative splanchnic mesodermal cells at the venous pole drives elongation of the cardiac structure. Consistent with in vivo phenotypes, TBX5 deletion results in shortened EHOs with reduced looping-like curvature and irregular contractions. Together, EHOs provide a human in vitro system that enables investigation of early cardiac morphogenesis. - Source: PubMed
Publication date: 2026/08/11
Lee JinwooKim AhriJeong YideulChoi EugeneKim Tae YoungNabukenya MariamKim DaesikLee JaecheolBae Gyu-UnKang Jong-Sun - Temperature critically regulates early development in fish, yet the cellular and molecular mechanisms underlying cold-induced developmental disruption in fish remain poorly defined. Here, we investigated the effects of graded low-temperature exposure on zebrafish embryonic and larval development using integrated organismal, cellular, and molecular analyses. We generated EGFP-transgenic zebrafish to enable direct in vivo fluorescence visualization and evaluation of multiple organs. Wild-type and EGFP-labeled embryos were reared at 28 °C (control) or reduced temperatures (22 °C, 16 °C). Fluorescence imaging showed 22 °C caused developmental delay, reduced growth, impaired eye and cardiac development, and abnormal caudal vein morphology, while 16 °C induced severe developmental arrest and early lethality. At the molecular level, low temperature suppressed growth and cardiac-related genes (igf1, nkx2.5, gata4, tbx5) and upregulated inflammation-, proapoptosis- and antioxidant-related genes (tnfa, il1b, bax, sod1), with concurrent reduced mitochondrial membrane potential indicating impaired mitochondrial function. Collectively, low temperature disrupts zebrafish embryogenesis via coordinated effects on growth signaling, stress responses, and mitochondrial function. These findings link environmental temperature stress to altered gene expression and cellular phenotypes during early zebrafish development, providing insights into mechanisms of cold-induced developmental disruption in this model. - Source: PubMed
Publication date: 2026/08/11
Wang XiaoshuaiXu NanaZhu AoLi ZixinZhang HuiliYang SiruiLiu ZaizeZhang JieRao Wei - Appendage degeneration is a notable morphological feature of some teleosts with specialized benthic lifestyles. The half-smooth tongue sole (Cynoglossus semilaevis) undergoes severe pectoral fin regression during metamorphosis. However, the molecular basis underlying rapid pectoral fin degeneration remains unclear. Here, we performed time-series transcriptome sequencing on pectoral fins at pre-metamorphosis, metamorphosis peak and post-metamorphosis to characterize the molecular changes associated with pectoral fin degeneration. Transcriptional dynamics and functional enrichment showed that no significant enrichment of classical apoptosis-related transcriptional pathways was detected during pectoral fin degeneration. Instead, sustained downregulation of twist1b, identified as a transcriptomic candidate, together with significant upregulation of ssh1, coupled with enrichment of lysosome and ubiquitin-proteasome system (UPS) pathways, suggested enhanced tissue remodeling during pectoral fin degeneration. Temporal expression clustering revealed heterochronic misalignment in the developmental gene expression: upstream initiator tbx5 was upregulated at early metamorphosis, while downstream maintenance signal fgf10 decreased synchronously. Distal patterning gene hoxd12a exhibited premature expression and rapid decay, losing sustained late-phase expression. Moreover, transient elevation of gli3 during metamorphosis may contribute to restricted distal fin growth. We conclude that pectoral fin degeneration in C. semilaevis is associated with heterochronic disruption of developmental signaling and extensive tissue remodeling. This study provides transcriptomic insights into pectoral fin degeneration in tongue soles and establishes a basis for future functional studies of appendage reduction in teleosts. - Source: PubMed
Publication date: 2026/07/20
Yang YifeiHuang JinxinFu XiangxiangCai YanxiangZha HouyangLiu LiqinLi FenghuiLiu JingZhu DenghuiLü ZhenmingGong Li - Dosage-sensitive transcription factors (TFs) underlie altered gene regulation in human developmental disorders, and cell type-specific gene regulation is linked to the reorganization of three-dimensional (3D) chromatin during cellular differentiation. In this work, we show dose-dependent regulation of chromatin organization by the congenital heart disease (CHD)-linked, lineage-restricted TF TBX5 in human cardiomyocyte differentiation. Genome organization, including compartments, topologically associated domains, and chromatin loops, was sensitive to reduced dosage in a human model of CHD, with variations in response across individual cells. Cohesin binding was reduced at TBX5-bound enhancer elements in a TBX5 dose-dependent manner, providing a potential mechanism for disrupted loop formation. These results highlight the importance of lineage-restricted TF dosage in cell type-specific 3D chromatin dynamics, suggesting a mechanism for TF-dependent disease. - Source: PubMed
Publication date: 2026/07/23
Grant Zoe LKuang ShuzhenZhang ShuHorrillo Abraham JChen ZheRao Kavitha SCelen CemreKameswaran VasumathiJoubran CarineLau Pik KiDong KeyiYang BingBartosik Weronika MZemke Nathan RRen BingSrivastava DeepakKathiriya Irfan SPollard Katherine SBruneau Benoit G