TBX5 antibody - N-terminal region (ARP33403_T100)
- Known as:
- TBX5 (anti-) - N-terminal region (ARP33403_T100)
- Catalog number:
- arp33403_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- TBX5 antibody - N-terminal region (ARP33403_T100)
Related genes to: TBX5 antibody - N-terminal region (ARP33403_T100)
- 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_T100)
Related articles to: TBX5 antibody - N-terminal region (ARP33403_T100)
- The developing vertebrate forelimb expresses seven T-box transcription factors, with several in overlapping expression domains. All T-box transcription family members share similarity within their DNA binding domain, the T-domain. Outside of the T-domain, these factors share little similarity, allowing family members to have different transcriptional properties and binding partners. Several human T-box genes show haploinsufficiency in the limb, including Tbx5 and Tbx3 that, when mutated, cause Holt-Oram and ulnar-mammary syndrome, respectively. This dosage sensitivity combined with the shared T-domain leads to our hypothesis that when co-expressed a competition between T-box factors at target genes can occur. To test this, we ectopically expressed two exogenous T-box factors, T and Tbx6, in the developing forelimb mesenchyme to examine how artificially changing the relative levels of T-box proteins affects forelimb formation. Skeletal, apoptotic, and gene expression assays were used to characterize the resulting phenotypes. While ectopic T and Tbx6 both affected the size and shape of the forearm bones and ossification, they differentially affected digit formation: T caused loss of digits and Tbx6 led to phalange bone duplications and extra digit formation. These dissimilar phenotypes suggest that these transcriptional activators differentially affect pathways critical for regulating forelimb development. - Source: PubMed
Denhart Mariah HChapman Deborah L - Sirtuin 1 () is known to regulate stem cell differentiation and cardiomyocyte function, yet its specific role and mechanism in human embryonic stem cell (hESC) differentiation into cardiomyocytes remain unclear. This study aimed to elucidate the functional contribution and molecular pathway of in cardiomyogenesis. : A knockout (/) hESC line was generated using CRISPR-Cas9 technology. The expression of key differentiation markers was analyzed by RT-qPCR at days 6, 8, and 9. The underlying mechanism was investigated through integrated RNA-sequencing (RNA-seq) analysis and dual-luciferase reporter assays. : deletion significantly downregulated the expression of mesodermal (TBX6, KDR), cardiac precursor (NKX2.5, TBX5), and mature cardiomyocyte (cTNT, Hand2) markers. Mechanistically, a competing endogenous RNA (ceRNA) axis, LncRNA XR_951230.1/miR-3663-3p/SMYD1, was identified. knockout reduced XR_951230.1 expression, which consequently elevated miR-3663-3p activity and suppressed its target gene SMYD1. : These findings indicate that is essential for promoting hESC differentiation into cardiomyocytes, potentially via the XR_951230.1/miR-3663-3p/SMYD1 pathway. This study provides new insights into the regulatory network of stem cell-based cardiomyogenesis and suggests potential targets for stem cell-based cardiac disease therapy. - Source: PubMed
Publication date: 2026/02/27
Li ChengyuMahemuti MairepatiMaimaiti YusupujiangWang TingZhang XinJiapaer Zeyidan - The natriuretic peptides A and B, encoded by and , respectively, have complementary and redundant functions in cardiovascular homeostasis. To establish their coordinated roles, we analyzed the cardiac phenotype of a mouse line in which the was deleted from the genome. At 8 weeks of age, mice (HOM) had significantly larger hearts and cardiomyocytic hypertrophy compared to wild-type and heterozygous mice. Electrocardiogram comparisons showed QRS prolongation in HOM mice. Hypertrophy was confirmed by echocardiography, which further indicated preservation of left ventricular systolic function. Bulk-transcriptomic analysis revealed moderate changes in gene expression of the left ventricle. Genes involved in fatty acid metabolism, ion handling and conductivity, including genes marking the ventricular conduction system, were down-regulated. Spatial transcriptomic analysis revealed the greatest changes in gene expression in the subendocardial wall, where the ventricular conduction system is located. , the encoding dosage-sensitive T-box transcription factor Tbx5 that is essential for the expression of ventricular conduction system genes and for and , was down-regulated in the ventricles of HOM mice, indicating that a positive feedback loop normally maintains expression. We conclude that homozygous deficiency in mice causes cardiac hypertrophy, including a likely perturbation of the ventricular conduction system. - Source: PubMed
Publication date: 2026/03/06
Giovou Alexandra EMulleners Otto JGünthel MarieMan Joyce C KJensen BjarkeGladka Monika MChristoffels Vincent M - Holt-Oram syndrome, also known as atrio-digital syndrome, is a rare autosomal dominant genetic disorder primarily characterized by upper limb malformations and congenital heart defects, associated with mutations in the TBX5 gene. Diagnosis is typically based on clinical presentation, and the prognosis for affected individuals is closely related to the severity of cardiac involvement. Our study aims to highlight some key features of Holt-Oram syndrome to improve the level of clinical diagnosis. - Source: PubMed
Publication date: 2026/03/01
Liu XuechenYang LeiCui JianLiao MengqianHou ZonghuiZhao MengqiWang Lianyi - Fate-mapping studies have challenged the longstanding view of the adult mammalian heart as a post-mitotic organ, suggesting limited cardiomyocyte renewal. This has spurred efforts to determine whether selected cardiac stromal cells have regenerative potential; however, their contribution to cardiac regeneration has been found to be minimal compared with that of cardiomyocyte proliferation. Despite this, transplantation of some cardiac stromal cell populations has shown therapeutic potential through paracrine signalling. The identity of the paracrine-active stromal cell populations remains unclear due to overlapping characteristics with other cardiac stromal cell populations, such as fibroblasts, mesenchymal cells, and pericytes. This study sought to clarify the transcriptional identity and heterogeneity of adult mouse cardiac stromal cells by developing a cardiac collagenase-trypsin protocol and comparing it to the established method for isolating cardiosphere-derived cells (CDCs). This novel protocol resulted in a higher cell yield and shorter expansion time, and the resulting cells showed superior survival under serum starvation compared to commercially acquired cardiac fibroblasts (CFs). Single-cell qRT-PCR analysis revealed that collagenase-trypsin cells (CTs) and CDCs share similar gene expression profiles, distinct from those of CFs. Notably, CTs exhibited higher expression of and lower expression of , suggesting an epicardial-derived fibroblast phenotype, whereas was enriched in CDCs and CFs, reflecting heterogeneity within the cardiac fibroblast compartment. This study offers insights into the complex identity of cardiac stromal cells and concludes that CTs closely resemble CDCs but can be generated more rapidly, making them a robust and efficient source of paracrine-active cardiac stromal cells. - Source: PubMed
Publication date: 2026/02/23
Alonaizan RitaChaves-Guerrero PatriciaSamari SaraNoseda MichelaSmart NicolaCarr Carolyn