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)
- Holt-Oram syndrome (HOS) is a rare autosomal-dominant genetic disorder caused by mutations in the TBX5 gene. It is characterized by skeletal abnormalities of the upper limbs and congenital heart defects, most frequently atrial septal defect (ASD) and ventricular septal defect. Middle-aged individuals often develop conduction disorders and atrial arrhythmias, most commonly atrial fibrillation and atrial flutter, while focal atrial tachycardia (AT) remains relatively rare. We present the successful catheter ablation of a right anteroseptal focal AT in a patient with HOS and a history of surgical ASD closure. - Source: PubMed
Publication date: 2026/08/18
Kojić DejanRadunović AnjaBožović-Ogarević SladjanaIlić IvanNiković VukTomović MilosavBojić Milovan - Skeletal muscle growth in poultry depends on the proliferation and differentiation of skeletal muscle satellite cells (SMSCs), yet the regulatory landscape governing these processes in quail remains poorly defined. In this study, primary SMSCs were isolated from embryonic day 15 quail pectoral muscle and validated by PAX7 immunostaining and MYHC immunostaining following induction of differentiation. rRNA-depleted RNA-seq was performed at three developmental stages: satellite cells after differential adhesion (DA), proliferating myoblasts (GM), and differentiated myotubes after 4 d (DM4). Transcriptome profiling identified 9,728 common genes expressed in three group, with 1,254 genes differentially expressed across all pairwise comparisons. Functional enrichment analyses indicated a coordinated shift from cell cycle progression in proliferating cells to muscle contraction, oxidative phosphorylation, and calcium signaling during differentiation. Short time-series expression miner (STEM) analysis revealed distinct temporal expression patterns, highlighting proliferation-associated regulators (e.g., KDR, PIK3R1, MYF5, MYF6, NOTCH1, and WNT2) and myotube-related genes (e.g., ALDH18A1, HOXC8, TBX5, and EN1) as central nodes within stage-specific networks. In addition, 935 lncRNAs and 13,588 circRNAs were detected, many displaying stage-specific expression patterns. Predicted lncRNA-mRNA interactions and circRNA host gene enrichment implicated these noncoding RNAs in muscle development and metabolic remodeling. A competing endogenous RNA network highlighted miR-466-x and novel-m0255-5p as potential post-transcriptional regulators of muscle-related genes, including VEGFA, HDAC4, MYLK4, and NOX4. These findings provide a comprehensive transcriptomic resource for quail myogenesis and identify candidate coding and noncoding regulators relevant to muscle growth in poultry. - Source: PubMed
Publication date: 2026/08/03
Liu JingJiang HongxiaXiao XiaoyunLiao ZurongWang YuxiangDing ZhenxvanChai XuewenLiu HaodongHuang XvwenWei WenhuaXie YunongLiu LuoyangWang ZikunHu XiaolongLiu SanfengChen BiaoMao Huirong - 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